Online newspaper of professor Yasser Metwally

The author: Professor Yasser Metwally

http://yassermetwally.com 

MANAGEMENT OF INTRACEREBRAL HAEMORRHAGE

The management of ICH involves two main issues: (a) the prevention and treatment of increased ICP; and (b) the choice between medical and surgical therapy.

• Prevention and treatment of increased intracranial pressure

In addition to the effects of the haematoma itself, there are a number of possible contributors to increased ICP in the acute stage of ICH. They need to be treated aggressively since any increases in ICP result in the lowering of cerebral perfusion pressure (CPP), which results in further compromise of neurological function. They include: hypertension, hypoxia, hyperthermia, seizures, and elevations of intrathoracic pressure (Ropper, 1993). Hypertension in patients with a mass lesion results in increased CPP in areas of brain with impaired autoregulation, contributing to the formation of brain oedema. There are no specific guidelines for the management of hypertension in this setting, except for the maintenance of normal CPP, in the 60-70 mmHg range. The medications of choice are those without cerebral vasodilator properties, and a useful combination is labetalol and furosemide (Ropper, 1993). However, in instances of severe hypertension the use of rapid-acting vasodilators such as nitroprusside is justified, as they produce rapid and easily titrable management of blood pressure in emergency situations. Hypoxia produces an increase in cerebral blood flow (CBF) and cerebral blood volume, with an increase in ICP in patients with poor cerebral compliance (Siesjb et al, 1976). Adequate oxygenation is thus essential in patients with ICH and increased ICP, with the aim of maintaining pO, in the 100-1 50 mmHg range. Hyperthermia increases CBF and ICP, and also elevates arterial pCO, the latter partially counteracting the effects of therapeutic hyperventilation (Ropper, 1993). This calls for vigorous treatment of fever and infections. The occurrence of seizures in the setting of acute ICH, especially likely in the lobar variety, can result in increased CBF, cerebral blood volume, and ICP. Their control is generally achieved by using intravenous diazepam, followed by loading doses of phenytoin or phenobarbitone. Elevations in intrathoracic pressure produced by endotracheal suction, coughing, chest therapy, and the use of positive end-expiratory pressure can result in transient elevations in ICP. These measures, otherwise critically important in maintaining airway potency and adequate oxygenation, need to be used judiciously and monitored closely in the setting of ICH with increased ICP.

The specific measures that are useful in the treatment of increased ICP are listed in Table 1. Hyperventilation reduces ICP by producing vasoconstriction, which is maximal in normal areas of the brain, where autoregulation is preserved (Lassen, 1974). The ideal partial pressure of carbon dioxide (pCO,) for this purpose is between 28 and 35 mmHg (Ropper, 1993). The effects of hyperventilation are transient, as compensatory mechanisms within the central nervous system overcome the vasoconstriction that results from hypocarbia. A potential side-effect of the use of therapeutic hyperventilation is hypotension, that results from lowered cardiac filling pressure. It can be avoided by maintaining a normal intravascular volume, with isotonic or slightly hypertonic solutions. The use of osmotic diuretics is highly effective in rapidly lowering elevated ICP. Their effect is exerted by shifting water from the brain substance into the intravascular space, along with a small additional effect of reducing cerebrospinal fluid production and volume (Ropper, 1993). High-dose intravenous barbiturates effectively reduce CBF and brain metabolism, resulting in a decrease in ICP (Shapiro, 1975). The most commonly used agent is thiopentone, 1-5 mg/kg. Its main side-effects are hypotension and markedly reduced neurological function, at times making the neurological examination useless as a way of monitoring therapy. The use of corticosteroids in the treatment of increased ICP in ICH is controversial, since their value in reducing brain oedema in other conditions, such as brain metastases, has not been established in patients with ICH. In a controlled, randomized, double-blind clinical trial conducted by Poungvarin et al (1987), dexamethasone was not superior to placebo in terms of mortality at 21 days from onset of ICH, and the rate of complications was significantly higher in the dexamethasone-treated group.

Table 1. Major therapies for acutely raised ICP Treatment

• Choice between medical and surgical therapy

This is a difficult decision, since there are no adequate data to assist the clinician in the therapeutic choice. Most of the reported series that compare both forms of therapy in ICH contain biases, primarily related to different pre-operative status in the two treatment groups, non-random selection of therapy, and delayed performance of surgery. These preclude any conclusions regarding the value of one form of treatment over the other.

The pre-CT series of McKissock et al (I 96 1) documented no difference in mortality (65 versus 5 1 %) or functional outcome (I I versus 12%, for full recovery) in a group of 180 patients with supratentorial ICH who were randomly assigned to surgical (N = 89) or medical (N = 9 1) therapy. They observed a better outcome in lobar than in deep hemispheric haemorrhages, but still without differences between surgical and non-surgical treatment. More recent series show essentially similar results. Waga and Yamamoto (1983) found no differences in outcome in a group of 74 patients with putaminal haemorrhage, 18 treated surgically and 56 non-surgically. Juvela et al (1989) reported disappointing results with surgical treatment in a group of 52 patients with supratentorial ICH randomly assigned to surgical (N = 26) or non-surgical (N = 26) therapy within 48 hours of ICH onset.

A different surgical approach was taken by Kaneko et al (1983), who performed ultra-early (within 7 hours from onset) drainage of intracerebral haematomas in 100 patients, with the use of microsurgical techniques. They reported a figure of 7% mortality, and 89% of the 93 survivors had an outcome rated as highly satisfactory. However, the results of this study need to be interpreted with caution, as there was no control group, and the study group was in a relatively good prognostic category, as only 22% of the patients were in the semicoma group with GCS of 6 to 9. Despite their limitations, these results stimulated Batjer et al (1990) to conduct a controlled trial of surgical versus non-surgical management in putaminal haemorrhage. Patients were randomized to three treatment groups:

• best medical management, with hyperventilation, osmotic diuresis, dexamethasone, and control of other medical complications;

• best medical management plus ICP monitoring by ventriculostomy, maintaining the ICP below 20 mmHg (with both medical therapy and cerebrospinal fluid drainage);

• surgical evacuation of the haematoma.

After randomizing 21 patients, an interim analysis showed very poor results in all treatment groups: 15 patients (71 %) had died or remained in a vegetative state at 6 months after treatment, and only four (19%) were independent and at home. These results led to the early termination of the trial.

In conclusion, the issue of surgical versus medical treatment of ICH remains unresolved. Randomized clinical trials should provide the data needed to determine the value of surgical treatment. These trials should include not only conventional surgical haematoma drainage, but also novel forms of surgical treatment of ICH, such as stereotactic needle aspiration of haematomas with instillation of thrombolytic agents (urokinase) in the cavity, in order to promote full haematoma evacuation (Matsumoto and Hondo, 1984).

• Surgical issues in lobar and cerebellar haemorrhage

Although the value of surgical therapy in ICH in general remains unproven, lobar and, especially, cerebellar haemorrhages have improved outcomes with surgical intervention, especially in the event of progressive decline in the level of consciousness and/or signs of brainstem compression.

In lobar haemorrhage, the superficial and surgically accessible position of the haematoma (in comparison with putaminal and thalamic haemorrhage), often leads to considering surgical therapy. This applies particularly to patients with intermediate size haemorrhages, with volumes in the 20-40 cm range, who have better outcomes after surgical drainage of the haematoma, especially in the face of a progressive decline in the level of consciousness and increase in haematoma size on CT (Kase et al, 1982). Patients with smaller (volume 40-50 cm) haematomas are generally not subjected to surgical treatment, since the former do uniformly well with non-surgical therapy and the latter have poor outcomes irrespective of the treatment modality used (Kase et al, 1982; Volpin et al, 1984).

Patients with cerebellar haemorrhage have generally good prognosis when the haematoma is small, of 1-2 cm in diameter. However, slightly larger haematomas have a considerable potential for sudden neurological deterioration secondary to brainstem compression, resulting in death unless emergency haematoma evacuation is undertaken (Fisher et al, 1965). Patients at high risk of this complication are those who have haematomas 3 cm in diameter, fourth ventricular compression with supratentorial hydrocephalus (Little et al, 1978), and effacement of the quadrigeminal cistern (Taneda et al, 1987). Any of these findings, along with signs of ipsilateral tegmental pontine dysfunction are indications for emergency surgical evacuation of the haematoma by suboccipital craniotomy. This procedure needs to be considered under these circumstances even in patients who are still alert or only drowsy, since their surgical mortality is markedly lower (17%) in comparison with that of patients who have reached the level of stupor or coma (75%) by the time they are subjected to surgical treatment (Ott et al, 1974) (Table 2). Surgical decision needs to be made ideally when patients are still responsive, since waiting for signs of deterioration in the level of consciousness carries the risk of abrupt and unpredictable change to stupor and coma, with the consequent worsening outcome after surgery.

Table 2. Cerebellar haemorrhage: surgical mortality according to preoperative mental status.

Ott et al [1974]

SUMMARY

The management of intracerebral haemorrhage involves: (a) the prevention and treatment of increased intracranial pressure; and (b) the choice between surgical and nonsurgical treatment, a clinical decision that is still controversial as a result of the paucity of controlled clinical data comparing both treatment modalities.

---

REFERENCES

Abe M, Kjellberg RN & Adams RD (1989) Clinical presentations of vascular malformations of the brain stem: comparison of angiographically positive and negative types. Journal of Neurology, Neurosurgery and Psychiatry 52: 167-175.

Barinagarrementeria F & Cantu C (1994) Primary niedullary hemorrhage: report of four cases and review of the literature. Stroke 25: 1684-1687.

Barraquer-Bordas L, Illa 1, Escartin A et al (1981) Thalamic hemorrhage: a study of 23 patients with diagnosis by computed tomography. Stroke 12: 524-527. Batjer HH, Reisch JS, Allen BC et al (1990). Failure of surgery to improve outcome in hypertensive putaminal hemorrhage: a prospective randomized trial. Archives of Neurology 47: 1103-1106.

Berger AR, Lipton RB, Lesser ML et at (1988) Early seizures following intracerebral hemorrhage: implications for therapy. Neurology 38: 1363-1365.

Biller J, Loftus CM, Moore SA et at (1987) Isolated central nervous system angiitis first presenting a spontaneous intracranial hemorrhage. Neurosurgery 20: 310-315.

Bogousslavsky J, Van Melle G & Regli F (1988) The Lausanne Stroke Registry: analysis of 1,000 consecutive patients with first stroke. Stroke 19: 1083-1092.

Broderick JP, Brott TG, Tomsick T et at (1990) Ultra-early evaluation of intracerebral hemorrhage. Journal of Neurosurgery 72: 195-199.

Caplan L (1988) Intracerebral hemorrhage revisited. Neurology 38: 624-627.

Caplan LR & Goodwin JA (1982) Lateral tegmental brainstem hemorrhages. Neurology 32: 252-260.

Citron BP, Halpem M, McCarron M et a] (1970) Necrotizing angiitis associated with drug abuse. New England Journal of Medicine 283: 1003-101 1.

Cole FM & Yates P (1967) Intracerebral microaneurysms and small ccrebrovascular lesions. Brain 90:759-767.

Crawford JV & Rusell DS (1956) Cryptic arteriovenous and venous hamartom&s of the brain. Journal of Neurology, Neurosurgery and Pvychiatry 19: 1 -1 I..

Delaney P & E&tes M (1980) Intracranial hemorrhage with Amphetamine use. Neurology .30: 1125-1128.

Dul K & Drayer BP (I 994) CT and MR imaging of intracerebral hemorrhage. In Kase CS & Caplan (ed&) Intracerebral Hemorrhage, pp 73-93. Boston: Butterworth-Heinemann.

Fisher CM (I 959) The pathologic and clinical aspects of thalamic hemorrhage, Transactions or the American Neurol(igical Association 84: 56-59.

Fisher CM (i961) The pathology and pathogenesis of intracerebral hemorrhage. In Fields WS (ed.) Pathogenesis and Treatment of Cerebrovascular Disease, pp 295-317. Springfield: Charles C Thomas.

Fisher CM (1971) Pathological observations in hypertensive cerebral hemorrhage. Journal of Neuropathology and Experimental Neurology 30: 536-550.

Fisher CM, Picard EH, Polak A et a] (I 965) Acute hypertensive cerebellar hemorrhage: diagnosis and surgical treatment. Journal of Nervous and Mental Diseases 140: 38-57.

Foulkes MA, Wolf PA, Price TR et at (1988) The Stroke Data Bank: design, methods and baseline characteristics. Stroke 19: 547-554.

Franke CL, de Jonge J, van Swieten JC et at (1990) Intracerebral hematomas during anticoagulant treatment. Stroke 21: 726-730.

Franke CL, van Swieten JC, Algra A et at (1992) Prognostic factors in patients with intracerebral haematoma. Journal of Neurology, Neurosurgery and Psychiatry 55: 653-657.

Furlan AJ, Whisnant JP & Elveback LR (1979) The decreasing incidence of primary intracerebral hemorrhage: a population study. Annals of Neurology 5: 367-373.

Glick R, Hoying J, Cerullo L & Perlman S (1987) Phenylpropanolamine: an over-the-counter drug causing central nervous system vasculitis and intracerebral hemorrhage. Neurosurgery 20: 969-974.

Gore JM, Sloan M, Price TR et at (I 99 1) Intracerebral hemorrhage, cerebral infarction,and subdural hematoma after acute myocardial infarction and thrombolytic therapy in the Thrombolysis In Myocardial Infarction study: Thrombolysis In Myocardial Infarction, phase 11, pilot and clinical data. Circulation 83: 448-459.

Gray F, Dubas F, Roullet E & Escouroulle R (1985) Leukoencephalopathy in diffuse hemorrhagic cerebral amyloid angiopathy. Annals of Neurology 18: 54-59.

Green RM, Kelly KM, Gabrielsen T et at (1990) Multiple intracerebral hemorrhages after smoking crack cocaine. Stroke 21: 957-962.

Gudmundsson G, Haligrimsson J, Jonasson TA & Bjamason 0 (1972) Hereditary cerebral haemorrhage with amyloidosis. Brain 95: 387-404.

Hankey GJ (1991) Isolated angiitis/angiopathy of the central nervous system. Cerebrovascular Disease 1: 2-15.

Helweg-Larsen S, Sommer W, Strange P et at (1984) Prognosis for patients treated conservatively foi spontaneous intracerebral hematomas. Stroke 15: 1045-1048.

Hier DB, Davis KR, Richardson EP et at (1977) Hypertensive putaminal hemorrhage. Annals oj Neurology 1: 152-159.

Juvela S, Heiskanen 0, Poranen A et at (1989) The treatment of spontaneous intracerebral hemorrhage: a prospective randomized trial of surgical and conservative treatment. Journal of Neurosurgery 70: 755-758.

Kaneko M, Tanaka K, Shimada T et at (1983) Long-term evaluation of ultra-early operation for hypertensive intracerebral hemorrhage in 100 cases. Journal of Neurosurgery 58: 838-842.

Kase CS (1986) Intracerebral hemorrhage: Non-hypertensive causes. Stroke 17: 590-595.

Kase CS & Caplan LR (1994) Intracerebral Hemorrhage. Boston: Butterworth-Heinemann.

Kase CS, Maulsby GO & Mohr JP (1980) Partial pontine hematomas. Neurology 30: 652-655.

Kase CS, Williams JP, Wyatt DA et at (1982) Lobar intracerebral hematomas: clinical and CT analysis of 22 cases. Neurology 32: 1146-1150.

Kase CS, Robinson RK, Stein RW et at (1985) Anticoagulant-related intracerebral hemorrhage. Neurology 35: 943-948.

Kase CS, Foster TE, Reed JE et at (1987) Intracerebral hemorrhage and phenylpropanolamine use. Neurology 37: 399-404.

Kase CS, O’Neal AM, Fisher M et at (1990) Intracranial hemorrhage after use of tissue plasminogen activator for coronary thrombolysis. Annals of Internal Medicine 112. 17-21.

Kase CS, Pcssin MS, Zivin JA et at (1993) intracranial hemorrhage after coronary thrombolysis with tissue plasminogen activator. American Journal of Medicine 92-.384-390.

Kikta DG, Devereaux Mw & Chandar K (1985) fntracranial hemorrhages due to phenytpropanolainine. Stroke 16: 510-512.

Kolodny EH, Rebeiz JJ, Caviness VS & Richardson EP (1968) Granulomatous angiitis of the central nervous system. Archives of Neurology 19: 510-524.

Kucharczyk W, Lemme-Pleghos L, Uske A et at (1985) Intracranial vascular malformations: MR and CT imaging. Radiology 156: 383-389.

Lassen NA (1974) Control of cerebral circulation in health and disease. Circulation Research 34: 749-760.

Levine SR, Brust JCM, Futrell N et at (1990) Cerebrovascular complications of the use of the crack form of alkaloidal cocaine. New England Journal of Medicine 323- 699-704.

Little JR, Tubman DE & Ethier R (1978) Cerebellar hemorrhage in adults: diagnosis by computerized tomography. Journal of Neurosurgery 48; 575-579.

Little JR, Dial B, Bellanger 0 et at (1979) Brain hemorrhage from intracranial tumor. Stroke 10: 283-288.

Loes DJ, Biller J, Yuh WTC et at (1 990) Leukoencephalopathy in cerebral amyloid angiopathy: MR imaging in four cases. American Journal of Neuroradiology 11: 485-488.

Luyendijk W (1972) Intracerebral haematoma. In Vinken PJ & Bruyn GW (eds) Handbook of Clinical Neurology, pp 660-719. Amsterdam: North Holland Publishing Co.

McCormick WF & Nofzinger JD (1966) Cryptic vascular malformations of the central nervous system. Journal of Neurosurgery 24: 865-878.

McKissock W, Richardson A & Taylor J (I 961) Primary intracerebral haemorrhage: a controlled trial of surgical and conservative treatment in 180 unselected cases. Lancet it: 221-226.

Margolis MT & Newton TH (1971) Methamphetamine (speed) arteritis. Neuroradiology 2: 179-182.

Massaro AR, Sacco RL, Mohr JP et at (1991) Clinical discriminator, of lobar and deep hemorrhages: the Stroke Data Bank. Neurology 41: 1881-1885.

Matsumoto K & Hondo H (1984) CT-guided stereotaxic evacuation of hypertensive intracerebral hematomas. Journal of Neurosurgery 61: 440-448.

Mohr JP, Caplan LR, Melski JW et at (1978) The Harvard Cooperative Stroke Registry: a prospective registry. Neurology 28: 754-762.

Moore PM & Copps TR (1983) Neurological complications of vasculitis. Annals of Neurology 14: 155-167.

Morel-Maroger A, Metzger J, Bories J et at (1982) Les h6matomes bdnins du tronc cdrobral chez les hypertendus artdriels. Revue Neurologique 138: 437-445.

New PFJ & Aronow S (1976) Attenuation measurements of whole blood and blood fractions in computed tomography. Radiology 121: 635-640.

Ott KH, Kase CS, Ojemann RG et at (1974) Cerebellar hemorrhage: diagnosis and treatment: a review of 56 cases. Archives of Neurology 31: 160-167.

Pendlebury WW, lole ED, Tracy RP & Dill BA (1991) lntracerebral hemorrhage related to cerebral amyloid angiopathy and t-PA treatment. Annals of Neurology 29: 210-213.

Poungvarin N, Bhoopat W, Viriyavejakul A et at (1987) Effects of dexamethasone in primary supra- tentorial intracerebral hemorrhage. New England Journal of Medicine 316: 1229-1233.

Rfidberg JA, Olsson JE & RAdberg CT (1991) Prognostic parameters in spontaneous intracerebral hematomas with special reference to anticoagulant treatment. Stroke 22: 571-576.

Requena 1, Arias M, L6pez-lbor L et al (199 1) Cavemomas of the central nervous system: clinical and neuroimaging manifestations in -47 patients. Journal of Neurology, Neurosurgery and Psychiatry 54:590-594.

Rigamonti D, Hadley MN, Drayer BP et al (1988) Cerebral cavernous malformations: incidence and familial occurrence. New England Joumal of Medicine 319: 343-347.

Roig C, Carvajal A, Illa I et al (1982) H6morragies mdsencdphaliques isoldes: trois cas diagnostiquds par tomodensitom6trie. Revue Neurologique 138: 53-61.

Ropper AH (1993) Treatment of intracranial hypertension. In Ropper AH (ed.) Neurological and Neurosurgical Intensive Care, pp 29-52. New York: Raven Press.

Ropper AH & Davis KR (1980) Lobar cerebral hemorrhages: acute clinical syndromes in 26 cases. Annals of Neurology 8: 141-147.

Russell DS (1954) The pathology of spontaneous intracranial haemorrhages. Proceedings of the Royal Society of Medicine 47: 689-693.

Shapiro HM (1975) Intracranial hypertension: therapeutic and anesthetic considerations. Anesthesiology 43: 445-47 1.

Siesjp BK, Carlsson C, Hagerdal M et al (1976) Brain metabolism in the critically ill. Critical Care Medicine 4: 283-294.

Simard JM, Garcia-Bengochea F, Ballinger WE et al (1986) Cavernous angioma: a review of 126 collected and 12 new clinical cases. Neurosurgery 18: 162-172.

Stahl SM, Johnson KP & Malainud N (1980) The clinical and pathological spectrum of brain-stem vascular malformations: long-term course simulates multiple sclerosis. Archives of Neurology 37: 25-29.

Stein RW, Kase CS, Hier DB et al (1984) Caudate hemorrhage Neurology 34: 1549-1554.

Sung C-Y & Chu N-S (1989) Epileptic seizures in intracerebral haemorrhage. Journal of Neurology, Neurosurgery and Psychiatry 52: 1273-1276.

Taneda M, Hayakawa T & Mogami H (1987) Primary cerebellar hemorrhage: quadiigeminal cistem obliteration on CT scans as a predictor of outcome. Journal of Neurosurgery 67: 545-552.

Tapia JF & Golden JA (1993) Case Records of the Massachusetts General Hospital (Case 27-1993). New England Journal of Medicine 329: 117-124.

Tapia JF, Kase CS, Sawyer RH et al (1983) Hypertensive putaminal hemorrhage presenting as pure motor hemiparesis. Stroke 14: 505-506.

The Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO) Ila Investigators (1994) Randomized trial of intravenous heparin versus recombinant hirudin for acute coronary syndromes. Circulation 90: 1631-1637.

The TIMI Study Group (1989) Comparison of invasive and conservative strategies after treatment with intravenous tissue plasminogen activator in acute myocardial infarction: results of the Thrombolysis in Myocardial Infarction (TIMI) phase 11 trial. New England Journal of Medicine 320:618-627.

Toffol GJ, Biller J & Adams HP (1987) Nontraumatic intracerebral hemorrhage in young adults. Archives of Neurology 44: 483-485.

Tomck RM (1975) Congophilic angiopathy complicated by surgery and massive hemorrhage: a light and electron microscopic study. American Joumal of Pathology 81: 349-366.

Tuhrim S, Datnbrosia JM, Price TR et al (1988) Prediction of intracerebral hemorrhage survival. Annals of Neurology 24: 258-263.

Vaquero J, Salazar J, Martinez R et al (1987) Cavemomas of the central nervous system: clinical syndromes, CT scan diagnosis, and prognosis after treatment in 25 cases. Acta Neurochirurgica 85:29-33.

Vinters HV (1987) Cerebral atnyloid angiopathy: a critical review. Stroke 18: 311-324.

Vinters HV & Gilbert JJ (1983) Cerebral ainyloid angiopathy: incidence and complications in the aging brain. II. The distribution of amyloid vascular changes. Stroke 14: 924-928.

Volpin L, Cervellini P, Colombo F et al (1984) Spontaneous intracerrbral hematomas: a new proposal about the usefulness and limits of surgical treatment. Neurosurgery 15: 663-666.

Vonsattel JPG, Myers RH, Hedley-Whyte ET et al (I 99 1) Cerebral amyloid angiopathy without and with cerebral hemorrhages: a comparative histological study. Annals of Neurology 30: 637- 649.

Waga S & Yamamoto Y (1983) Hypertensive putaminal hemorrhage: treatment and results: is surgical treatment superior to a conservative one? Stroke 14: 480-485.

Waga S, Okada M & Yamamoto Y (1979) Reversibility of Parinaud syndrome in thalamic hemorrhage. Neurology 29: 407-409.

Waga S, Fujimoto K, Okada M et al (1986) Caudate hemorrhage. Neurosurgery 18: 445-450.

Wakai S, Yamakawa K, Manaka S & Takakura K (1982) Spontaneous intracranial hemorrhage caused by brain tumor: its incidence and clinical significance. Neurosurgery 10: 437-444.

Walshe TM, Davis KR & Fisher CM (1977) Thalaniic hemorrhage: a computed tomographic-clinical correlation. Neurology 27: 217-222.

Weisberg LA (1984) Caudate hemorrhage. Archives of Neurology 41: 971-974.

Weisberg LA (1985) Subcortical lobar intracerebral haemoffhage: clinical-computed tomographic correlations. Joumal of Neurology, Neurosurgery and Psychiatry 48: 1078-1084.

Weisberg LA & Wall M (1987) Alexia without agraphia: clinical-computed tomographic correlations. Neuroradiology 29: 283-286.

Weisberg LA & Stazio A (1988) Nontraumatic frontal lobe hemorrhages: clinical-computed tomo- graphic correlations. Neuroradiology 30: 500-505.

Weisberg LA & Stazio A (1989) Nontraumatic parietal subcortical hemorrhage: clinical-computed tomographic correlations. Computerized Medical Imaging and Graphics 13: 355-361.

Weisberg LA, Stazio A, Shainsnia M et al (1990) Nontraumatic temporal subcortical hemorrhage: clinical computed tomographic analysis. Neuroradiology 32: 137-141.

Whisnant JP, Cartlidge NEF & Elveback LR (1978) Carotid and vertebral-basilar transient ischemic attacks: effect of anticoagulants, hypertension, and cardiac disorders on survival and stroke occurrences population study. Annals of Neurology 3: 107-115.

Wijdicks EFM & Jack CR (1993) Intracerebral hemorrhage after fibrinolytic therapy for acute myocardial infarction. Stroke 24: 554-557.

Wintzen AR, de Jonge H, Loeliger EA & Bots GTAM (1984) The risk of intracerebral hemorrhage during oral anticoagulant treatment: a population study. Annals of Neurology 16: 553-558.

Yamasaki T, Handa H, Yamashita J et al (1986) Intracranial and orbital cavernous angiomas: a review of 30 cases. Journal of Neurosurgery 64: 197-208.

Zimmerman RD, Leeds NE & Naidich TP (1977) Ring blush associated with intracerebral hematoma. Radiology 122: 707-71 1.