Armored Brain, Giant Calcified Chronic Subdural Hematoma, in 97-Year-Old Patient: Systematic Review

Abstract

Calcified chronic subdural hematoma (CCSDH) is a rare neurosurgical entity. Due to limited reported cases, its diagnosis and management remain poorly understood. This study aims to enhance the understanding of CCSDH and improve familiarity with its clinical presentation, imaging features, and treatment strategies. A comprehensive search was performed using PubMed, Scopus, DOAJ (Directory of Open Access Journals), BASE (Bielefeld Academic Search Engine), and ScienceDirect with the keyword “calcified chronic subdural hematoma,” without date restrictions. Out of 354 articles initially identified, 163 unique records remained after merging duplicates. Following abstract and full-text screening, 76 articles describing 93 cases were included. One additional case from our institution was added, resulting in 94 cases reviewed. The average patient age was 41.88 years, with a strong male predominance (sex ratio 4.53). No past medical history was noted in 24 cases; ventriculoperitoneal shunt was present in 33 cases. While 14% were asymptomatic, 34% presented with intracranial hypertension, 12.5% with altered consciousness, 33% with motor deficits, and 25.5% with seizures. Bilateral CCSDH was observed in 21 patients, totaling 115 hematomas. Imaging showed: capsule-only calcification (52%), total (28%), or partial (20%) calcification. Hematoma shapes were biconvex (37%), concave (29%), bean-like (20%), irregular (7%), and thin lamina (6%). Computed tomography (CT) was used in 90.5%, and magnetic resonance imaging in 43.6%. Twenty-seven were visible on plain X-ray. Twenty cases were managed conservatively; two later required surgery. About 70 surgical procedures were performed: 60 via craniectomy, 9 burr holes procedures, and 1 via twist drill. Outcomes were favorable in 75% of conservatively treated cases and 87.5% of craniectomy cases. Six surgical deaths occurred. CCSDH primarily affects young males, often with a history of shunting. CT remains the imaging modality of choice. Conservative treatment is suitable for noncompressive, asymptomatic cases, while surgical evacuation via craniectomy offers the best outcomes when intervention is required.

 

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Keywords

armored or armored brain - calcified subdural hematoma - chronic subdural hematoma - calcified empyema - epilepsy

Introduction

The first mention of calcified chronic subdural hematoma (CCSDH) in the literature dates back to the 19th century, by von Rokitansky in 1844.[1] Years later, Rudolf Virchow was the first to associate chronic subdural hematoma with an inflammatory process. He coined the term “pachymeningitis hemorrhagica” in 1857, reflecting his belief that the condition was primarily inflammatory. CCSDH has been described in the literature as “Armored brain”[2]; “Armoured brain”[3]; “Matrioska head”[4]; or “Double skull.”[5] We report a case of a nonagenarian patient who, we believe, is the oldest case of CCSDH reported in the literature. Additionally, we conduct a comprehensive literature review on this rare pathology to understand its biological, clinical, paraclinical, and therapeutic aspects.

 

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Case Report

History and Examination

The patient is a male of 97-year-old with a past medical history of ischemic stroke 5 years prior and a femur fracture that was operated on years before. Two months ago, the patient experienced cranial trauma without immediate consequences. The patient presented 24 hours before admission with a consciousness disorder. At admission, the patient was drowsy, scored 13/15 on the Glasgow Coma Scale, and had right hemiparesis rated ⅗. Pupils were isochoric and reactive. Osteoarticular reflexes were exaggerated, with a positive Babinski reflex on the right side. There was no sensory deficit, but generalized muscle atrophy was noted. Laboratory tests revealed no abnormalities.

 

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Imaging Findings

A brain computed tomography (CT) scan revealed a left hemispheric hyperdense, heterogeneous subdural hematoma, surrounded by a hyperdense, calcified thick capsule. The lesion was bean-shape 34 mm in thickness ([Fig. 1]). No further imaging was needed.

Fig. 3 Flowchart of study selection process.

Fig. 1 A preoperative brain computed tomography (CT) scan revealed a totally calcified frontoparietal subdural hematoma in a bean-like shape. (A) The upper level of the hematoma and (B) the lower level.

 

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Surgical Procedure

The patient was operated on under general anesthesia and orotracheal intubation. A frontoparietal bone flap and a U-shaped dural opening were performed, exposing the outer membrane. Once the outer membrane was excised, the hematoma was exposed. It was a brown, chocolate-colored solid matter with the consistency of “leather-hard clay” ([Fig. 2]). It was removed using a freer to cut it into pieces until the inner membrane was exposed. The inner membrane was unexpectedly thicker than the dura and adhered closely to the cortex surface, where superficial veins were hypotrophic. Therefore, further membrane excision was avoided. Once the hematoma was evacuated, the large cavity was filled with normal saline, and closure was performed in the usual fashion. The patient was extubated and regained consciousness promptly in the operating room.

Fig. 2 A piece of the hematoma with a leather-hard clay aspect (the arrow).

 

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Postoperative Course

Postoperatively, the patient showed improvement in motor function but no significant change in his deteriorated mental status. At his last follow-up appointment 2 months after surgery, he maintained an acceptable clinical condition: alert, noncooperative, but moving his limbs spontaneously. His family was satisfied with his condition and chose not to seek further consultation unless notable worsening occurred.

 

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Literature Review

A comprehensive search was conducted in PubMed, Scopus, DOAJ (Directory of Open Access Journals), BASE (Bielefeld Academic Search Engine), and ScienceDirect to retrieve journal articles using the keywords “calcified chronic subdural hematoma.” There were no date restrictions applied during the search. In total, 354 articles were identified: 97 in PubMed, 122 in Scopus, 13 in DOAJ, 81 in BASE, and 41 in ScienceDirect (where the keyword was put in quotation marks). All records were imported into an online version of EndNote, where duplicates were merged, resulting in 163 unique records. A total of 138 abstracts were screened (25 records had no abstract). Twenty-four articles were excluded after abstract screening: 14 not focusing on CCSDH, 3 comments, 5 with no cases, 1 with spinal CCSDH, and 1 veterinary case. There was no full text available for 18 articles. Ninety-six full texts were screened. Twenty articles were excluded after screening the full text: 7 in Japanese, 3 in Spanish, 3 in Turkish, 1 in German, 1 where the hematoma was not calcified, 2 with epidural hematoma, and 3 with no cases. One case of a calcified subdural hygroma was included, as the authors who managed the case believed it was originally a subdural hematoma. Another case of postsurgery cerebellopontine angle calcified subdural hematoma was included. In total, 76 articles were added to this review, describing 93 cases. Five cases of subdural empyema were not excluded from this study because they were considered more as complicated preexisting subdural hematomas (admitted in a noninfectious state, presence of trauma, or ventriculoperitoneal [VP] shunt). Additionally, the clinical case of a patient managed by our team, which we believe is directly relevant to this review, was presented and included. As a result, a total of 94 cases were included in this study ([Table 1, Fig. 3]). The initial literature search was conducted by one author. Data extraction and full-text assessment were performed independently by two authors. There were no notable disagreements during this process. Final inclusion decisions were based on seniority and academic consensus, with deference to academic rank when needed (resident, assistant professor, professor). This study was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA)[6] statement from 2009. However, the protocol for this systematic review was not registered ([Supplementary Material], available in the online version).

Table 1 Summary of reviewed cases

Authors	Year	Gender	Age		Management	Outcome
Arseni and Iacob[29]	1970	F	22		Craniotomy	Improvement
Norman and Dubowy[30]	1971	M	47		Conservative	Seizures controlled by treatment
Ludwig et al[31]	1983	M	34		/	/
	1983	F	37		/	/
	1983	F	3		/	/
	1983	F	8		/	/
	1983	M	18		/	/
Matsumura and Noriji[1]	1984	M	77		Conservative	Stable
Spadaro et al[32]	1986	M	11		Conservative	/
Yamashida et al[14]	1987	M	75		Craniotomy	/
Ito et al[22]	1988	F	61		Craniotomy	Stable
Lunardi and Guidetti[33]	1988	M	37		Burr holes	/
Niwa et al[10]	1988	M	25		Craniotomy	Recidivism of a calcified hematoma
Hirakawa et al[13]	1989	F	59		Conservative then craniotomy	Uneventful
Kondoh et al[34]	1989	M	62		Craniotomy	Improvement
Yamada et al[3]	1992	M	22		Craniotomy	Transient aphasia and right hemiparesis then improvement
Ide et al[15]	1993	M	49		Craniotomy	Seizures occurred in the immediate postoperative period but subsided within one day. Discharged one month after surgery with improvement.
	1993	M	83		Conservative	Stable
	1993	M	78		Conservative	Died from trauma
Kulali et al[11]	1993	M	4		Craniotomy en bloc	Slow recovery
	1993	M	28		Craniotomy en bloc	Improvement
Sharma et al[35]	1999	M	10		Craniotomy	Improvement
	1999	M	9		Craniotomy	Improvement
Imaizumi et al[7]	2001	M	3		Craniotomy	Improvement
	2001	M	3		Craniotomy	Improvement
	2001	M	78		Craniotomy	Improvement
	2001	M	69		First burr hole then craniotomy	Failure of burr holes, then improvement after craniotomy
	2001	M	77		Craniotomy	Uncomplicated
Parc et al[20]	2003	M	37		Craniotomy	Improvement
Yang et al[36]	2004	M	59		Craniotomy	Improvement
He and Zhang[37]	2005	M	15		Craniotomy	Improvement
Kaspera et al[38]	2005	F	47		Craniotomy	Improvement
Dammers et al[39]	2006	M	67		First twist drill then craniotomy	Failure of twist drill, then improvement after craniotomy
Dimogerontas and Rovilas[40]	2006	M	43		Conservative	/
Hikawa et al[17]	2006	M	44		First burr hole the craniotomy	Failure of burr holes, then improvement after craniotomy
Per et al[41]	2006	M	4		Craniotomy	Improvement
Moon et al[28]	2007	F	47		Craniotomy	Deterioration from acute subdural hematoma. Reoperated then improved.
Amr et al[42]	2008	F	30		Conservative	Seizures controlled by treatment
Papanikolaou et al[43]	2008	M	33		Conservative	Stable
Galldiks et al[44]	2009	M	86		Burr holes	Improvement
Kasliwel et al[45]	2009	F	17		Craniotomy	Improvement
Pruna et al[46]	2009	F	26		Craniotomy	Improvement (continued anticonvulsant)
Babafemi et al[47]	2010	M	68		Craniotomy	Died 12 hours after surgery.
Marini et al[23]	2010	M	9		Mini craniotomy failed then craniotomy	Ischemia then improvement
Oda et al[8]	2010	F	32		Craniotomy	Improvement
Rao et al[48]	2010	M	75		Craniotomy	Improvement
Tatli et al[49]	2010	M	16		Craniotomy	Contralateral subdural hematoma operated; then improvement
Akhdar et al[50]	2011	M	7		Conservative	Seizures controlled by treatment
Petraglia et al[51]	2011	F	38		Conservative	Stable
Dagan et al[52]	2012	M	20		Conservative	Seizures controlled by treatment
Juan et al[53]	2012	M	10		Craniotomy	Improvement
	2012	F	35		Craniotomy	Improvement
Rahman et al[54]	2012	M	65		Craniotomy en bloc	Improvement
Sugita et al[9]	2012	M	77		Small craniectomy	/
Taha[2]	2012	M	12		Conservative	Seizures controlled by treatment
Tandon et al[5]	2012	F	54		Conservative	Seizures controlled by treatment
Garg et al[55]	2013	M	24		/	/
Goyal et al[56]	2013	F	15		Craniotomy	Improvement
Pappamikail et al[57]	2013	M	73		Craniotomy	Improvement
Salunke et al[58]	2013	M	15		Burr holes	Improvement
Cai et al[59]	2014	M	77		Craniotomy en bloc	Hemorrhage reoperated, kept deficit.
Djoubario et al[60]	2015	M	22		Conservative	Stable
Gupta et al[61]	2015	M	30		Craniotomy	Intubated for 5 days. Postoperative seizure then liberated
Li Xinwei et al[62]	2015	M	26		Craniotomy	Improvement
Seddiqui et al[12]	2016	M	30		Craniotomy en bloc	Improvement
Gosh et al[63]	2017	M	60		Craniotomy	Improvement
	2017	M	30		Craniotomy	Succumbed due to septicemia.
	2017	F	10		Craniotomy	Improvement
Haciyakupoglu et al[64]	2017	F	35		Craniotomy	/
	2017	M	58		Craniotomy	/
Li Huan et al[65]	2017	M	61		Burr holes two times then craniotomy	Transient Broca's aphasia, which fully resolved2weeks later
Xiao et al[66]	2017	M	62		Craniotomy	Encountered severe cerebral edema, then died
Chan and Gallo[67]	2018	M	/		Craniotomy	Improvement then died from glioblastoma.
Satyathree et al[68]	2018	M	8		Burr holes	Improvement
Viozzi et al[69]	2018	F	15		Conservative	Stable
Zhang et al[70]	2018	M	60		Craniotomy	Improvement
Ding et al[71]	2019	M	15		Conservative	Resolve of the hematoma and not calcifications
Liu et al[72]	2019	M	41		Conservative then craniotomy	Failure of conservative, improved after.
Prasard et al[73]	2019	M	50		Craniotomy en bloc	Died from intraparenchymal hematoma
Qin et al[74]	2019	M	58		Craniotomy	Stable
Turgut et al[75]	2019	M	59		Craniotomy	Pneumoencephaly operated then improvement
Bhadjway et al[76]	2020	M	25		Craniotomy	Improvement
Songnatsiri et al[18]	2020	M	83		Craniotomy en bloc	Takotsubo cardiomyopathy. Died from severe pneumonia
Sponko et al[21]	2020	F	81		Craniotomy	Improvement
Januarman and Parenrengi[77]	2021	M	20		Conservative	Improvement
	2021	M	18		Conservative	/
Pakrasi et al[26]	2021	M	75		Craniotomy	Died from pulmonary infection
Rong et al[16]	2022	M	46		Craniotomy en bloc	Improvement
Giroto and Gago[78]	2023	M	62		First burr hole the craniotomy	Failure of burr holes, then improvement after craniotomy
Mansour et al[27]	2023	F	34		Craniotomy en bloc	Improvement persistence of seizure
Tafera et al[79]	2023	M	84		Craniotomy	Improvement
Wang et al[80]	2023	M	69		Craniotomy	Improvement
Yadav et al[81]	2023	M	69		Craniotomy	Improvement
Our case	2024	M	97		Craniotomy	Improvement

Abbreviations: F, female; M, male.

 

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Results

Thirty cases were reported before 2004 and 64 cases were reported after 2004.

Nomination

The lesion was referred to as “calcified” in 84 cases (89.5%), “organized” in 7 cases (7.5%), and “ossified” in 3 cases (3%).

 

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Demographics

Cases were mostly reported from Japan (18), India (15), China (12), Germany (6), Turkey (7), Taiwan (3), and Italy (3). The ages ranged from 3 to 97 years, with an average age of approximately 41.88 years. The number of males was 77, and the number of females was 17, resulting in a sex ratio of 4.53.

 

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Past Medical History

No past medical history in 24 patients; VP shunt placement was noted in 33 cases, and 2 cases had subdural peritoneal shunts; cranial trauma in only 22 cases; 8 cases with brain infections (empyema, meningitis); 3 patients presented with craniocerebral neoplasms (2 glioblastomas, 1 skull angiosarcoma) and 1 lymphoproliferative disorder; only 1 case with coagulopathy; and neurofibromatosis type 1 in 2 cases.

 

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Clinical Findings

Clinical presentation was given in all patients. Thirteen cases were totally asymptomatic (14%); in 9 patients, the clinical presentation was related to other pathologies (glioblastoma, ruptured aneurysm, recent violent trauma, cerebellopontine angle tumor, meningitis, and cerebral palsy) (9.5%). Other symptoms were variable and present inconsistently from one patient to another: intracranial hypertension (headache, vomiting, disk anomalies, oculomotor palsy) was present in 32 patients (34%); 12 cases had impaired consciousness (12.5%); in 7 patients, this intracranial hypertension was complicated with vision impairment and papillary disk anomalies (7.5%); 31 patients had motor deficits (33%); 24 patients had seizures (25.5%); amnesia, personality behavior changes, cognitive disturbance, or even psychotic signs were present in 7 cases (7.5%); in 5 patients, there was urinary dysfunction (5.5%); gait disturbance and dizziness were present in 4 patients (4%); and one case had skull deformities, one case had tremor, one case had trigeminal neuralgia, and one case had polyuria and polydipsia.

 

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Radiologic Finding

All studied cases included a radiological description of the CCSDH using either simple X-rays, CT scans, or magnetic resonance imaging (MRI). In 21 cases, investigations found bilateral hematomas, resulting in 115 CCSDHs being studied. The amount of calcification was evaluated in 111 hematomas. Images were categorized as: totally calcified in 31 hematomas (28%) (total hyperdensity on CT, totally black on MRI, and/or total hyperclarity on X-rays); partially calcified in 22 hematomas (20%) (based on CT only); and only calcification of the capsule in 58 hematomas (52%) (based on CT only). The volume of the hematoma was grossly evaluated according to the shift effect in three categories: clearly compressive with a large shift effect in 73 patients (63.5%); causing focal compression in 30 cases (26%); and presenting as a thin blade in 12 cases (10.5%). The shape on the axial plane was evaluated in 113 hematomas: classic crescentic concave shape in 33 hematomas (29%); biconvex lentiform shape in 42 hematomas (37%); bean-like aspect in 23 hematomas (20%); irregular in 8 hematomas (7%); and thin lamina in 7 hematomas (6%). In 27 cases, a clear coronal slice was provided, with the shape being convex in 13 cases (48%), concave in 12 hematomas (44.5%), and irregular in 2 patients (7.5%) ([Fig. 4]).

Fig. 4 Chronic calcified subdural hematoma shapes on imaging (arrow): (A) concave crescentic (29%), (B) biconvex lentiform shape (37%), (C) bean-like aspect (20%), (D) irregular (7%), (E) thin lamina (6%).

 

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X-Rays

Twenty-seven hematomas (in 21 patients) were detected on simple X-rays. In one case, an X-ray was confirmed to have been performed but did not show the hematoma.

 

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CT

One hundred seven hematomas were identified using CT scans (in 85 patients). The density of calcification was measured in two cases: 480 Hounsfield units in the first case and 650 Hounsfield units in the other.

 

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MRI

Forty-one MRI descriptions were provided (in 35 patients). The signal was heterogeneous in 28 hematomas and homogeneous in 13 hematomas. T1 signal characteristics were reported for 34 hematomas (30 patients): it was hyperintense in 24 (70.5%), hypointense in 7 (20.5%), and isointense in 3 (9%). The T1 capsule signal was evaluated in 27 hematomas (24 patients): no identifiable capsule in 8 hematomas (29.5%), while a thin black egg-shell-like capsule was identified in 19 hematomas (70.5%). T2 signal characteristics were reported for 27 hematomas (22 patients): it was hyperintense in 4 hematomas (15%) and hypointense in 23 (85%). The T2 capsule signal was evaluated for 22 hematomas (18 patients): in 8 hematomas (36.5%), the signal was black and indistinguishable from the rest of the hematoma; in 12 hematomas (54.5%), there was a black signal surrounding the hematoma easily differentiated from the rest, and in 2 cases (9%), the capsule was hyperintense compared with the rest of the hematoma. Around the capsule, 20 hematomas (74%) were supposed to have a cerebrospinal fluid (CSF) plane with the parenchyma, indicated by a thin hyperintense signal; this plane was absent in 7 hematomas (26%). T2 echo gradient signal characteristics were reported for 4 hematomas (in 3 patients): it was hyperintense in 3 hematomas (75%) and hypointense in 1 (25%). The T2 echo gradient capsule signal was reported for 3 hematomas (in 2 patients): in all 3 hematomas (100%), there was a black signal surrounding the hematoma easily differentiated from the rest. Fluid-attenuated inversion recovery (FLAIR) images were provided for 4 hematomas (in 4 patients), and they were hyperintense in all 4 cases with a black capsule (100%). Gadolinium-injected sequences were provided for 5 hematomas (in 5 patients), revealing a peripheral rim enhancement on gadolinium administration in all 5 hematomas (100%).

 

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Other Diagnosis Modalities

Brain angiography was performed in 5 cases, all of which showed no specific abnormalities except for the shift effect. A radioisotope brain scan (99m Tc) was performed in one case, which showed no abnormal accumulation of the isotope.

 

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Management Options

In 6 cases, the management strategy was not clear. Twenty patients were managed conservatively, either with medical treatment for seizures or simple observation. In two cases, patients underwent surgery after the failure of conservative strategies. All other patients underwent initial surgery.

 

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Surgical Technic

In total, around 70 patients were operated on: 60 patients were initially managed with craniectomy, 9 patients were initially managed with burr holes, and 1 with a twist drill. The twist drill patient and 5 of the burr hole procedures s were reoperated on, with the hematoma being evacuated through bone flaps (one patient was operated on two times with burr holes before the craniectomy). Overall, around 66 patients were managed with craniectomy.

 

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Epilepsy Management

In the 24 patients with seizures, in one case, the management tool was not clear; 7 were managed with antiepileptic drugs; 10 were initially operated on due to the presence of supplementary intracranial hypertension signs or neurologic deficits in addition to seizures; in 3 patients, the hematoma was clearly compressive (according to the given images), so the patients were operated on initially; and in 5 patients, the hematoma exerted only focal compression with clinical presentation limited to seizures, but the surgeons opted for surgery.

 

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Peroperative Findings

Macroscopically, the hematoma was described as paste-like in 5 cases, mud-like in 14 cases, clay-like in 3 cases, coal-like in 4 cases, bone-like in 2 cases, fluid in 4 cases, and other aspects such as semisolid, cheese-like, and blood clot. The hematoma was described as gray in 5 cases, yellow in 9 cases, brown in 5 cases, and dark in one case.

 

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Outcome

Follow-up was provided in 80 cases, ranging from 10 days to 7 years, with an average of 16 months after surgery. In 20 patients managed conservatively, the outcome was not clear in three cases; one case died from polytraumatic complications; two were operated on; in the other cases, the outcome was summarized in the table. In operated patients, the only case managed with a twist drill failed. Five of the 9 burr holes procedures (8 patients) failed; in one case, the outcome was not clear (62.5% clear failure); and only three cases showed improvement with only burr holes (37.5% clear improvement). In the 66 cases managed with bone flap evacuation, the outcome was not clear in three cases. Forty-five patients (71.5%) improved initially after surgery or maintained tolerable clinical signs. There was a transient conscious disorder in one case, transient seizures in two cases, and transient neurologic deficits in three patients. Four patients were reoperated on: three for acute bleeding and one for pneumoencephaly. In the long term, 55 patients (87.5%) had a good outcome. Two patients remained dependent on antiepileptic drugs after surgery. Six patients died after surgery: two due to pulmonary infection, one from glioblastoma, one from postoperative septicemia, one from intraparenchymal hematoma, one from subdural hemorrhage, and one from severe cerebral edema.

 

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Discussion

While organized tissue can sometimes be associated with calcifications, the two are not inherently linked, and the presence of organized tissue does not necessarily mean calcifications will be present. Consequently, there is a lot of confusion in the literature regarding the difference between simply organized tissue and CCSDH. Therefore, the selection of cases was also based on the presence of calcification on imaging. In fact, in the seven cases where the authors referred to the hematomas as “organized,” they confirmed the presence of calcifications.[7] [8] [9] With the development of health care, particularly in neurosurgery, more cases of CCSDH are being discovered, and most cases were reported in the last 20 years. Based on our analysis, while Asia shows a significant proportion (over 53% of cases), the high p-value (0.963) indicates no statistically significant difference in pathology frequency compared with other regions. The 95% confidence interval (43.19–63.19%) suggests a broad range where the true proportion of cases in Asia likely falls, reflecting the global distribution observed. However, this sample suggests a higher proportion of males compared with females with a high degree of confidence (p-value < 0.001; sex ratio = 4.53), which can be easily compared with most traumatic pathologies where there is a higher frequency in the male population. The exact mechanism underlying calcification in chronic subdural hematomas remains uncertain. Many authors have suggested that a systemic predisposition to calcification, possibly due to metabolic factors, could be responsible.[10] Afra proposed that impaired circulation and absorption within the subdural space, along with vascular thrombosis, may contribute to the calcification process.[10] Interestingly, McLaurin and McLaurin[10] reported a case of bilateral hematomas in which calcification was present only on one side, suggesting that local factors may influence calcification. It is known that chronic inflammation can lead to the deposition of calcium salts, so most authors of the reviewed cases attribute the formation of hematoma calcifications to a similar process.[2] [7] [11] In some cases, metaplastic bone formation occurs, where fibroblasts within the hematoma differentiate into osteoblasts, leading to ossification.[12] Hyalinized fibrous tissue, calcifications, and fresh bleedings were noted in both inner and outer membranes.[3] [11] [13] [14] [15] [16] Membranes with well-developed sinusoidal blood vessels were noted in one case[17]; absent in two cases.[15] Membranes also contained hemosiderin-laden macrophages or hemosiderin[7] [13] [17] [18] and cholesterol, cholesterol clefts, or cholesterol crystals.[7] [11] [13] [19] The inner membrane had highly vascular granulation tissue tightly adhered to leptomeninges.[13] [20] [21] Osteoid tissue was present in the outermost layer.[15] The content of the mass was blood clot containing degenerated blood cells,[3] [22] mostly fibrin,[3] [7] and calcified areas.[3] [8] [23] Although a quarter of the patients presented no past medical history in this review, a third of the cases were under VP shunt, which largely influenced age distribution. In fact, while classic chronic subdural hematoma is considered a third-age pathology, less commonly seen in the young population, more than half of the reviewed cases were under 40 years old, and 66% were less than 60 years old ([Fig. 5]). In the second row after VP shunt, less than a quarter of the cases were declared to be victims of trauma, which could not eliminate the presence of a benign remote trauma. Otherwise, no other medical condition seems to be strongly related to CCSDH formation. The pathology could remain inexpressive for a long time, and a large part of the reviewed cases (23.5%) were either totally asymptomatic or presenting symptoms related to other pathologies. Despite this, the pathology evolves through an infinite cycle of chronic inflammation, fragile neovascularization, and bleeding. Outside of this cycle, more intracranial volume is occupied by granulomatous tissue, calcifications, and blood itself, causing increasing intracranial pressure (seen in more than a third of the reviewed patients) and even consciousness disturbances (in more than 12% of cases). The mass could cause focal compression resulting in motor deficits in a third of the patients and epilepsy in a quarter of the cases, as well as cognitive and psychotic disorders. In addition to cognitive signs, 5.5% of cases presented with urinary dysfunction, which could evoke an exaggerated micturition reflex similar to what is seen in stroke or normal pressure hydrocephalus,[24] especially with the presence of gait disturbance in 4% of the reviewed cases and some cases with cognitive disturbance (mimicking Hakim and Adams triad). The most iconic form of CCSDH calcification is presented with hematoma capsule calcification; indeed, more than half of the reviewed cases presented calcification limited to the capsule. However, calcification could also involve the hematoma inside, whether partially or, more frequently, totally. Although compressive CCSDH is the most seen form in our review, we think that less voluminous forms are underestimated due to asymptomatic undetected individuals. Typically, subdural hematoma is differentiated from epidural hematoma by its crescentic concave shape; paradoxically, in this review, the biconvex form of CCSDH is more frequently encountered in more than a third of the cases, followed by the concave form. When the hematoma spreads along the anteroposterior axis, it can resemble a bean or kidney shape, a form frequently seen in this review ([Figs. 1] and [4]). The CCSDH could present an irregular form or be limited to a thin lamina of two calcified superposed capsules. Although the diagnosis of intracranial calcification can be performed with simple X-rays, as in many cases of this review, this exam lacks specificity, and some cases of CCSDH are not detected. Thus, the value of simple X-rays is to prompt the physician to demand further investigation in asymptomatic patients with suspected intracranial calcifications. The superiority and specificity of brain CT in detecting calcifications is widely acknowledged.[25] Moreover, the rapidity and accessibility make brain CT the exam of choice in detecting CCSDH. On the Hounsfield CT scale, the radiodensity is very high, helping to differentiate bleeding from calcification in the case of CT hyperdensity. MRI is useful for diagnosis, providing supplementary information such as the presence of a dissectible plane with the brain and the density of the different compartments inside the hematoma. Wide variations in hematoma signal can induce confusions. Plus, in the same patient, both sides may not have the same intensity,[2] and inside the hematoma, the signal is—in most cases of this review—heterogeneous. Where given, the signal for the hematoma was mostly: hyperintense in T1 weighted imaging (WI), hypointense in T2 WI, hyperintense in FLAIR, and hyperintense in T2 echo gradient, with no enhancement inside the hematoma after gadolinium injection. For the capsule, the signal was mostly black in T1 WI, T2 WI, FLAIR, and T2 echo gradient, with enhancement after gadolinium injection. In some cases, the capsule is not distinguishable from the rest of the hematoma, especially in T2 WI (the black signal of the hematoma interferes with the black signal of the capsule). In most cases, we supposed the presence of a CSF plane with the parenchyma since a thin hypersignal is present in T2 sequences. Both angiography and radioisotope scans are not useful for diagnosis and lack sensitivity and specificity. Management options include observation, medical treatment for seizures, and surgery. Simple observation seems a good option for asymptomatic patients with noncompressive hematomas, with surgery reserved for these patients in case of deterioration. In patients with isolated seizures without clear brain compression, management with anticonvulsant drugs provides relief in most cases; in fact, most patients where medical treatment was judiciously indicated reported improvement. Furthermore, some patients remained dependent on anticonvulsants even after surgery. For patients with signs of intracranial hypertension, neurologic deficit, failure of medical treatment, or clearly compressive hematoma on imaging, surgery is indicated. Most patients operated on with twist drill or burr holes failed. Small skull openings will limit evacuation of the hard, organized hematoma, making burr holes or twist drill nonfavorable surgical options. The majority of patients operated on with bone flap improved after surgery; some transient complications, such as seizures or neurologic deficits, could occur. Other complications could lead to reoperation, such as intracranial bleeding or pneumocephalus. Unfortunately, some of these complications could be fatal, such as brain edema and intraparenchymal hemorrhage. Some technical points through this review must be noted. First, poor exposure results in suboptimal removal; the surgeon must expect a hard, brown, gray, or yellowish bone-like, mud-like, clay-like, or coal-like matter that does not get through the skull opening either by washing or by section. Second, some authors of this review preferred en bloc rather than stepwise resection[11] [26]; we think that such a maneuver carries supplementary risk unless the hematoma is ossified or hardly solidary,[27] where cracking it carries more risk. Dissecting the inner membrane could hold a risk of injury to pial vascularization, and leaving some pieces of the inner membrane is advised if attached to the pial surface to prevent brain edema or even brain herniation through a tear of the internal calcified membrane into the subdural cavity.[23] Finally, the brain likely will not return immediately, so the surgeon must fill the space with normal saline.[10] [28]

Fig. 5 Graphical representation of the age distribution of reviewed cases of calcified chronic subdural hematoma.

 

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Conclusion

CCSDH is a rare pathology with global distribution that predominates in young males, caused by calcium deposits during chronic inflammation. It is most commonly seen in patients with a history of VP shunt rather than those with notable cranial trauma. In most cases, CCSDH is asymptomatic or presents with signs of increasing intracranial pressure, deficits, or more specifically, seizures. On imaging, the extent of calcification varies from being limited to the capsule to a totally calcified or ossified hematoma. CCSDH is mostly diagnosed in a compressive form. The hematoma is mostly convex or bean-shaped; the classic crescentic concave shape is less common. CCSDH can be detected on simple X-rays, but CT, due to its rapid accessibility and superiority in detecting calcification, is considered the exam of choice. MRI, although sensitive and useful for diagnosis, can cause some confusion due to the wide variety of signal changes. CCSDH can be distinguished from other calcified intracranial conditions on imaging first by its extra-axial location, then by the calcification limited to the hematoma membrane in most cases. For partially or totally calcified hematomas, the concave or kidney shape can help differentiate it from other lesions. Unfortunately, the more commonly seen biconvex shape may lead to misdiagnosis with a calcified epidural hematoma. Observation or medical treatment is preferred in asymptomatic cases or in patients with isolated seizures and noncompressive hematoma. Otherwise, surgery is performed, and the hematoma is evacuated through a sufficiently exposed bone flap to remove the hard encapsulated tissue. The outcome is generally good, but some serious complications have been reported that could lead to death. Thus, surgeons must be careful in removing the lesion, and pieces of the internal capsule should be left if tightly adherent to the pial surface.

 

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Conflict of Interest

None declared.

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Artikel online veröffentlicht:
23. September 2025