Delayed traumatic intracerebellar hematoma

Delayed Traumatic Intracerebellar Hematoma PhiUip A. Tibbs, M.D., Steven J. Ooldstein, M.D., and John R. Smithson, Jr., M.D.

displacement of the fourth ventricle, consistent with a contusion of the cerebellum (Fig. 1). The patient was observed closely in the neurosurgical intensive care unit. Twelve hours after admission he became more difficult to arouse, although he would still awaken and was oriented. A repeat C-q" scan revealed a highdensity intmcerebellar mass indicative of a large hematoma in the left cerebellar hemisphere, with compression of the fourth ventricle and obstructive hydrocephalus (Fig. 2). During the scanning procedure the patient became deeply obtunded and decerebrate. A catheter was immediately Detection of posttraumatic delayed intracerebral he- placed into the right lateral ventricle through a frontal twist matomas has been greatly expedited by the advent of drill hole, and the patient was taken to the operating room. computed tomographic (CT) scanning [5, 6]. However, A left suboccipital craniectomy revealed a dural laceration delayed traumatic intracerebellar hematomas have re- beneath the linear fracture; intradurally a bulging contused mained rare; there have been only 3 previous cases reported left cerebellar hemisphere was found. A large acute hein the literature [1, 9]. matoma was evacuated through a cortical incision. We report a case in which a large intracerebellar Several hours after the operation the patient was able to hematoma developed in a patient whose initial CT scan obey commands and was noted to have a right: sixth nerve showed only contusion of the left cerebellar hemisphere. palsy. Over the next several days he became ambulatory We believe this case is the first reported in which early use with normal mentation. Follow-up CT scan (Fig. 3) of serial CT scans led to immediate evacuation of a de- showed complete evacuation of the hematoma and reconlayed traumatic intracerebellar hematoma and in which the stitution of a normal fourth ventricle. The patient's most patient survived. recent evaluation in March, 1981, revealed that he is functioning normally; a partial right sixth nerve palsy is the Case Report only remaining neurological deficit. A 30-year-old man sustained a head injury in a motorcycle accident on August 8, 1980. On initial examination the Discussion patient was lethargic but easily arousable. There was ten- In all large series of head-injured patients, hematomas of demess, edema, and ecchymosis over the left occipital area. the posterior fossa are unusual [7, 8]; subdural and epidural Optic disks were normal and there were no abnormal cranial hematomas far outnumber intraparenchymal lesions [4, nerve findings. Motor and reflex examinations were nor- 10]. In the 14 cases of traumatic hematomas in:the posterior mal. Roentgenograms of the skull demonstrated a linear fossa reported by Fisher and associates [4], only 2 had innondepressed fracture of the left occipital bone extending tracerebellar hematomas and neither had a delayed onset. into the foramen magnum. CT scan of the head revealed Wright's [10] 17 cases of hematomas in the posterior fossa abnormal density of the left cerebellar hemisphere with included 6 intracerebellar clots, all of which were apparently acute. Only 3 cases of delayed traumatic intracerebellar heFrom the Departmentof Surgery, Divisionof Neurosurgery,and the De- matomas have been described (Table). Barantham and partment of Radiology, University of Kentucky Medical Center, Dennyson [1] reported 2 cases of intracerebellar hematoma Lexington, KY. in 21 cases of delayed traumatic hematomas in a population Addressreprintrequeststo Dr. PhillipA. Tibbs, Divisionof Neurosurgery, of 7,866 head injuries. One case resulted from a blow to the University of KentuckyMedical Center, 800 Rose St., Lexington,KY 40536. occiput that produced an occipital fracture and laceration Key words: hematoma;cerebellum;head injury; delayedhematoma;CT of the underlying cerebellum; the other was a contrecoup scan; trauma. lesion secondary to a blow on the brow. Olin and colleagues

A case of delayed traumatic intracerebellar hematoma is presented in which the patient survived after diagnosis and surgical intervention. The computed tomographic and clinical features of this entity are reported, and theories of pathogenesis are discussed. We advise a high index of suspicion for delayed intracerebellar hematomas in patients with cerebellar contusion following trauma. Tibbs PA, OoldsteinSJ, SmithsonJR Jr: Delayed traumatic intracerebellarhematoma.SurgNeurol 16:309-311, 1981

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Fig. 1. The initial unenhanced C T scan demonstrates swelling of an abnormally dense left cerebellar hemisphere with anterior and left lateral displacement of the fourth ventricle. These findings are indicative of posttraumatic cerebeUar contusion.

Fig. 3. Three weeks after the patient's injury the C T scan is normal except for postoperative changes. The fourth ventricle has retumecl to its normal position and there is no evidence of residual hematoma or ventriculomegaly.

Summary of Data from Reported Cases of Delayed Traumatic Intracerebellar Hematoma Mechanism Author Barantham [1], 1972 Olin [9], 1980 Tibbs (present study)

Fig. 2. A repeat C T scan nine hours later reveals a high.density intracerebeUar mass on the left not present initially and thought to be a large cerebellar hematoma. The fourth ventricle and aqueduct are compressed by the mass, resulting in supratentorial ventricular enlargement.

No. of Patients

ContreCoup coup Survivors

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1

1

0

1 1

... 1

1 ...

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[9] recently described a second patient who had delayed brainstem injury is to be prevented. Although traumatic onset of an intracerebellar hematuma with a contrecoup cerebellar hemorrhages or hemorrhagic contusions may be managed conservatively in selected cases, evidence on CT mechanism of origin. None of these 3 patients survived. A number of pathophysiological mechanisms have been scan of an expanding hematoma correlated with neurologiinvoked to explain the development of delayed post- cal deterioration, brainstem signs, and obliteration or shift traumatic hematomas. B611inger [2], who in 1891 coined of the fourth ventricle makes evacuation of the delayed inthe term traumatische Sp;~t.apoplexie, theorized that cranial tracerebellar hematoma mandatory. trauma produces focal softening and necrosis of the parenchyma and vessels, resulting in delayed hemorrhage. Evans References and Scheinker [3] described petechial hemorrhages in au1. Barantham G, Dennyson WG: Delayed traumatic intracerebral hemorrhage. J Neurol Neurosurg Psychiatry 35:698-706, 1972 topsy specimens of head-injured patients and concluded 2. B6llinger O: Ueber traumatische Sp~t-apoplexie: Etn Beitrag zur that these may coalesce to form larger hematomas. In the Lehre yon der Himershtitterung, in lnternationale 8eitrage zur wiscase reported by Olin et al [9], the intracerebellar hesenschaftlichen Medizin, Festschrift, Rudolf Virchow gewidmet zur Vollendung seines 70 Lebenjahres. Berlin: Hirschwald, 1891, Vol 2, matuma was preceded by a cerebellar contusion docupp 457-470 mented by CT scan and later by postmortem examination. 3. Evans JP, Scheinker IM: Histologic studies of the brain following Our case also suggests that delayed intracerebellar hehead trauma. 1I. Post-traumatic petechia[ and massive intracerebral hemorrhage. J Neurosurg 3:101-113, 1946 matomas may derive from late hemorrhage into an area 4. Fisher RG, Kim JK, Sachs E Jr: Complicationsin the posteriorfossa of cerebellar contusion detectable on the initial C T scan. due to occipital trauma--their operability. JAMA 167:176-182, The lethal nature of previously reported delayed traumat1958 5. Gudeman SK, Kishore PRS, Miller JD, Giaevendulis AK, Lippes ic intracerebellar hematomas suggests that early diagnosis MH, Becker DP: The genesis and significance of delayed traumatic is all important in preventing fatal brain injury. Previous hematomas. Neurosurgery5:309-313, 1979 cases had a fatal outcome because of delay in diagnosis be6. Hirsh LF: Delayed traumatic intracerebral hematomas after surgical decompression. Neurosurgery5:653-655, 1979 fore the advent of C T scanning [1] or because of the sever7. Jamieson KG, Yelland JDN: Extradural hematomas: report of 167 ity of coexisting supratentorial injury [9]. We believe that cases. J Neurosurg 29:13-23, 1968 the head-injured patient who has evidence of cerebellar 8. McKissockW, Richardsbn A, Bloom WH: Subdural hematoma, a review of 389 cases. Lancet 1:1365, 1960 contusion on initial C T examination should be considered 9. Olin MS, Young HA, Schmidek HH: Contracoup intracerebellar at risk for development of delayed intracerebellar hemorhemorrhage: report of a case. Neurosurgery7:271-2~3, 1980 rhage. Even minor degrees of neurological deterioration 10. Wright RL: Traumatic hematomas of the posterior cmniat fossa. J Neurosurg 25:402-409, 1966 should prompt immediate repeat C T scanning if irreversible

Book Review' Current Surgical Management of Neurologic Disease edited by Charles B. Wilson, M.D., and Julian T. Hoff, M.D., New York, Edinburgh, London, Churchill Livingstone, 1980 355 pp., $39.50 Reviewed by James D. Geissinger, M.D., F.A.C.S., Tallahassee, Florida As the title might imply, the editors state that this text has been written for nonneurosurgeons to keep them informed of the changing pattern of neurological surgery. To accomplish this goal, 29 authorities have combined their expertise in writing specific chapters under the broad headings of: congenital disorders, neoplastic disease, vascular disorders, trauma, and infectious and "acquired" disorders. As one might imagine, virtually every ailment confronting the neurosurgeon is included in this work. To satisfy the objectives of the book, the contributors have been carefully chosen, and would be considered by

their neurosurgical colleagues as both authoritative and scholarly in their approach. Historical background, up-tudate statistics, and clinical material from their own experience all serve to hold the reader's interest. Old theories on the pathogenesis and treatment of disease are reviewed, along with the current concepts that are replacing them. Such changing attitudes are portrayed no more vividly than in the chapters on syringomyelia or those on tumors of the pituitary and pineal regions. The book is succinct and easy to read. Yet, with the important statistics, graphs, appropriate case histories, roentgenograms, and pertinent illustrations the reader is left with a more than basic understanding of the diseases discussed. There are many salient features to the book but none any more important than the manner in which the authors have condensed the vast volume of world literature on particular subjects into a workable text. For those desiring more detail, bibliographies are included. The readers also benefit from the personal experience of the individual