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EDITORIAL
Year : 2011  |  Volume : 59  |  Issue : 4  |  Page : 504-505

Chronic encapsulated intracerebral hematoma


Department of Neurosurgery, Apollo Specialty Hospital, Tamil Nadu, India

Date of Submission13-Jul-2011
Date of Decision17-Jul-2011
Date of Acceptance17-Jul-2011
Date of Web Publication30-Aug-2011

Correspondence Address:
K Ganapathy
Department of Neurosurgery, Apollo Specialty Hospital, 320 Anna Salai, Chennai-600 035, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.84327

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How to cite this article:
Ganapathy K. Chronic encapsulated intracerebral hematoma. Neurol India 2011;59:504-5

How to cite this URL:
Ganapathy K. Chronic encapsulated intracerebral hematoma. Neurol India [serial online] 2011 [cited 2019 Dec 14];59:504-5. Available from: http://www.neurologyindia.com/text.asp?2011/59/4/504/84327


Chronic encapsulated intracerebral hematoma (CEIH) is a rare condition first described by Hirsh [1] in 1981. Two years later Takahashi [2] reported a chronic multilocular encapsulated intracerebral hemorrhage (ICH), parts of which were liquid, xanthochromic, semisolid and solid. Since then about 60 cases have been documented worldwide, mostly from Japan. Affecting all age groups, clinical symptoms progress slowly, over a long period, suggesting a low-grade neoplasm. Traditionally, intracerebral hemorrhage is thought of when there is a hyper-acute dramatic onset of neurological deficit. In a non-traumatic clinical setting one does not immediately include CEIH in the differential diagnosis, even in a contrast-enhancing encapsulated Intracranial space occupying lesion (ICSOL) containing blood. There are no imaging features pathognomonic of CEIH. In fact they are often misleading. While computed tomography (CT) and magnetic resonance imaging (MRI) may indicate the presence of blood in different states, peripheral ring enhancement often leads one to think of more common conditions like metasatic deposits, gliomas or even brain abscess, particularly when there is mass effect and perifocal edema. It is unusual for such an SOL to contain a cavernous angioma or a residual arteriovenous malformation (AVM). Even when there is a history of previous treatment of a vascular anomaly, as in the case reported [3] angiography may be inconclusive. A definitive diagnosis of CEIH is normally made only at surgery.

Operative findings include finding a thick, fibrous capsule consisting of an outer layer of dense collagenous tissue and an inner layer of granulation tissue enclosing old and recent areas of hemorrhage possibly due to the rupture of vessels near the inner surface of the thickest part of the fibrous capsule. The mechanism of capsule formation and self-perpetuating expansion still remains uncertain, as is the causal relationship with vascular malformations. Occasionally, the fibrous capsule has been found histologically to arise from an occult angiomatous malformation or a cavernous angioma. It has been suggested that repeated subclinical hemorrhages could mask the macroscopic evidence of a cavernous angioma or vascular malformation. Detailed histological study of CEIH is therefore necessary.

In this [3] first report from South Asia, the CEIH appears to be causally related to the original AVM. The relationship of the CEIH to embolization, and radiosurgery is probably fortuitous, rather than causal, though there is a suggestion that radiation could stimulate the production of vascular endothelial growth factor (VEGF) promoting angiogenesis. The authors have mentioned the high prevalence of a residual nidus in CEIHs following radiosurgery for cerebral AVMs. The authors have also suggested at least 10 years' careful follow-up following radiosurgery for AVM. How common or rare is CEIH following stereotactic radio surgery (SRS) for AVM? It is unlikely that we will ever be able to quantify the true incidence and prevalence of these uncommon conditions due to incomplete follow-up - particularly long-term. Most of these delayed 'complications' are seen even 15 to 20 years after SRS and often are not overtly symptomatic. Lundsford [4] is of the opinion that there is a 1% lifetime risk of hemorrhage in an AVM treated with radiosurgery, despite documentation of total obliteration. Does it mean that follow-up should be lifelong? Are we justified in creating a possible fear psychosis in a patient, by discussing uncommon, delayed, long-term, possibly innocuous, conditions which could theoretically occur? The Supreme Court of India has opined that a doctor should use his discretion and judgment before discussing the "rarest of the rare" complications, which could occur after a procedure, lest the patient be frightened into refusing treatment which is more important. At the same time should patients be forewarned so that they come for regular follow-up? From a pragmatic view although the condition is uncommon, chronic encapsulated intracerebral hematoma needs to be considered in the differential diagnosis, when an encapsulated mass lesion is present in the brain.

 
  References Top

1.Hirsh LF, Spector HB, Bogdanoff BM Chronic encapsulated intracerebral haematoma. Neurosurgery 1981;9:169-72  Back to cited text no. 1
    
2.Takahashi N, Kikuchi H, Kobayashi K, Karasawa J Multilocular encapsulated intracerebral haematoma. No Shinkei Geka 1983;11:739-43.  Back to cited text no. 2
    
3.Takeuchi S, Takasato Y, Masaoka H. Chronic encapsulated intracerebral haematoma formation after radiosurgery for cerebral arteriovenous malformation. Neurol India 2011;59:624-6.  Back to cited text no. 3
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4.Lunsford D, Niranjan A, Kano N, Flickinger JC, Kondziolka D. Stereotactic Radiosurgery for Arteriovenous Malformations. In: Lunsford D, Sheehan JP, editors. Intracranial stereotactic radiosurgery. Stuttgart, Germany: Thieme; 2009.p.29-40.  Back to cited text no. 4
    



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