traumatic_interhemispheric_subdural_hematoma

Traumatic Interhemispheric Subdural Hematoma

It accounts for approximately 6% of all traumatic SDH, or 0.8% of all hospitalized patients after head trauma 1) 2).


IHSDHs are often referred to as rare entities. Results show they are common 3).


The most likely pathogenic mechanism of posttraumatic ISH is linked to traumatic venous tearing frequently involving the parasagittal bridging veins, which are stretched by the tangential forces that develop after frontal or occipital impact 4) 5) 6) 7). The mechanism principally responsible for laceration of the bridging veins is the linear acceleration provoked, in most cases, by a frontal or occipital impact. Posttraumatic ISH is commonly caused by a mechanism of ‘inertia’ rather than fracture or cerebral contusion by direct impact 8) ; this theory is consistent with the lack of fracture in most published cases 9)

Interhemispheric Subdural Hematoma treatment.

420 patients had Interhemispheric Subdural Hematomas (1.9% of admissions and 35.5% of Subdural Hematoma), 35 (8.3% of IHSDH) were ≥8 mm in width. IHSDH was isolated in 16 (3.8%) of the cases. Average age was 61.7 ± 21.5 years for all IHSDHs and 77.1 ± 10.4 for large IHSDH (p < 0.001). For large IHSDH, a transient loss of consciousness (LOC) occurred in 51.5% of individuals, post-traumatic amnesia (PTA) in 47.8% of cases, and motor weakness in 37.9% of patients. Five of the large IHSDH patients presented with motor deficits directly related to the IHSDH, and weakness resolved in four of these five individuals. None were treated surgically. Progression of IHSDH width occurred in one patient 10).


A prospectively collected, single-institution trauma database was searched for patients with isolated traumatic iSDH causing falx syndrome in the period from January 2008 to January 2018. Information on demographic and radiological characteristics, serial neurological examinations, clinical and radiological outcomes, and posttreatment complications was collected and tallied. The authors subsequently dichotomized patients by management strategy to evaluate clinical outcome and 30-day survival.

Twenty-five patients (0.4% of those with intracranial injuries, 0.05% of those with trauma) with iSDH and falx syndrome represented the study cohort. The average age was 73.4 years, and most patients (23 [92%] of 25) were taking anticoagulants or antiplatelet medications. Six patients were managed nonoperatively, and 19 patients underwent craniotomy for iSDH evacuation; of the latter patients, 17 (89.5%) had improvement in or resolution of motor deficits postoperatively. There were no instances of venous infarction, reaccumulation, or infection after evacuation. In total, 9 (36%) of the 25 patients died within 30 days, including 6 (32%) of the 19 who had undergone craniotomy and 3 (50%) of the 6 who had been managed nonoperatively. Patients who died within 30 days were significantly more likely to experience in-hospital neurological deterioration prior to surgery (83% vs 15%, p = 0.0095) and to be comatose prior to surgery (100% vs 23%, p = 0.0031). The median modified Rankin Scale score of surgical patients who survived hospitalization (13 patients) was 1 at a mean follow-up of 22.1 months 11).


21 patients with Traumatic Interhemispheric Subdural Hematoma (TISH) who were treated with microsurgery were analyzed retrospectively. Prognostic factors for outcome were analyzed by univariate analysis.

Long-term follow up with outcome assessment according to the Glasgow Outcome Scale (GOS) showed good recovery in 16 cases, moderate disability in two cases, severe disability in one case, and death in two cases. During surgery the origin of bleeding could be identified in all 21 cases. A rupture of the distal anterior cerebral artery or veins in the interhemispheric fissure was seen more frequently in patients with whole interhemispheric fissure hematoma, while hemorrhage from brain tissue laceration was seen more frequently in patients with more localized hematomas. The outcome in patients with an identified rupture of a vessel was better than in those with cortical laceration. Preoperative GCS score and thickness of the interhemispheric hematoma were correlated with outcome (P=0.001 and P=0.004, respectively) 12).


1) , 2)
Takeda N, Kurihara E, Matsuoka H, Kose S, Tamaki N, Matsumoto S. [Three cases of acute interhemispheric subdural hematoma]. No Shinkei Geka. 1988 Jan;16(1):87-92. Japanese. PMID: 3283592.
3) , 10)
Léveillé E, Schur S, AlAzri A, Couturier C, Maleki M, Marcoux J. Clinical Characterization of Traumatic Acute Interhemispheric Subdural Hematoma. Can J Neurol Sci. 2020 Jul;47(4):504-510. doi: 10.1017/cjn.2020.44. Epub 2020 Mar 3. PMID: 32122420.
4)
Bartels RH, Verhagen WI, Prick MJ, Dalman JE. Interhemispheric subdural hematoma in adults: case reports and a review of the literature. Neurosurgery 36:1210-1214, 1995
5)
Okamoto J, Ban M, Sakamoto M, Takasugi S, Matumoto K. [Acute interhemispheric subdural hematoma–report of a case (author’s transl)]. No Shinkei Geka 10:209-213, 1982
6)
Rapanà A, Lamaida E, Pizza V, Lepore P, Caputi F, Graziussi G. Inter-hemispheric scissure, a rare location for a traumatic subdural hematoma, case report and review of the literature. Clin Neurol Neurosurg 99:124-129, 1997
7)
Romano VA, Toffol GJ. Confirmation of traumatic interhemispheric subdural hematoma by magnetic resonance imaging. J Emerg Med 12:369-373, 1994
8) , 9)
Delfini R, Santoro A, Innocenzi G, Ciappetta P, Salvati M, Zamponi C. Interhemispheric subdural hematoma (ISH). Case report. J Neurosurg Sci 35:217-220, 1991
11)
Tonetti DA, Ares WJ, Okonkwo DO, Gardner PA. Management and outcomes of isolated interhemispheric subdural hematomas associated with falx syndrome. J Neurosurg. 2019 Jan 11;131(6):1920-1925. doi: 10.3171/2018.8.JNS181812. PMID: 30641843.
12)
Wang Y, Wang C, Cai S, Dong J, Yang L, Chen L, Maas A. Surgical management of traumatic interhemispheric subdural hematoma. Turk Neurosurg. 2014;24(2):228-33. doi: 10.5137/1019-5149.JTN.8377-13.0. PMID: 24831365.
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