Chronic subdural hematoma

Chronic subdural hematoma

Chronic subdural hematoma (CSDH) is an encapsulated collection of old blood, mostly or totally liquefied and located between the dura mater and the arachnoid mater.

They are arbitrarily defined as those hematomas presenting 21 days or more after injury. These numbers are not absolute, and a more accurate classification of a subdural hematoma usually is based on imaging characteristics.

The first description of a chronic subdural hematoma was made in 1658 by J.J. Wepfer, followed in 1761 by Morgagni. A possible case was described by Honoré de Balzac in 1840 including its traumatic origin and surgical treatment.

Virchow, in 1857, denied a traumatic origin, and gave the name of “pachymeningitis hemorrhagica interna” to this pathology which he explained by inflammatory processes.

The traumatic etiology of chronic subdural hematoma was recognized in the XXth century, especially by Trotter in 1914. Pathophysiology was considered later on in the XXth century.

It was first described by Rudolf Ludwig Karl Virchow, in 1857, as “an internal hemorrhagic pachymeningitis” 1).

Later, in 1914, Trotter launched the theory of traumatic brain injury and the consecutive lesion of the “bridging veins”, as being the cause of what he called “hemorrhagic subdural cyst” 2).

Chronic subdural hematoma epidemiology.

see Chronic subdural hematoma etiology.

Chemokines in Chronic Subdural Hematoma

see Chronic subdural hematoma classification.

Chronic subdural hematoma pathophysiology.

cSDHs have a tendency to persist and gradually increase in volume over time. The disease is thought to be related to a cycle of chronic inflammation and angiogenesis. An original hemorrhage forms and fibrinolysis ensues with the liquefaction of the initial clot. The subsequent blood breakdown products stimulate inflammation and thickening of the inner dural layer (ie, ‘dural border cells). This process incites angiogenesis with the ingrowth of immature capillaries, which chronically leak blood. These microhemorrhages result in the progressive enlargement of the collection with increased fibrinolytic activity, inflammation, and further angiogenesis, membrane formation, and vessel proliferation. The rate of accumulation of blood products outpaces physiological reabsorption and the collection gradually enlarges. Thus the entire basis for the pathology is the formation of leaky vascular membranes, which incite a positive feedback cycle of continued hemorrhage, inflammation, and angiogenesis 3) 4)


Chronic subdural hematoma (CSDH) is characterized by an “old” encapsulated collection of blood and blood breakdown products between the brain and its outermost covering (the dura).

It is delimited by an outer and inner membrane. In between are bloodplasmacerebrospinal fluid, membranes, and a mixture of inflammatory angiogenic fibrinolytic and coagulation factors. These factors maintain a self-perpetuating cycle of bleeding, lysis, and growing of neo-membranes and neo-capillaries 5).

see Chronic subdural hematoma clinical features.

Glasgow Coma Scale.

Markwalder grading score.

Modified Rankin Scale.

Chronic subdural hematoma diagnosis

The association between the biomarkers of inflammation and angiogenesis, and the clinical and radiological characteristics of CSDH patients, need further investigation. The high number of biomarkers compared to the number of observations, the correlation between biomarkers, missing data and skewed distributions may limit the usefulness of classical statistical methods.

Pripp et al. explored lasso regression to assess the association between 30 biomarkers of inflammation and angiogenesis at the site of lesions, and selected clinical and radiological characteristics in a cohort of 93 patients. Lasso regression performs both variable selection and regularization to improve the predictive accuracy and interpretability of the statistical model. The results from the lasso regression showed analysis exhibited lack of robust statistical association between the biomarkers in hematoma fluid with age, gender, brain infarct, neurological deficiencies and volume of hematoma. However, there were associations between several of the biomarkers with postoperative recurrence requiring reoperation. The statistical analysis with lasso regression supported previous findings that the immunological characteristics of CSDH are local. The relationship between biomarkers, the radiological appearance of lesions and recurrence requiring reoperation have been inclusive using classical statistical methods on these data, but lasso regression revealed an association with inflammatory and angiogenic biomarkers in hematoma fluid. They suggest that lasso regression should be a recommended statistical method in research on biological processes in CSDH patients 6).

Chronic subdural hematoma (CSDH) is a disease of the meninges and is to be distinguished from hygroma and subdural empyema.

Subdural effusion in the setting of dural metastases is very rare and may be difficult to be distinguished from chronic subdural hematoma. Such lesions could be missed and could be the cause of recurrence in CSDH. A contrast-enhanced brain CT scan is recommended to diagnose dural metastases.

Rosai–Dorfman disease may be mistaken for a CSDH on imaging. This disease is an uncommon, benign systemic histioproliferative disease characterized by massive lymphadenopathy, particularly in the head and neck region, and is often associated with extranodal involvement. CSDH can also develop in multifocal fibrosclerosis (MFS) which is a rare disorder of unknown etiology, characterized by chronic inflammation with dense fibrosis and lymphoplasmacytic infiltration into the connective tissue of various organs. The mechanism of the formation of CSDH is presumed to involve reactive granular membrane together with subdural collection. On the other hand, the extramedullary erythropoiesis within CSDH can be confused with metastatic malignant tumors, such as lymphoma, carcinoma, and malignant melanoma 7).

A 44-year old woman with gastric adenocarcinoma was presented with headache and a hypodense subdural collection in right fronto-parietal in brain CT. Burr-hole irrigation was performed with the impression of chronic subdural hematoma, but nonhemorrhagic xantochromic fluid was evacuated without malignant cell. Brain CT on the 11th day depicted fluid re-accumulation and noticeable midline shift, necessitating craniotomy and removing the affected dura.

Because the affected dura can be supposed as the main source of subdural effusion, resection of the involved dura is obligatory for the appropriate palliative management of such patients 8).

see Chronic subdural hematoma treatment.

Routine postoperative CT

Routine post-operative CT brain for burr hole drainage of CSDH may be unnecessary in view of the good predictive value of pre-operative volume, and also because it is not predictive of the clinical outcome 9).

Scheduled postoperative cranial imaging with indwelling drains was not shown to be beneficial and misses information of intracranial damage inflicted by removal of drains. Brokinkel et al recommend CT-scanning after drainage removal 10).

see Chronic subdural hematoma surgery complications.

see Chronic subdural hematoma recurrence.

see Chronic subdural hematoma outcome.

A study aimed to quantify the heterogeneity of data elements in the pre-operative, operative, and post-operative phases of care, and build the basis for the development of a set of common data elements (CDEs) for CSDH. This systematic review adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement and was registered with the PROSPERO register of systematic reviews (CRD42014007266). All full-text English studies with more than 10 patients (prospective) or more than 100 patients (retrospective) published after 1990 examining clinical outcomes in CSDH were eligible for inclusion. One hundred two eligible studies were found. Only 40 studies (39.2%) reported the main presenting symptom/feature and 24 (23.5%) reported additional symptoms/features. Admitting neurological/functional status was classified by the Glasgow Coma Scale (25 studies; 24.5%), the Markwalder Score (26 studies; 25.5%) and the modified Rankin Scale (three studies; 2.9%). Fifty-four studies (52.9%) made some mention of patient comorbidities and 58 studies (56.9%) reported the proportion or excluded patients on anticoagulant medication. Eighteen studies (17.6%) reported baseline coagulation status. Sixty-four studies (62.7%) stratified or assessed severity based on radiological findings, although the methods used varied widely. There was variable reporting of surgical technique and post-operative care; 32 studies (31.4%) made no mention of whether the operations were performed under general or local anesthetic. This study, a part of the Core Outcomes and Common Data Elements in CSDH (CODE-CSDH) project, confirms and quantifies the heterogeneity of data elements collected and reported in CSDH studies to date. It establishes the basis for the consensus-based development of a set of common data elements, facilitating robust cross-study comparisons and resulting improvements in patient outcomes 11).

see Chronic subdural hematoma case series.

see Chronic subdural hematoma case reports.

Attempts to create CSDH have been made in mice, rats, cats, dogs and monkeys. Methods include injection or surgical implantation of clotted blood or various other blood products and mixtures into the potential subdural space or the subcutaneous space. No intracranial model produced a progressively expanding CSDH. Transient hematoma expansion with liquification could be produced by subcutaneous injections in some models. Spontaneous subdural blood collections were found after creation of hydrocephalus in mice by systemic injection of the neurotoxin, 6-aminonicotinamide. The histology of the hematoma membranes in several models resembles the appearance in humans. None of the models has been replicated since its first description.

D’Abbondanza et al. did not find a report of a reproducible, well-described animal model of human CSDH 12).


1) 
Weigel R, Krauss JK, Schmiedek P. Concepts of neurosurgical management of chronic subdural haematoma: historical perspectives. Br J Neurosurg. 2004 Feb;18(1):8-18. PubMed PMID: 15040710.
2) 
Guénot M. [Chronic subdural hematoma: historical studies]. Neurochirurgie. 2001 Nov;47(5):461-3. French. PubMed PMID: 11915757.
3) 
Ito H , Yamamoto S , Komai T , et al . Role of local hyperfibrinolysis in the etiology of chronic subdural hematoma. J Neurosurg 1976;45:26–31.doi:10.3171/jns.1976.45.1.0026
4) 
Edlmann E , Giorgi-Coll S , Whitfield PC , et al . Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy. J Neuroinflammation 2017;14:108.doi:10.1186/s12974-017-0881-y
5) 
Frati A, Salvati M, Mainiero F, Ippoliti F, Rocchi G, Raco A, Caroli E, Cantore G, Delfini R (2004) Inflammation markers and risk factors for recurrence in 35 patients with a posttraumatic chronic subdural haematoma: a prospective study. J Neurosurg 100:24–32
6) 
Pripp AH, Stanišić M. Association between biomarkers and clinical characteristics in chronic subdural hematoma patients assessed with lasso regression. PLoS One. 2017 Nov 6;12(11):e0186838. doi: 10.1371/journal.pone.0186838. eCollection 2017. PubMed PMID: 29107999.
7) 
Yadav YR, Parihar V, Namdev H, Bajaj J. Chronic subdural hematoma. Asian J Neurosurg. 2016 Oct-Dec;11(4):330-342. Review. PubMed PMID: 27695533; PubMed Central PMCID: PMC4974954.
8) 
Mirsadeghi SM, Habibi Z, Meybodi KT, Nejat F, Tabatabai SA. Malignant subdural effusion associated with disseminated adenocarcinoma: a case report. Cases J. 2008 Nov 18;1(1):328. doi: 10.1186/1757-1626-1-328. PubMed PMID: 19019205; PubMed Central PMCID: PMC2611978.
9) 
Ng HY, Ng WH, King NK. Value of routine early post-operative computed tomography in determining short-term functional outcome after drainage of chronic subdural hematoma: An evaluation of residual volume. Surg Neurol Int. 2014 Sep 19;5:136. doi: 10.4103/2152-7806.141299. eCollection 2014. PubMed PMID: 25298918.
10) 
Brokinkel B, Ewelt C, Holling M, Hesselmann V, Heindel WL, Stummer W, Fischer BR. Routine postoperative CT-scans after burr hole trepanation for chronic subdural hematoma – better before or after drainage removal? Turk Neurosurg. 2013;23(4):458-63. doi: 10.5137/1019-5149.JTN.7269-12.0. PubMed PMID: 24101264.
11) 
Chari A, Hocking KC, Edlmann E, Turner C, Santarius T, Hutchinson PJ, Kolias AG. Core Outcomes and Common Data Elements in Chronic Subdural Hematoma: A Systematic Review of the Literature Focusing on Baseline and Peri-Operative Care Data Elements. J Neurotrauma. 2016 Sep 1;33(17):1569-75. doi: 10.1089/neu.2015.4248. Epub 2016 Jan 28. PubMed PMID: 26541092.
12) 
D’Abbondanza JA, Loch Macdonald R. Experimental models of chronic subdural hematoma. Neurol Res. 2014 Feb;36(2):176-88. doi: 10.1179/1743132813Y.0000000279. Epub 2013 Dec 6. Review. PubMed PMID: 24172841.

Subdural Grid Monitoring

Subdural Grid Monitoring

.

A useful technique for intra-operative functional mapping, for the surgical treatment of epilepsy.

○ Grids are frequently used for extra-operative functional mapping (helpful in children or in the mentally retarded). Subdural grid electrodes are placed with a craniotomy.

○ Surface strip electrodes may be placed through a burr hole.


https://adtechmedical.com/subdural-electrodes.

Subdural grid monitoring (SDG) has the advantage to provide continuous coverage over a larger area of cortex, direct visualization of electrode location and functional mapping. However, SDG can cause direct irritation of the cortex or postoperative headaches due to cerebrospinal fluid fistula. Epidural grid monitoring (EDG) without opening the dura is thought to reduce the possibility of these complications. Park et al. reported the experience with Epidural grid monitoring.

see Epidural grid monitoring.

Traditionally, for subdural grid electrode placement, large craniotomies have been applied for optimal electrode placement. Nowadays, microneurosurgeons prefer patient-tailored minimally invasive approaches. Absolute figures on craniotomy size have never been reported. To elucidate the craniotomy size necessary for successful diagnostics, Schneider et al. reviewed there single-center experience in the Charité.

Within 3 years, 58 patients with focal epilepsies underwent subdural grid implantation using patient-tailored navigation-based craniotomies. Craniotomy sizes were measured retrospectively. The number of electrodes and the feasibility of the resection were evaluated. Sixteen historical patients served as controls.

In all 58 patients, subdural electrodes were implanted as planned through tailored craniotomies. The mean craniotomy size was 28 ± 15 cm2 via which 55 ± 16 electrodes were implanted. In temporal lobe diagnostics, even smaller craniotomies were applied (21 ± 11 cm2). Craniotomies were significantly smaller than in historical controls (65 ± 23 cm2, p < 0.05), while the mean number of electrodes was comparable. The mean operation time was shorter and complications were reduced in tailored craniotomies.

Craniotomy size for subdural electrode implantation is controversial. Some surgeons favor large craniotomies, while others strive for minimally invasive approaches. For the first time, they measured the actual craniotomy size for subdural grid electrode implantation. All procedures were straightforward. They therefore advocate for patient-tailored minimally invasive approaches – standard in modern microneurosurgery – in epilepsy surgery as well 1).


Subdural strip and grid electrode (SDE) implantations have long been used as the mainstay of intracranial seizure localization in the United States. Stereoelectroencephalography (SEEG) is an alternative approach in which depth electrodes are placed through percutaneous drill holes to stereotactically defined coordinates in the brain. Long used in certain centers in Europe, SEEG is gaining wider popularity in North America, bolstered by the advent of stereotactic robotic assistance and mounting evidence of safety, without the need for catheter-based angiography. Rates of clinically significant hemorrhage, infection, and other complications appear lower with SEEG than with SDE implants. SEEG also avoids unnecessary craniotomies when seizures are localized to unresectable eloquent cortex, found to be multifocal or nonfocal, or ultimately treated with stereotactic procedures such as laser interstitial thermal therapy (LITT), radiofrequency thermocoagulation (RF-TC), responsive neurostimulation (RNS), or deep brain stimulation (DBS). While SDE allows for excellent localization and functional mapping on the cortical surface, SEEG offers a less invasive option for sampling disparate brain areas, bilateral investigations, and deep or medial targets. SEEG has shown efficacy for seizure localization in the temporal lobe, the insula, lesional and nonlesional extra-temporal epilepsy, hypothalamic hamartomas, nodular periventricular heterotopias, and patients who have had prior craniotomies for resections or grids. SEEG offers a valuable opportunity for cognitive neurophysiology research and may have an important role in the study of dysfunctional networks in psychiatric disease and understanding the effects of neuromodulation 2).

Hamer et al retrospectively reviewed the records of all patients who underwent invasive monitoring with subdural grid electrodes (n = 198 monitoring sessions on 187 patients; median age: 24 years; range: 1 to 50 years) at the Cleveland Clinic Foundation from 1980 to 1997.

From 1980 to 1997, the complication rate decreased (p = 0.003). In the last 5 years, 19/99 patients (19%) had complications, including two patients (2%) with permanent sequelae. In the last 3 years, the complication rate was 13.5% (n = 5/37) without permanent deficits. Overall, complications occurred during 52 monitoring sessions (26.3%): infection (n = 24; 12.1%), transient neurologic deficit (n = 22; 11.1%), epidural hematoma (n = 5; 2.5%), increased intracranial pressure (n = 5; 2.5%), and infarction (n = 3; 1.5%). One patient (0.5%) died during grid insertion. Complication occurrence was associated with greater number of grids/electrodes (p = 0.021/p = 0.052; especially >60 electrodes), longer duration of monitoring (p = 0.004; especially >10 days), older age of the patient (p = 0.005), left-sided grid insertion (p = 0.01), and burr holes in addition to the craniotomy (p = 0.022). No association with complications was found for number of seizures, IQ, anticonvulsants, or grid localization.

Invasive monitoring with grid electrodes was associated with significant complications. Most of them were transient. Increased complication rates were related to left-sided grid insertion and longer monitoring with a greater number of electrodes (especially more than 60 electrodes). Improvements in grid technology, surgical technique, and postoperative care resulted in significant reductions in the complication rate 3).


From 1987 to 1992, invasive EEG studies using subdural strips, subdural grids or depth electrodes were performed in a total of 160 patients with medically intractable epilepsy, in whom scalp EEG was insufficient to localize the epileptogenic focus. Dependent on the individual requirements, these different electrode types were used alone or in combination. Multiple strip electrodes with 4 to 16 contacts were implanted in 157 cases through burrholes, grids with up to 64 contacts in 15 cases via boneflaps, and intrahippocampal depth electrodes in 36 cases using stereotactic procedures. In every case, localization of the electrodes with respect to brain structures was controlled by CT scan and MRI. Visual and computerized analysis of extra-operative recordings allowed the localization of a resectable epileptogenic focus in 143 patients (89%), who subsequently were referred for surgery, whereas surgery had to be denied to 17 patients (11%). We did not encounter any permanent morbidity or mortality in our series. In our experience, EEG-monitoring with chronically implanted electrodes is a feasible technique which contributes essentially to the exact localization of the epileptogenic focus, since it allows nearly artefact-free recording of the ictal and interictal activity. Moreover, grid electrodes can be used for extra-operative functional topographic mapping of eloquent brain areas 4).


1)

Schneider UC, Oltmanns F, Vajkoczy P, Holtkamp M, Dehnicke C. Craniotomy Size for Subdural Grid Electrode Placement in Invasive Epilepsy Diagnostics. Stereotact Funct Neurosurg. 2019 Jul 30:1-9. doi: 10.1159/000501235. [Epub ahead of print] PubMed PMID: 31362296.
2)

Youngerman BE, Khan FA, McKhann GM. Stereoelectroencephalography in epilepsy, cognitive neurophysiology, and psychiatric disease: safety, efficacy, and place in therapy. Neuropsychiatr Dis Treat. 2019 Jun 28;15:1701-1716. doi: 10.2147/NDT.S177804. eCollection 2019. Review. PubMed PMID: 31303757; PubMed Central PMCID: PMC6610288.
3)

Hamer HM, Morris HH, Mascha EJ, Karafa MT, Bingaman WE, Bej MD, Burgess RC, Dinner DS, Foldvary NR, Hahn JF, Kotagal P, Najm I, Wyllie E, Lüders HO. Complications of invasive video-EEG monitoring with subdural grid electrodes. Neurology. 2002 Jan 8;58(1):97-103. PubMed PMID: 11781412.
4)

Behrens E, Zentner J, van Roost D, Hufnagel A, Elger CE, Schramm J. Subdural and depth electrodes in the presurgical evaluation of epilepsy. Acta Neurochir (Wien). 1994;128(1-4):84-7. PubMed PMID: 7847148.

Interhemispheric subdural hematoma

Interhemispheric subdural hematoma

Interhemispheric acute subdural hematomas (ASDHs) were first described by Aring and Evans 1).

Interhemispheric Subdural Hematoma Epidemiology.

Spontaneous Interhemispheric Subdural Hematoma.

Traumatic Interhemispheric Subdural Hematoma.

Acute Interhemispheric Subdural Hematoma.

Chronic Interhemispheric Subdural Hematoma

Its natural history is still quite unknown in terms of potential origin and course.

They usually occur in patients with bleeding disorders and are associated with trauma in 83% of cases 2).

Other causes include history of birth trauma, forceps delivery, child abuse with shaking, hemodialysis, anticoagulation and aneurysmal bleeding 3).

Fruin et al. 4) suggested that an occipital blow in the sagittal plane lead to an interhemispheric ASDH because of the anatomic orientation of the veins in the interhemispheric fissure, which tend to course antero-medially from the cortex to the midline sinuses. Before the CT era, it was difficult to detect an interhemispheric ASDH. Though removal of the blood has proved to be an option in the management of these patients, there is danger due to the close proximity of the superior sagittal sinus and bridging veins. Some of these hematomas migrate superiorly (to a more favorable position) with time, as they liquefy. It is also conceivable that if a patient with an interhemispheric ASDH is relatively asymptomatic, initial conservative management might be followed by migration of the clot to a position over the convexity where removal is considerably less dangerous. Thus there is no consensus on the ideal management of these rare hematomas, conservative treatment may be followed in those who are neurologically stable or have concurrent risk factors, while surgical treatment should be reserved for those who have pronounced symptoms or neurological deficits 5).

The hyperdense hematoma can best be visualized on the coronal and sagittal views. This is in contrast with typical subdural hematomas, which can be best appreciated on the axial views. Thus, it is important to image all three main views of the brain looking out for interhemispheric hematoma 6).

Interhemispheric Subdural Hematoma Treatment.

Interhemispheric Subdural Hematoma Case Series.

Interhemispheric Subdural Hematoma Case Reports.


1)

Aring CD, Evans JP. Aberrant location of subdural hematoma. Arch Neurol Psychiatry. 1940;44:1296–306.
2)

Houtteville JP, Toumi K, Theron J, Derlon JM, Benazza A, Hubert P. Interhemispheric subdural haematomas: seven cases and review of the literature. Br J Neurosurg. 1988;2:357–67. doi: 10.3109/02688698809001007.
3)

Ishikawa E, Sugimoto K, Yanaka K, Ayuzawa S, Iguchi M, Moritake T, Kobayashi E, Nose T. Interhemispheric subdural hematoma caused by a ruptured internal carotid artery aneurysm: case report. Surg Neurol. 2000;54:82–6. doi: 10.1016/S0090-3019(00)00262-7.
4)

Fruin AH, Juhl GL, Taylon C. Interhemispheric subdural hematoma. Case report. J Neurosurg. 1984;60:1300–2. doi: 10.3171/jns.1984.60.6.1300.
5)

Kawoosa NN, Bhat AR, Rashid B. Interhemispheric acute subdural hematomas. Iran Red Crescent Med J. 2011 Apr;13(4):289-90. Epub 2011 Apr 1. PubMed PMID: 22737484; PubMed Central PMCID: PMC3371964.
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