Neurological Research A Journal of Progress in Neurosurgery, Neurology and Neurosciences ISSN: 0161-6412 (Print) 1743-1328 (Online) Journal homepage: http://www.tandfonline.com/loi/yner20 Symptomatic subacute subdural hematoma associated with cerebral hemispheric swelling and ischemia Nobuhiko Aoki, Akihiro Oikawa & Tatsuo Sakai To cite this article: Nobuhiko Aoki, Akihiro Oikawa & Tatsuo Sakai (1996) Symptomatic subacute subdural hematoma associated with cerebral hemispheric swelling and ischemia, Neurological Research, 18:2, 145-149, DOI: 10.1080/01616412.1996.11740393 To link to this article: http://dx.doi.org/10.1080/01616412.1996.11740393 Published online: 21 Jul 2016. Submit your article to this journal View related articles Citing articles: 4 View citing articles Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=yner20 Download by: [Australian Catholic University] Date: 22 August 2017, At: 09:04 Symptomatic subacute sub~ural hematoma associated with cerebral .· hemispheric swelling · and ischemia Nobuhiko Aoki, Akihiro Oikawa and Tatsuo Sakai Downloaded by [Australian Catholic University] at 09:04 22 August 2017 Department of Neurosurgery, Tokyo Metropolitan Ohkubo Hospital Tokyo, japan A 55-year-old man with traumatic acute subdural hematoma (SOH) was managed. l10nsurgically because of having isolated mild headache that resolved within a week. However, the patient developed an acute onset of amnestic aphasia 12 days post-trauma. Although the SOH itself did not increase in volume, remarkable swelling of the ipsilateral cerebral hemisphere was observed on CT scanning. CraniotQmy was required since the main component of the SOH was solid and partially organized. Post-operative recovery from · his speech disturbance · \-\las delayed, . necessitating speech therapy for more than two month?. Additionally, decreased cerebral blood flow on the affectedoside was observed even 3 months after injury. Symptomatic subacute SOH exclusively presenting as focal neurological deficits, though very rare, is worthwhile to be kept in mind as a pitfall in nonsurgical management of acute SOH. [Neural Res 1996; 18: 145-149] Keywords: Acute subdural hematoma; amnestic aphasia; head trauma; subacute subdural hematoma INTRODUCTION Most neurosurgeons seem to hesitate to operate on patients with acute subdural hematoma (SOH) which is thiri and represents minimal mass effect on computed tomography (CT) scans. This is a particularly practical dilenima in patients complaining of isolated mild headache without neurological findings. When acute SOH is managed neurosurgically, however, the patients may carry significant risks during the clinical course; i ~e., rapid increase of the hematoma volume in the acute stage 1, symptomatic subacute SDH 2- 5 , and evolution to chronic SDH 6 •7 . Among these pathological processes, subacute SOH has received less a:ttention, and the mechanism of its symptom onset has oeen considered to be secondary to the increase in the volume of hematoma2 -4. Recently, the authors encountered a patient with acute SOH which caused rapid onset of a focal neurologica l defi cit in the subacute stage. In addition, the mechanism of the pathophysiological process in this patient was considered to be different from that reported previously. Details of the clinical course in this patient are described, and the pitfall of nonsurgically manrJ.ged acute SDH in the subacute stage is highlighted. CASE REPORT A 55-year-old right-hand male journalist was referred to us for further management of acute SOH on November Correspondence and reprint requests to: Nobukiko Aoki, MD, Department of Neurosurgery, Tokyo Metropo litan Ohkubo Hosp ital~ 44-1, Kabukicho 2-chome, Shinjuku-ku, Tokyo 160, Japan. Accepted for publication December 1995. © 1996 Forefront Publishi ng Group 01 61 -6412/96/020145- 06 29, 1994. He struck the left parietal region urider a heavily drunken state at midnight on November 27. He ignored his symptom until 2 days later when he complained of headache, and presented to a nearby hospital, whereCT scans revealed acute SDH on the left side: His medical history was significant for hypertension, diabetes mellitus and duodenal ulcer w ithout treatment. Examination At the time of transfer to our hospital the patient complained of mild headache, but was alert and cooperative. His neurological examination did not show any abnormalities. A bruise was found on the left parietal region. A skull x-ray series failed to reveal fractures. CT scans of the head performed on admission demonstrated high-density SOH on the left side together with mild compression of the left lateral ventricle (Figure 1). Results of laboratory studies including coagu lation tests were all within normal range. Clinical course Because of having tolerable but persistent headache coupled with the possibil ity of evolution to symptomatic subacute SOH, he w as scheduled for inpatient observation. His headache resolved one week after admission without treatment. CT scans obtained on December 5 (8 days post-trauma) showed seemingly minimal reduction of the hematoma volume w ithout decrease of mass effect. He w as confirmed to remain neurologica lly intact and flu ently talked to his primary nurse at the time of lunch on December 9. At 1:30 p.m., (1 2 days post- Neurological Research, 1996, Volume 18, April 145 Downloaded by [Australian Catholic University] at 09:04 22 August 2017 Subacute subdural hematoma: Nobuhiko Aoki et a/. (A) (A) (B) (B) Plain computed tom98~<1PflY .scans ..on admission show . high-density subdural hematoma on the left side, associated with mild compression of the left lateral ventricle Figure 1: trauma), however, the nurse noted abnormality in his speech. An emergency neurological examination revealed that he was alert, but was unable to name any objects. He could repeat words and follow simple onestep commands. No other abnormalities in the motor, sensory and cranial nerve functions were observed. His neurological symptomatology was evaluated as amnestic aphasia by the neuropsychologist. Emergency CT scans showed rather slightly reduced volume of the 146 Neurological Research, 1996, Volume 18, April Figure 2: Plain computed tomography scans 12 day post-trauma reveal rather slight reduction of the subdural hematoma with . deE:rea5ed ·density, but demvhstrafe· deliii'ite iiic're-ase.. in 'the sliift ci'f · the midline structures to the right side hematoma with decreased density, but revealed definite increase in the shift of the midline structures to the right side. (Figure 2) T2-weighted magnetic resonance (MR) images showed SOH, shift of the midline structures and multiple lacunar infarctions in the left basal ganglia, corona radiata and pons; however, no pathological features producing swelling of the left cerebral hemispheric parenchyma were noted. (Figure 3) Arterial occlusion or veno- sinus thrombosis were not exhibited on MR angiography. Subacute subdural hematoma: Nobuhiko Aoki et a/. speech function was evidenced by global aphasia showing complete loss of auditory comprehension. Because of his neurological worsening associated with persistent mass effect on CT scans despite administration of steroids and osmotic agents, an emergency craniotomy was performed. Downloaded by [Australian Catholic University] at 09:04 22 August 2017 Surgery A left parieto-occipital craniotomy revealed partially organized, clots. Removal of these clots al lowed drainage of liquid hematoma from the frontal region. The miter membrane of the hematoma was present, but the inner membrane or other abnormal findings were not seen on the exposed cortical surface. Post-operative ~T scans did not show residual hematoma or cerebral parenchymal abnormalities. Recovery of his speech deficits was unexpectedly delayed; nominating dysphasia was observed at the time of discharge from this hospital two months after surgery. In addition, one month after discharge, although his speech function was completely normalized, and MR images failed to exhibit ) abnormalities apart from preexisting lacunar infarctions. Single photon emission computed tomography (SPECT) images revealed definite reduction of cerebral blood flow (CBF) on the . left fronto-temporo-parietal regions. (Figure 4) DISCUSSION (B) T2-weighed magnetic resonance images 12 days after injury show subdual hematoma, shift of the midline structures and multiple lacunar infarctions, but fail to exhibit other pathological features producing swelling of the left cerebral hemispheric parenchyma Figure 3: Under a diagnosis of symptomatic subacute subdural hematoma, percutaneous subdural tappin~ was performed at the bedside on an emergency basis . Although this procedure resulted in drainage of only 15 ml of liquid hematoma, his speech function improved to the level of being able to name simple objects. On the following morning, however, rapid deterioration of his Unlike acute or chronic SDH, there have been no large series of subacute SDH 8 , necessitating accumulation of detailed documentation of sporadic cases with subacute SDH. When summarizing previously reported cases, nonsurgically managed acute SDH, though rarely encountered, becomes symptomatic most frequently eleven or twelve days after injur/-4. The mechanism of symptomatic subacute SDH has been reported to be secondary to influx of cerebrospinal fluid (CSF) into the subdural space either by colloid-osmotic pressure difference between the liquid hematoma and CSF 2 , or by tearing of the arachnoid membrane3 A. Thus, the pathogenesis of symptomatic subacute SDH has been considered exclusively attributable to the progressive volume expansion of the hematoma with corresponding increase in the intracranial pressure. For this reason, it has not been difficult to predict possible development of symptomatic subacute SDH on serial CT studies and neurological observation. Additionally, the liquid hematoma has consisted of the main component in the pathological process, facilitating evacuation of the hematoma via percutaneous subdural tapping 2 or burrhole craniostomy in most cases. Based on our experience and the previously reported series 3A, the authors have closely observed this patient at the neurosurgical ward. Unexpectedly, however, the patient developed rapid onset of isolated speech disturbance without association of increase in the volume of the hematoma. The pathophysiological basis for his focal neurological deficit characterized by aphasia seems to be produced by relatively long-standing compression of the cortical surface, similar to transient ischemic attack Neurological Research, 1996, Volume 18, April 147 Downloaded by [Australian Catholic University] at 09:04 22 August 2017 Subacute subdural hematoma: Nobuhiko Aoki eta/. Figure 4: Single photon emission computed tomography images three months after injury demonstrate definite reduction of cerebral blood flow (arrows) on the left hemisphere in the chronic SOH 9 , resulting in cerebrovascular hypoperfusion 10 • This hypothesis is supported by the results of SPECT study which revealed definite reduction of CBF at least until three months after injury despite evacuation of the hematoma. Moreover, since it has been reported that SOH is usually associated with cerebrovascular hypoperfusion 11 ' 12 , surgical consideration may be usefully assessed by serial CBF studies in patients with minimally or mildly symptomatic acute SOH. Of particular note in the present patient is that remarkable increase of the hemispheric swelling is not associated with volume expansion of the hematoma itself, indicating the importance of repeat CT follow-up irrespective of neurological symptomatology. Although no evidence could be obtained by MR angiography on the venous phase, the above-described phenomenon may be related to altered venous hemodynamics due to mild but persistent compression of the cortex. To summarize, in patients with nonsurgically mana148 Neurological Research, 7996, Volume 78, April ged acute SOH which is delayed in resolution, it is essential to be aware of rapid development of focal neurological deficits with delayed recovery even after emergency craniotomy. 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