Printed in the USA ??Copyright 0 1989 Pergamon Press plc The Journal of Emergency Medicine, Vol. 7, pp. 603-610. 1989 TRAUMATIC LACERATION OF PERICALLOSAL ARTERY RESULTING IN INTERHEMISPHERIC SUBDURAL HEMATOMA: A CASE REPORT John J. Gartman, Jr, MD, Eliot A. Atstupenas, BA, Dennis G. Vollmer, MD, Stephen K. Powers, MD Division of Neurosurgery, University of North Carolina, Chapel Hill, North Carolina Reprint address: John J. Gartman, MD, Division of Neurosurgery, CB#7060 UNC-School of Medicine, Chapel Hill, NC 27514-7060 CASE REPORT 0 Abstract - Interhemispheric subdural hematoma (IHSDH) usually manifests itself in a delayed fashion after trauma as a slow neurological deterioration with signs of the falx syndrome (paresis or seizures of the lower extremity contralateral to the hematoma). Several etiologies of IHSDH have been described, with tearing of bridging veins being especially associated with trauma. We present the second reported case of IHSDH due to traumatic arterial laceration. This lesion demonstrates a benign and delayed initial presentation. Conservative observation has been employed in the past with mixed results. Patients receiving early definitive surgical treatment have a lower mortality rate then those treated similarly having convexity SDHs. This review of 31 cases discusses the salient aspects of this clinical entity, emphasizing the need for prompt diagnosis and treatment, despite the patient’s seemingly stable neurological status. E. I., a 34-year-old female, was an unrestrained passenger involved in an automobile accident. By report, at an outside institution she was responsive, alert, and had a normal neurological exam. A history of loss of consciousness was unobtainable secondary to alcohol intoxication (plasma ethanol level=460mg/ dL). A head computed tomography (CT scan) reportedly revealed a left-sided interhemispheric hematoma. (A CT scan in this situation can be supported by a recent article by Feuerman [ 11.They recommend CT scanning for all patients with a minor head injury [Glascow Coma Scale < 151 and altered mental status, or hemispheric neurological deficits.) She was transferred via air ambulance, arriving at our hospital approximately six hours postinjury. 0 Keywords-subdural hematoma; interhemispherlc; anterior cerebral artery; falx syndrome; trauma; head injury Examination Initially, she was lethargic but awake. She opened her eyes spontaneously, followed commands with all four extremities and was conversant but confused (Glascow Coma Scale of 14). CT scan showed an anteriorly located, left interhemispheric subdural hematoma, without midline shift (Figure 1). The hematoma was relatively small and not enlarging, so close observation without intracranial pressure monitoring was felt to be appropriate. She was under close observation and her condition remained unchanged. Then approximately eight hours postinjury, over a matter of minutes she became confused, then unresponsive and experienced an acute respiratory arrest. She was intubated, hyperventilated, and given 50 gm of mannitol. INTRODUCTION Interhemispheric subdural hematoma (IHSDH) represents a rare form of subdural hematoma (SDH). Study of this usually traumatic lesion demonstrates consistencies within previously described cases relative to the mechanism of injury, time course in clinical signs of presentation, and natural history. These characteristics appear to separate it into a distinctive type of SDH. We present a case of IHSDH and describe peculiarities of this intracranial mass derived from a review of the literature. RECEIVED:12 December 1988; FINALSUBMISSION RECEIVED:17 April 1989; ACCEPTED:1 May 1989 603 0736-4679/89 $3.00 + .OO 604 J. J. Gartman, Jr, E. A. Atstupenas, D. G. Vollmer, S. K. Powers A repeat CT scan showed expansion of the hematoma posteriorly, with extension over the left frontal convexity and significant mass effect (Figure 2). Operation An emergent left frontoparietal craniotomy was performed with removal of the convexity hematoma. The interhemispheric portion of the hematoma was completely evacuated, followed by brisk bleeding. A laceration of the pericallosal artery on the medial aspect of the left frontal lobe and against the free edge of the falx cerebrio was identified as the source of bleeding and was coagulated and clip ligated. It appeared that the laceration resulted from direct injury to the vessel by the edge of the falx that had torn the vessel and disrupted the integrity of the surrounding cingulate gyrus . Postoperative Course (4 She was initially noted to have 3 mm nonreactive pupils, intact gag and cornea1 reflexes. Wo hours postoperatively her condition deteriorated, with 6 mm fixed pupils, absent corneal, doll’s eyes and gag reflexes. A subsequent CT scan revealed a large pontine hemorrhage (Figure 3). Her condition never improved and she expired approximately 36 hours postinjury. DISCUSSION (W Figure 1. CT scan approximately six hours post-Injury (patient GCS = 14). (a) The left frontal interhemispheric subdural hematoma is seen and the midllne is not deviated. (b) Coronal view shows the left interhemispheric hematoma with depression of the corpus callosum and effacement of the lateral ventricle. Acute subdural hematomas (ASDHs) have long been recognized as the most common and most lethal of traumatic intracranial mass lesions. The majority of ASDHs have a definite predilection for occurring over the convexities or on the basal surface of the frontal or temporal lobes. A much rarer variety of acute ASDH occurs between the cerebral hemispheres, in the interhemispheric fissure. Several similarities in the cases of IHSDH reported in the literature warrant further discussion and appear to separate this lesion as a distinct entity within the various intracranial traumatic mass lesions. The rapidity with which ASDHs are surgically evacuated has been show to have a significant effect upon improving the patient’s ultimate outcome (2). Presumably this shortens the amount of time during which the intracranial anatomy is distorted and exposed to elevated intracranial pressure, which causes focal tissue ischemia with or without brainstem compression. Despite aggressive attempts to minimize the time elapsed between injury and surgical interven- Interhemispheric 605 Hematoma (4 (4 Figure 2. CT scan approximately eight hours postinjury after patlent suffered acute respiratory arrest. (a and b) There is an increase In hematoma size, with extension posteriorly and marked midline shift. (c) More inferior cuts show compression of the basilar cisterns and no evidence of hemorrhage. 606 Figure 3. CT scan 2 hours postoperatively demonstrates a hemorrhage in the pontine tegmentum. tion, traumatic ASDH has remained a devastating injury. Overall mortality in most large series of ASDH reported is over 50% (3). Our review of 31 patients has shown a somewhat lower mortality rate of 32% for IHSDHs. A significant number of these deaths (40%) actually represent postoperative complications, not specifically related to head trauma. These results imply that IHSDHs are a more benign traumatic lesion than acute ASDHs of other locations. The first description of IHSDH was published by Aring (4) in 1940, and the first correct diagnosis of IHSDH in life was made by Jacobson in 1955 (5). Since then our review of literature has produced 28 separate cases described in sufficient detail for a comparison and analysis (Table 1). By far, the most common cause has been trauma, and this more specifically has a distinct predilection for the occipital area. Other authors have commented on the apparent minor severity of the head trauma (6,7). Toffol et al., note that in the nine cases reviewed, none lost consciousness at the time of injury (7). The cause of most traumatic ASDHs is the tearing of bridging veins with subsequent hemorrhage into the subdural space. It has been proposed that, be- J. J. Gartman, Jr, E. A. Atstupenas, D. G. Vollmer, S. K. Powers cause the bridging veins in the region of the interhemispheric fissure run in an anteromedial direction to the superior sagittal sinus, a blow to the occiput would provide a large shearing and stretch force upon these vessels. This would result in tearing of the veins and subsequent interhemispheric clot formation (8,9). Several other causes of IHSDH have been described including rupture of a callosomarginal and of a posterior communicating aneurysm (10,l l), ventriculoperitoneal shunt in the presence of minor trauma (12), shaken baby syndrome (13) and both systemic anticoagulation and von Willebrand’s disease in combination with head trauma (6,14,15,16,17,18). Our case is the second in the literature to demonstrate an arterial bleeding source. At operation the arterial bleeding point corresponded with the inferior edge of the falx. We suspect that the falcine border lacerated the artery upon impact, with subsequent hemorrhage into the interhemispheric space. “Falx syndrome”, originally described by List (19) in 1955, denotes the combination of signs that are often present with an acute interhemispheric mass, including hematoma or empyema (20) or ischemia of this region by occlusion of an anterior cerebral artery. This consists of paresis or seizures of the contralateral leg, sometimes with weakness of the arm or face but to a much lesser degree. Table 1 indicates that 20 of 3 1 (65 %) cases presented with the falx syndrome. The anatomic correlate to this is the contralateral lower extremity motor cortex on the medial aspect of the hemisphere effected by the ischemia. If unaware of this ischemic syndrome, especially in the case of bilateral lesion, one might mistakenly localize the lesion to the cervical or thoracic spine when evaluating the trauma patient. Given this situation both possibilities must be thoroughly investigated. Interestingly, Clein and Bolton emphasized a very flattened affect in their patient with IHSDH which cleared immediately after evacuation of the mass (21). Although this finding has only been alluded to in one other case in the literature (lo), it may be considered as further clinical evidence of localizing the lesion to the region of the frontal lobes and cingulate gyrus. Admittedly, this is a difficult finding to interpret in the acute trauma situation. Whereas the majority of ASDHs produce neurologic deficits that may be obvious during the initial evaluation of the trauma patient, a recurrent theme in the presentation of IHSDH is a delay in appearance of a localizing neurologic deficit. The range of delay in presentation is from several hours up to ten days or more (2,9). Our case and others (6) demonstrate the potential for these lesions to produce rapid neurolog- Interhemispheric 607 Hematoma Table 1. Summary of 31 Interhemispheric Subdural Hematoma Cases Etiol. Presentation Delay Diagnosis Treatment Result Year Ref Pt 1940 4 45M trauma 2 days * L-hemiparesis L-LE seizure coma necropsy trephine openings 1955 5 23M trauma 5 days *L-leg paresis angio burr holes recovered 1961 23 old trauma hours ‘RUE movement spasticity angio burr holes expired (unrelated) 1964 18 74M trauma anticoag 12-24 hrs *L-leg paresis angio burr holes recovered 1969 21 38M trauma 24 days PEGlangio craniotomy recovered 1970 17 42F trauma anticoag 10 days angio craniotomy recovered ?? L-hemiparesis expired LE>UE 10 73M callosomarginal aneurysm 4 days ‘R-LE paresis R-babinski HyperDTRs angio craniotomy recovered -flat affect -sI. paresis 1977 14 80M anticoag 10 days progressive obutundation CT scan IH + ICH burr holes expired (pulm. emboli) 1978 9 27M trauma 24 hours *leg weakness R>L, UEUE; 1979 1982 HA 44M trauma 4 days vertex HA confusion CT scan angio burr holes recovered 12 43F trauma VP shunt 4 days *paraparesis arm weakness CT scan B-hematoma craniotomy recovered 25 24M trauma 36 hours * L-hemiparesis LE>UE CT scan craniotomy recovered 6 54M trauma 2 days decerebrate CN Ill palsy CT scan IH +SDH trephine openings expired (renal failure) 62M trauma anticoag 2-4 days decerebrate no OC reflex CT scan IH+ICH craniotomy expired (fatal arrhythmia) 1983 11 55M PcoA aneurysm immediate HA, LOC CN Ill palsy Angio CT scan craniotomy w/clipping recovered 1984 24 61M trauma 6-8 hours L-LE paresis lethargy CT scan angio craniotomy recovered 8 59M trauma l-2 L-hemiparesis LE>UE CT scan ICP monitor mannitol recovered 1985 7 66M trauma 24 hours seizure wide gait CT scan Dilantin recovered 1987 16 80M trauma anticoag 3 days ‘R-hemislegia R-seizures LE>UE CT scan craniotomy expired (unrelated) 81F trauma anticoag 24-38 hrs ‘comatose movement R>L, UE>LE CT scan IH + SDH craniotomy expired (unrelated) 55M trauma anticoag 3 hours ‘R-hemiplegia CT scan angio craniotomy recovered 40M trauma anticoag 24 hours ?? L-hemiparesis CT scan craniotomy recovered anticoag immediate CT scan none expired 1988 15 65M days ?? ?? LE>UE decerabrate coma (continued) J. J. Gartman, Jr, E. A. Atstupenas, 608 D. G. Vollmer, S. K. Powers Table 1. Continued Year Ref 77M 1988 Etiol. R Delay Presentation trauma 7 hours ?? R-hemiplegia coma CT scan craniotomy expired trauma 3 days seizure, HA CT scan trephine openings recovered IH+SDH Diagnosis Treatment Result trauma VW dz 12 days ‘L-hemiparesis LE>UE CT scan burr holes recovered trauma 5 days seizure CT scan IH + SDH burr hole recovered -hydrocephalus pres case 34F trauma 8 hours lethargy acute resp. arrest CT scan craniotomy expired (pontine hemorrhage) ## 73F trauma immediate ‘L-hemiparesis CT scan craniotomy recovered ## 49M trauma 2 days ?? R-LE focal motor seizure CT scan IH+SDH Dilantin recovered ‘Falx syndrome present L = left. R = right, B = bilateral HA = headache LOC = loss of consciousness LUUE = lower/upper extremity PEG = pneumoencephalography VP Shunt =ventriculopertoneal shunt OC reflex = oculocephalic reflex Uu = personal communication of Dr. B. Walters PccA = posterior communicating artery IH = interhemispheric subdural hematoma SDH I subdural hematoma ICH = intracerebral hematoma DTRs = deep tendon reflexes VW dz = von Willebrand’s disease ic deterioration after a previously stable course. Seventy-four percent of patients with IHSDH exhibited localizing neurological deficits 24 hours or longer after injury (see Table 1). Whether this represents acute decompensation due to brain edema or ischemia in the presence of a stable hematoma or rehemorrhage is unclear from the descriptions provided in the literature. The noncontrasted CT scan remains the diagnostic test of choice for IHSDH. In the past both arteriography and pneumoencephalography have been used to establish the diagnosis of interhemispheric mass. Neither of these modalities plays a significant role at this time. The obvious exception to this occurs when aneurysmal hemorrhage is a serious diagnostic consideration (6). Despite recent advancements in high speed MRI, the advantage of this modality over routine CT scan for ASDHs remains to be demonstrated. Further, CT scan allows visualization of the bony anatomy, which is of practical importance in the setting of acute head trauma. IHSDH presents a characteristic picture on noncontrasted CT scan (see Figure 1). When acute and unilateral, the hematoma appears as a high density midline mass that is convex to the ipsilateral side of the lesion but respects the falx and maintains the midline position medially (14). The ipsilateral hemisphere will often display the effects of a midline mass with ventricular shift and effacement of the gyri and sulci. The clot may extend anteriorly to the crista gali and floor of the anterior fossa, or posteriorly to the torcula with clot layering out over the tentorium. Glista et al. have proposed that the acute hematoma is confined to the interhemispheric region by firm adherence of the arachnoid trabeculations between the brain and the parasagittal dura (9). Cases exist with concurrent ipsilateral convexity SDHs (6,16,18). Whether this represents clot migration or simultaneous tearing of a convexity-bridging vein with independent second clot formation is unclear. This possibility implies the need to search for a second bleeding source in the acute surgical situation. Ho et al. point out that the most important differential diagnosis of this CT abnormality in the traumatic setting is intracerebral hematoma, which may also appear as a concurrent lesion (6,14). Intracerebral hematomas may be distinguished by their round shape and are usually more peripheral when of traumatic origin. The natural history of IHSDHs has been alluded to in several previous articles. Based upon a few lesions treated nonoperatively it has been suggested that as the hematoma ages it liquifies, leaving the interhemispheric fissure to migrate over the convexities (8,22). Fruin et al. suggest that many convexity chronic SDHs may actually originate as IHSDHs and come to be located over the convexities by the natural relocation of the mass (8). This would assume that the firm arachnoid trabeculations between the brain Interhemispheric 609 Hematoma and parasagittal dura that restricted the original hematoma no longer provide a barrier to the liquifying clot. Sibayan et al. presented a case of IHSDH that was operated upon in a delayed fashion and described a well-formed capsule that continued to retain the hematoma in its interhemispheric position (17). Toffol et al. describe a case of nonoperative treatment where the hematoma was shown to resolve on sequential CT scans but did not demonstrate the appearance of a convexity collection (7). IHSDHs have been treated by several approaches. Early accounts employed burr-hole drainage and trephination with mixed results. Given the potential for disastrous intraoperative hemorrhagic complications involving lacerations of structures in close proximity to the superior sagittal sinus (6,23), recent authors have advocated formal craniotomy with wide exposure of the fissure and control over the sinus (9,24). In our opinion this represents the more conservative option, providing for maximal evacuation of the clot and exposure of the lacerated vessel. A nonoperative approach has been described for patients with a definite diagnosis who are neurologitally intact or who are not surgical candidates (8,22). This approach assumes that if intracranial pressure can be monitored and intracranial pressure and seizures can be controlled, the clot will resolve in situ or will liquify and migrate to a convexity position where it may be evacuated by a less invasive burr hole approach. This may be justified in the intact patient with a small clot in the setting of continuous monitoring and rapid access to full operating facilities. The danger of leaving a known mass lesion within the intracranial compartment with the potential for rapid decompensation should not be underestimated (6). This point deserves additional emphasis in light of our documentation of an arterial source of hemorrhage in IHSDHs of traumatic origin. The pontine hemorrhage that we describe probably occurred as a result of herniation in the period between the accumulation of the clot and the patient’s clinical deterioration. Had our patient undergone evacuation of the clot and repair of the offending vessel while she was still in good condition (GCS = 14), she perhaps would have avoided herniation with subsequent pontine hemorrhage and made a full recovery. SUMMARY IHSDs are a rare and more benign form of SDH. They present in a delayed fashion, most typically after occipital trauma. The falx syndrome is commonly seen at the time of presentation and is an important localizing feature. Disruption of the bridging veins is the most common etiology, however, bleeding from a lacerated arterial source can occur. Our review of the literature concludes that there is a need for prompt diagnosis and treatment, despite a patient’s relatively stable neurological status. Acknowledgement-The authors would like to thank Bradford B. Walters, MD, Pm, for reviewing the manuscript and providing two additional cases for the analysis. REFERENCES 1. Feuerman T, Wackym PA, Gade GF, Becker DP. 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