Neurology_Adams

Neurology_Adams. Rabkin SW, Mathewson FAL, Tate RB: Long-term changes in blood pressure and risk of cerebrovascular disease. Stroke 9:319, 1978. Reivich M, Holling HE, Roberts B, Toole JF: Reversal of blood flow through the vertebral artery and its effect on cerebral circulation. N Engl J Med 265:878, 1961. Rice GPA, Boughner DR, Stiller C, Ebers GC: Familial stroke syndrome associated with mitral valve prolapse. Ann Neurol 7:130, 1980. Roach GW, Kanchuger M, Mangano CM, et al: Adverse cerebral outcomes after coronary bypass surgery. N Engl J Med 335:1857, 1996. Roehmholdt ME, Palumbo PJ, Whisnant JP, Elveback LR: Transient ischemic attack and stroke in a community-based diabetic cohort. Mayo Clin Proc 58:56, 1983. Roffe C, Nevatte T, Sim J, et al: Effect of routine low-dose oxygen supplementation on death and disability in adults with acute stroke: The Stroke Oxygen Study Randomized Clinical Trial. JAMA 318:1125, 2017.


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Neurology_Adams. Rosenfield K, Matsumura JS, Chaturvedi S, et al: Randomized trial of stent versus surgery for asymptomatic carotid stenosis. N Engl J Med 374:1011, 2016. Ropper AH: Tipping point for patent foramen ovale closure. N Engl J Med 377:1093, 2017. Ropper AH, Davis KR: Lobar cerebral hemorrhages: Acute clinical syndromes in 26 cases. Ann Neurol 8:141, 1980. Ropper AH, Fisher CM, Kleinman GM: Pyramidal infarction in the medulla. A cause of pure motor hemiplegia sparing the face. Neurology 21:91, 1979. Ropper AH, King RB: Intracranial pressure monitoring in comatose patients with cerebral hemorrhage. Arch Neurol 41:725, 1984. Ropper AH, Shafran B: Brain edema after stroke: Clinical syndrome and intracranial pressure. Arch Neurol 41:26, 1984. Rost NS, Smith EE, Chang Y, et al: Prediction of functional outcome in patients with primary intracerebral hemorrhage: The FUNC score. Stroke 39:2304, 2008.


Neurology_Adams

Neurology_Adams. Rost NS, Smith EE, Chang Y, et al: Prediction of functional outcome in patients with primary intracerebral hemorrhage: The FUNC score. Stroke 39:2304, 2008. Rothwell PM, Elisziw M, Gutnikov SA, et al: Endarterectomy for symptomatic carotid artery stenosis in relation to clinical subgroups and timing of surgery. Lancet 363:915, 2004. Rothwell PM, Giles MF, Flossman E, et al: A simple score (ABCD) to identify individuals at high risk of stroke after transient ischemic attack. Lancet 366:29, 2005. Ruigrok TM, Rinkel GJ, Algra A, et al: Characteristics of intracranial aneurysms in patients with familial subarachnoid hemorrhage. Neurology 62:891, 2004. Ruiz DSM, Yilmaz Y, Gailloud P: Cerebral developmental venous anomalies: Current concepts. Ann Neurol 66:271, 2009. Sacco RL, Diener HC, Yusuf S, et al: Aspirin and extended-release dipyridamole versus clopidogrel for recurrent stroke. N Engl J Med 359:1238, 2008.


Neurology_Adams

Neurology_Adams. Sacco RL, Diener HC, Yusuf S, et al: Aspirin and extended-release dipyridamole versus clopidogrel for recurrent stroke. N Engl J Med 359:1238, 2008. Sacco RL, Ellenberg JH, Mohr JP, et al: Infarcts of undetermined cause: The NINCDS stroke data bank. Ann Neurol 25:382, 1989. Sacco SE, Whisnant JP, Broderick JP, et al: Epidemiological characteristics of lacunar infarcts in a population. Stroke 22:1236, 1991. Sage JI, Lepore FE: Ataxic hemiparesis from lesions of the corona radiata. Arch Neurol 40:449, 1983. Sahs AL, Nibbelin KDW, Torner JC (eds): Aneurysmal Subarachnoid Hemorrhage. Baltimore, Urban & Schwarzenberg, 1981. Sahs AL, Nishioka H, Torner JC, et al: Cooperative study of intracranial aneurysms and subarachnoid hemorrhage: A long term prognostic study. Arch Neurol 41:1140, 1142, 1147, 1984. Samuels MA: Can cognition survive heart surgery? Circulation 113:2784, 2006.


Neurology_Adams

Neurology_Adams. Samuels MA: Can cognition survive heart surgery? Circulation 113:2784, 2006. Sandok BA, Giuliani ER: Cerebral ischemic events in patients with mitral valve prolapse. Stroke 13:448, 1982. Sanna T. Diener H-C, Passman RS, et al: Cryptogenic stroke and underlying atrial fibrillation. N Engl J Med 370:2478, 2014. Saver JS, Goyal M, Bonafe A, et al: Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke. N Engl J Med 372:2285, 2015. Schievink WI: Intracranial aneurysms. N Engl J Med 336:28, 1997. Schievink WI, Bjornsson J, Parisi JE, Prakash UB: Arterial fibromuscular dysplasia associated with severe alpha 1-antitrypsin (alpha 1-AT) deficiency. Mayo Clin Proc 69:1040, 1994. Schon F, Martin RJ, Prevett M, et al: “CADASIL coma”: An underdiagnosed acute encephalopathy. J Neurol Neurosurg Psychiatry 74:249, 2003. Schwab S, Steiner T, Aschoff A, et al: Early hemicraniectomy in patients with complete middle cerebral artery infarction. Stroke 29:1888, 1998.


Neurology_Adams

Neurology_Adams. Schwab S, Steiner T, Aschoff A, et al: Early hemicraniectomy in patients with complete middle cerebral artery infarction. Stroke 29:1888, 1998. Scott RM, Smith ER: Moyamoya disease and moyamoya syndrome. N Engl J Med 360:1226, 2009. Shah AK: Non-aneurysmal primary subarachnoid hemorrhage in pregnancy-induced hypertension and eclampsia. Neurology 61:117, 2003. Shields RW Jr, Laureno R, Lachman T, Victor M: Anticoagulant-related hemorrhage in acute cerebral embolism. Stroke 15:426, 1984. Shroyer AL, Grover FL, Hattler B, et al: On-pump versus off-pump coronary bypass surgery. N Engl J Med 361:1827, 2009. Shuaib A, Lees KR, Lyden P, et al: NXY-059 for the treatment of acute ischemic stroke. N Engl J Med 357:562, 2007. Siesjo BK: Historical overview: Calcium, ischemia, and death of brain cells. Ann N Y Acad Sci 522:638, 1988. Singhal AB, Caviness VS, Begleiter AF, et al: Cerebral vasoconstriction and stroke after use of serotonergic drugs. Neurology 58:130, 2002.


Neurology_Adams

Neurology_Adams. Singhal AB, Caviness VS, Begleiter AF, et al: Cerebral vasoconstriction and stroke after use of serotonergic drugs. Neurology 58:130, 2002. Singhal AB, Topcuoglu MA: Glucocorticoid-worsening in reversible vasoconstriction syndrome. Neurology 88:228, 2016. Sirin S, Kondziolka D, Niranjan A, et al: Prospective staged volume reduction for large arteriovenous malformations: Indications and outcomes in otherwise untreatable patients. Neurosurgery 58:17, 2006. Sneddon JB: Cerebrovascular lesions and livedo reticularis. Br J Dermatol 77:180, 1965. So EL, Toole JF, Dalal P, Moody DM: Cephalic fibromuscular dysplasia in 32 patients: Clinical findings and radiologic features. Arch Neurol 38:619, 1981. Solomon RA, Connolly ES: Arteriovenous malformations of the brain. N Engl J Med 376:1859, 2017. Solomon RA, Fink ME: Current strategies for the management of aneurysmal subarachnoid hemorrhage. Arch Neurol 44:769, 1987.


Neurology_Adams

Neurology_Adams. Solomon RA, Fink ME: Current strategies for the management of aneurysmal subarachnoid hemorrhage. Arch Neurol 44:769, 1987. Spetzler RF, Martin NA: A proposed grading system for arteriovenous malformations. J Neurosurg 65:476, 1986. Spetzler RF, McDougall CG, Albuquerque FC, et al. The Barrow Ruptured Aneurysm Trial: 3-year results. J Neurosurg 119:146, 2013. Stam J: Thrombosis of the cerebral veins and sinuses. N Engl J Med 352:1791, 2005. Stapf C, Mast H, Sciacca RR, et al: Predictors of hemorrhage in patients with untreated brain arteriovenous malformations. Neurology 66:1350, 2006. Starkstein SE, Robinson RG, Price TR: Comparison of cortical and subcortical lesions in the production of post-stroke mood disorders. Brain 110:1045, 1987. St. Louis, Wijdicks EF, Li H: Predicting neurologic deterioration in patients with cerebellar haematomas. Neurology 51:1364, 1998.


Neurology_Adams

Neurology_Adams. St. Louis, Wijdicks EF, Li H: Predicting neurologic deterioration in patients with cerebellar haematomas. Neurology 51:1364, 1998. Stockhammer G, Felber SR, Zelger B, et al: Sneddon’s syndrome: Diagnosis by skin biopsy and MRI in 17 patients. Stroke 24:685, 1993. Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) Investigators, The: High-dose atorvastatin after stroke or transient ischemic attack. N Engl J Med 355:549, 2006. Susac JO, Hardman JM, Selhorst JB: Microangiopathy of the brain and retina. Neurology 29:313, 1979. Susac JO, Murtagh R, Egan RA, et al: MRI findings in Susac’s syndrome. Neurology 61:1783, 2003. Swanson RA: Intravenous heparin for acute stroke: What can we learn from the megatrials? Neurology 52:1746, 1999. Takayasu M: A case with peculiar changes of the central retinal vessels. Acta Soc Ophthalmol Jpn 12:554, 1908.


Neurology_Adams

Neurology_Adams. Takayasu M: A case with peculiar changes of the central retinal vessels. Acta Soc Ophthalmol Jpn 12:554, 1908. Takebayashi S, Sakata N, Kawamura A: Reevaluation of miliary aneurysm in hypertensive brain: Recanalization of small hemorrhage? Stroke 21(Suppl):1, 1990. Taneda M, Hayakawa T, Mogami H: Primary cerebellar hemorrhage: Quadrigeminal cistern obliteration as a predictor of outcome. J Neurosurg 67:545, 1987. Teasdale GM, Wardlaw JM, White PM, et al: The familial risk of subarachnoid hemorrhage. Brain 128:1677, 2005. The EC/IC Bypass Study Group. Failure of extracranial-intracranial arterial bypass to reduce the risk of ischemic stroke: Results of an international randomized trial. N Engl J Med 313:1191, 1985. Thieme H, Mehrholz J, Pohl M, et al: Mirror therapy for improving motor function after stroke. Cochrane Database Syst Rev 14:3, 2012. Ueda K, Toole JF, McHenry LC: Carotid and vertebral transient ischemic attacks: Clinical and angiographic correlation.


Neurology_Adams

Neurology_Adams. Ueda K, Toole JF, McHenry LC: Carotid and vertebral transient ischemic attacks: Clinical and angiographic correlation. Neurology 29:1094, 1979. Vahedi K, Hofmeijer J, Juettler E, et al: Early decompressive surgery in malignant infarction of the middle cerebral artery—a pooled analysis of three randomized controlled trials. Lancet Neurol 6:215, 2007. van Beijnum J, van der Worp HB, Buis DR, Treatment of brain arteriovenous malformations: A systematic review and meta-analysis. JAMA 306:2011, 2011. van den Bergh WM, van der Schaaf I, van Gijn J: The spectrum of presentations of venous infarction caused by deep cerebral venous thrombosis. Neurology 65:192, 2005. van Gijn J, Van Donegen KJ, Vermeulen M, et al: Perimesencephalic hemorrhage: A nonaneurysmal and benign form of subarachnoid hemorrhage. Neurology 35:493, 1985. Verreault S, Joutel A, Riant F, et al: A novel hereditary small vessel disease of the brain. Ann Neurol 59:353, 2006.


Neurology_Adams

Neurology_Adams. Verreault S, Joutel A, Riant F, et al: A novel hereditary small vessel disease of the brain. Ann Neurol 59:353, 2006. Vessey MP, Lawless M, Yeates D: Oral contraceptives and stroke: Findings in a large prospective study. Br Med J 289:530, 1984. Viswanathan A, Greenberg SM: Cerebral amyloid angiopathy in the elderly. Ann Neurol 70:871, 2011. Volhard F: Clinical aspects of Bright’s disease. In: Berglund H, et al (eds): The Kidney in Health and Disease. Philadelphia, Lea & Febiger, 1935, pp 665–688. Vonsattel JP, Myers RH, Hedley-Whyte ET, et al: Cerebral amyloid angiopathy without and with cerebral hemorrhages: A comparative histological study. Ann Neurol 30:637, 1991. Waga S, Yamamoto Y: Hypertensive putaminal hemorrhage—treatment and results: Is surgical treatment superior to conservative? Stroke 14:480, 1983. Wang Y, Wang Y, Zhao X, et al for the CHANCE Investigators: Clopidogrel with aspirin in acute minor stroke or transient ischemic attack. N Eng J Med 369:11, 2013.


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Neurology_Adams. Wang Y, Wang Y, Zhao X, et al for the CHANCE Investigators: Clopidogrel with aspirin in acute minor stroke or transient ischemic attack. N Eng J Med 369:11, 2013. Weiller C, Ringelstein B, Reiche W, et al: The large striatocapsular infarct. A clinical and pathophysiological entity. Arch Neurol 47:1085, 1990. Weinberger J, Biscarra V, Weisberg MK: Factors contributing to stroke in patients with atherosclerotic disease of the great vessels: The role of diabetes. Stroke 14:709, 1983. Weisman AD, Adams RD: The neurological complications of dissecting aortic aneurysm. Brain 67:69, 1944. Whisnant JP, Matsumoto N, Elveback LR: Transient cerebral ischemic attacks in a community: Rochester, Minnesota, 1955 through 1969. Mayo Clin Proc 48:194, 1973. White HD, Simes JS, Anderson NE, et al: Pravastatin therapy and the risk of stroke. N Engl J Med 343:317, 2000.


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Neurology_Adams. White HD, Simes JS, Anderson NE, et al: Pravastatin therapy and the risk of stroke. N Engl J Med 343:317, 2000. Whiteley WN, Adams, HP, Bath MWP, et al: Targeted use of heparin, heparinoids, or low-molecular-weight heparin to improve outcome after acute ischaemic stroke: An individual patient data meta-analysis of randomised controlled trials. Lancet Neurol 12: 539, 2013. Wiebers DO: Ischemic cerebrovascular complications of pregnancy. Arch Neurol 42:1106, 1985. Wiebers DO, Whisnant JP, O’Fallon WM: The natural history of unruptured intracranial aneurysms. N Engl J Med 304:696, 1981. Wiebers DO, Whisnant JP, Sandok BA, O’Fallon WM: Prospective comparison of a cohort with asymptomatic carotid bruit and a population-based cohort without carotid bruit. Stroke 21:984, 1990. Wiebers DO, Whisnant JP, Sundt TM, O’Fallon WM: The significance of unruptured intracranial saccular aneurysms. J Neurosurg 66:23, 1987.


Neurology_Adams

Neurology_Adams. Wiebers DO, Whisnant JP, Sundt TM, O’Fallon WM: The significance of unruptured intracranial saccular aneurysms. J Neurosurg 66:23, 1987. Wijdicks EF, St. Louis E: Clinical profiles predictive of outcome in pontine hemorrhage. Neurology 49:1342, 1997. Wijdicks EFM, Ropper AH, Hunnicut EJ, et al: Atrial natriuretic factor and salt wasting after subarachnoid hemorrhage. Stroke 22:1519, 1991. Wolf ME, Szabo K, Griebe M, et al: Clinical and MRI characteristics of acute migrainous infarction. Neurology 76:1911, 2011. Wolf PA, Kannel WB, McGee DL, et al: Duration of atrial fibrillation and imminence of stroke: The Framingham Study. Stroke 14:664, 1983. Wolf SL, Winsten CJ, Miller JP, et al: Effect of constraint-induced movement therapy on upper extremity function 3 to 9 months after stroke. JAMA 296:2095, 2006. Wood JH, Fleischer AS: Observations during hypervolemic hemodilution of patients with acute focal cerebral ischemia. JAMA 248:2999, 1982.


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Neurology_Adams. Wood JH, Fleischer AS: Observations during hypervolemic hemodilution of patients with acute focal cerebral ischemia. JAMA 248:2999, 1982. Yamashita M, Oka K, Tanaka K: Histopathology of the brain vascular network in moyamoya disease. Stroke 14:50, 1983. Yanagihara P, Piepgras DG, Klass DW: Repetitive involuntary movement associated with episodic cerebral ischemia. Ann Neurol 18:244, 1985. Lacrimal AAngular ANasal ASupraorbital AOphthalmic APersistenttrigeminal ACommoncarotid ABasilar AExt.carotid AAscendingcervical AVertebral AR. subclavian AInnominate AAortic archThyrocervical ADeepcervical AInt.carotid AVertebral AAngular APost. parietal ARolandic APost. communicating ACentralretinal AMiddlecerebral stem Ant. cerebral AOphthalmic APost. cerebral AAABCCDDB


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Neurology_Adams. Figure 33-1. Arrangement of the major arteries on the right side carrying blood from the heart to the brain. Also shown are collateral vessels that may modify the effects of cerebral ischemia. For example, the posterior communicating artery connects the internal carotid and the posterior cerebral arteries and may provide anastomosis between the carotid and basilar systems. Over the convexity, the subarachnoid interarterial anastomoses linking the middle, anterior, and posterior cerebral arteries are shown, with inset A illustrating that these anastomoses are a continuous network of tiny arteries forming a border zone between the major cerebral arterial territories. Occasionally a persistent trigeminal artery connects the internal carotid and basilar arteries proximal to the circle of Willis, as shown in inset B. Anastomoses between the internal and external carotid arteries via the orbit are illustrated in inset C. Wholly extracranial anastomoses from muscular branches of the cervical


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Neurology_Adams. as shown in inset B. Anastomoses between the internal and external carotid arteries via the orbit are illustrated in inset C. Wholly extracranial anastomoses from muscular branches of the cervical arteries to vertebral and external carotid arteries are indicated in inset D.


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Neurology_Adams. Posterior cerebral A (P1 segment)A1 segment, anterior cerebral arteryM1 segment, middle cerebral arteryBasilar APenetrating branches ofmiddlecerebral AOptic NInternal carotid AAnterior communicating AParamedianarteriesPosteriorcommunicatingAAnterior inferiorcerebellar A5th N6th N7th N8th N9th, 10th, 11th NPosterior inferiorcerebellar AShort circumferential AAnt. spinal AVertebral AA 4 mm below upperborder of ponsC 2 mm above ponto-medullary junctionD 6 mm below ponto-medullary junctionB Mid-pontineSuperior cerebellar A3rd N


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Neurology_Adams. Figure 33-2. Diagram of the base of the brain showing the principal vessels of the vertebrobasilar system (the circle of Willis and its main branches). The term M1 is used to refer to the initial (stem) segment of the middle cerebral artery; A1 to the initial segment of the anterior cerebral artery proximal to the anterior communicating artery; A2 to the postcommunal segment of the anterior cerebral artery; and P1 and P2 to the corresponding preand post-communicating segments of the posterior cerebral artery. The letters and arrows on the right indicate the levels of the four cross-sections following: A = Fig. 33-16; B = Fig. 33-15; C = Fig. 33-14; D = Fig. 33-13. Although vascular syndromes of the pons and medulla have been designated by sharply outlined shaded areas, one must appreciate that because satisfactory clinicopathologic studies are scarce, the diagrams do not always represent established fact. The frequency with which infarcts fail to produce a well-recognized syndrome and


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Neurology_Adams. that because satisfactory clinicopathologic studies are scarce, the diagrams do not always represent established fact. The frequency with which infarcts fail to produce a well-recognized syndrome and the special tendency for syndromes to merge with one another must be emphasized.


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Neurology_Adams. Figure 33-3. MRI showing acute infarctions. The upper images show a right middle cerebral artery infarction that appears bright on diffusion-weighted imaging (DWI) (upper left). There is subtle hyperintensity representing early vasogenic edema on T2-FLAIR sequence (upper right). The lower images show an acute cerebellar infarction in the territory of the posterior inferior cerebellar artery (PICA) that is bright on DWI (lower left) and faintly bright on T2-FLAIR (arrow, lower right). There is also a previous infarction just anterior to the acute cerebellar stroke, that is dark on DWI and bright on T2 due to gliosis.


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Neurology_Adams. Figure 33-4. In perfusion imaging, a time-intensity curve (A) is generated by measurement of the passage of contrast material through brain tissue. The slope of the curve represents blood flow and the area under the curve represents blood volume. Voxel measurements of these parameters are converted to color maps showing blood flow, volume, and contrast transit time throughout the brain. Arterial occlusions alter the time-intensity curve by either flattening the slope of the curve or reducing the area under the curve. As an example, an acute occlusion of the proximal segment of the right middle cerebral artery produces a region of signal abnormality on diffusion-weighted imaging (B) that is matched in size by an area of reduced blood volume (C). This area represents infarcted tissue. The area of prolonged transit time (D) affects a larger territory, particularly posteriorly. The difference between this territory and the infarcted zone represents the ischemic penumbra, and is often


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Neurology_Adams. area of prolonged transit time (D) affects a larger territory, particularly posteriorly. The difference between this territory and the infarcted zone represents the ischemic penumbra, and is often referred to as the diffusion-perfusion mismatch.


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Neurology_Adams. AREA FOR CONTRAVERSIONOF EYES AND HEADAnt. parietal AMOTORSENSORYPost. parietal AAngular AVISUALCORTEXPost. temporal AAnt. temporal ATemporal polar AMiddle cerebral stemSup. division ofmiddle cerebral APrerolandic ABROCA AREA(MOTOR APHASIA)Inf. division ofmiddle cerebral ALateralorbito-frontal ALateral geniculate bodyAUDITORY AREAWERNICKE AREA(SENSORY APAHSIA)PO = PARIETAL OPERCULUM (CONDUCTION APHASIA)PPR = POST. PARIETAL REGION (ALEXIA WITH AGRAPHIA)Rolandic APPR VISUAL RADIATION MOUTHHIPTRUNKHANDSFINGERSTHUMBFACETONGUELIPSARMPO Figure 33-5. Diagram of the left cerebral hemisphere, lateral aspect, showing the courses of the middle cerebral artery and its branches and the principal regions of cerebral localization. Below is a list of the clinical manifestations of infarction in the territory of this artery and the corresponding regions of cerebral damage.


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Neurology_Adams. Figure 33-6. Diagram of one cerebral hemisphere, coronal section, showing the regions of blood supply of the major cerebral vessels. Figure 33-7. A. Diagram of the right cerebral hemisphere, medial aspect, showing the branches and distribution of the anterior cerebral artery and the principal regions of cerebral localization. Below is a list of the clinical manifestations of infarction in the territory of this artery and the corresponding regions of cerebral damage. Also shown is the course of the main branch of the posterior cerebral artery on the medial side of the hemisphere. Note: Hemianopia does not occur; transcortical aphasia occurs rarely (isolation of the language areas) (see Chap. 22). B. Axial diffusion-weighted MRI showing an acute ischemic infarction in the anterior cerebral artery territory.


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Neurology_Adams. Figure 33-8. Corrosion preparations with plastics demonstrating penetrating branches of the anterior and middle cerebral arteries. The medial and lateral lenticulostriate arterioles are labeled, along with the recurrent artery of Heubner. (Reproduced by permission from Krayenbühl and Yasargil.)


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Neurology_Adams. Figure 33-10. A. Inferior aspect of the left hemisphere showing the branches and distribution of the posterior cerebral artery and the principal anatomic structures supplied. The vessel is considered from the perspective of its proximal and distal territories. Listed below are the clinical manifestations produced by infarction in these territories and the corresponding regions of damage. Tremor in repose has been omitted because of the uncertainty of its occurrence in the posterior cerebral artery syndrome. Peduncular hallucinosis may occur in thalamic-subthalamic ischemic lesions, but the exact location of the lesion is unknown. B. Axial diffusion-weighted MRI showing an acute ischemic infarction in the posterior cerebral artery territory.


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Neurology_Adams. Figure 33-11. The posterior cerebral and basilar arteries. A. The terminus of the basilar artery and branches originating from the P1 through P3 segments. (Reproduced by permission from Stroke 34:2264, 2003.) B. Lateral view of the brain showing the branches of the posterior cerebral artery. (Reproduced by permission from Krayenbühl and Yasargil.) C. Axial diffusion-weighted MRI showing an acute ischemic infarction due to occlusion of an artery of Percheron, an anatomic variant, in which an azygos paramedian artery supplies both sides of the posterior-medial thalamus. Figure 33-9. Diagram of the regions of blood supply of the diencephalon. Distribution of the (1) anterior cerebral artery, (2) posterior cerebral artery, (3) anterior and posterior choroidal arteries, (4) posterior communicating artery, and (5) internal carotid artery. (Reproduced by permission from Krayenbühl and Yasargil.)


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Neurology_Adams. Figure 33-12. Regions supplied by the posterior segment of the circle of Willis, lateral view (A) and basal view (B). A. (1) Posterior cerebral artery; (2) superior cerebellar artery; (3) basilar artery and superior cerebellar artery; (4) posterior inferior cerebellar artery; (5) vertebral artery (posterior inferior cerebellar artery, anterior spinal artery, posterior spinal artery). B. (1) Posterior cerebral artery; (2) superior cerebellar artery; (3) paramedian branches of the basilar artery and spinal artery; (4) posterior inferior cerebellar artery; (5) vertebral artery; (6) anterior inferior cerebellar artery; (7) dorsal spinal artery. (Reproduced by permission from Krayenbühl and Yasargil.) Figure 33-13. Transverse section through the upper medulla, reflecting regions supplied by the vertebral arteries and their branches.


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Neurology_Adams. Figure 33-13. Transverse section through the upper medulla, reflecting regions supplied by the vertebral arteries and their branches. Figure 33-14. Transverse section through the lower pons, reflecting the regions supplied by the lower basilar artery including its anterior inferior cerebellar artery branch. Figure 33-15. Transverse section through the midpons in the regions supplied by the mid-basilar artery and its short circumferential and paramedian branches. Figure 33-16. Transverse section through the upper pons and the regions supplied by the upper basilar artery and its superior cerebellar artery branch. Figure 33-17. Axial diffusion-weighted MRI of acute lacunar infarctions. A. Left capsular infarction causing a right pure motor hemiplegia. B. Left pontine infarction causing a clumsy hand–dysarthria syndrome.


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Neurology_Adams. Figure 33-18. Large ischemic infarction of the left cerebral hemisphere mainly in the distribution of the superior division of the middle cerebral artery. CT at 24 h (left) and 72 h (right) following the onset of stroke symptoms. The second scan (right) demonstrates marked swelling of the infarcted tissue and rightward displacement of central structures. Figure 33-19. A. Axial diffusion-weighted MRI showing multifocal acute infarctions in the left ACA-MCA arterial border zone (watershed). B. Magnetic resonance angiography displays severe stenosis of the left internal carotid artery (arrow), just above the common carotid artery bifurcation.


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Neurology_Adams. Figure 33-20. Cervical artery dissections. T1 MRI with fat saturation (left) and magnetic resonance angiography (right). The upper images show bilateral internal carotid artery dissections (arrows). The lower images show a left vertebral artery dissection (arrows). The T1 hyperintensity that is shown in the left upper and lower images is due to thrombus within the false lumen of the vessel. Figure 33-21. Moyamoya disease. Digital subtraction angiography in the coronal plane of the left common carotid artery. On the left image, there is occlusion of the left internal carotid artery near its terminus, and evidence of abnormal vascular proliferation involving the lenticulostriate vessels (arrow). The external carotid artery branches fill normally. The right image shows the same contrast injection during the early capillary phase; the characteristic “puff of smoke” is encircled.


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Neurology_Adams. Figure 33-22. Axial T2-FLAIR MRI of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). There is confluent symmetric abnormal hyperintensity within the periventricular white matter and internal and external capsules (left) and characteristically, also in the anterior temporal lobes (right). Figure 33-23. Two axial T2-FLAIR images of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS). Multifocal asymmetric areas of cortical and subcortical T2 hyperintensity are seen. Figure 33-24. Unenhanced CT showing hypertensive hemorrhages in the putamen (A), thalamus (B), pons (C), and cerebellum (D). The thalamic hemorrhage (B) has extended into the posterior horn of the right lateral ventricle and the cerebellar hemorrhage (D) has extended into the fourth ventricle.


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Neurology_Adams. Figure 33-25. Diagram of the circle of Willis showing the principal sites of intracranial aneurysms. Approximately 90 percent of aneurysms arise from branches of the anterior half of the circle. The sizes of the aneurysms depicted correspond roughly to the frequency of occurrence at those sites. Figure 33-26. Subarachnoid hemorrhage as a result of rupture of a basilar artery aneurysm. Left: Axial CT at the level of the lateral ventricles showing widespread hyperdense blood in the subarachnoid spaces and layering within the ventricles with resultant hydrocephalus. There is a blood–CSF level in the posterior horns of the lateral ventricles, typical of recent bleeding. Right: At the level of the basal cisterns, blood can be seen surrounding the brainstem, in the anterior sylvian fissures, and the anterior interhemispheric fissure. The temporal horns of the lateral ventricles are enlarged, reflecting acute hydrocephalus.


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Neurology_Adams. Figure 33-27. Aneurysm of the anterior communicating artery. Left: CT angiogram showing the aneurysm (arrow) arising from the branch point of the anterior communicating artery and the A1 segment; Right: Reconstructed image from CT angiogram data showing the aneurysm (arrow) in relation to the adjacent bony and vascular structures. Figure 33-28. Vasospasm following subarachnoid hemorrhage due to rupture of an anterior communicating artery aneurysm. Sagittal CT angiography reveals multifocal narrowing of segments of the anterior cerebral artery (arrows). Figure 33-29. Giant aneurysm of the anterior cerebral artery. Left: T1-weighted MRI without gadolinium infusion. The white signal is thrombus within the anterior aspect of the aneurysm; there is some blood flow within the lesion evidenced by the darker signal. Right: Cerebral angiogram, left common carotid injection, lateral view, showing the residual flow in the posterior aspect of the aneurysm.


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Neurology_Adams. Figure 33-30. Left parietal arteriovenous malformation. Upper left: T2-weighted MRI shows a tangle of vessels interspersed throughout the parietal lobe. The largest of these vessels are dilated draining veins. Upper right: CT angiography demonstrates enhancement of the abnormal vessels throughout the left hemisphere. The AVM is fed primarily via branches of the left MCA. Cerebral angiography. Contrast injected into the left internal carotid artery reveals the feeding arteries (lower left) and abnormal early filling of dilated draining veins (lower right) due to blood bypassing the capillary bed. Figure 33-31. Cerebral angiogram of a cerebral dural arteriovenous malformation. The nidus is located at the cerebral convexity (arrow). There is rapid filing of the cerebral venous system after injection of contrast into one internal carotid artery.


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Neurology_Adams. Figure 33-32. Cavernous malformation in the right parietal lobe. Axial T2 MRI (left) shows a round lesion which is heterogeneously hyperintense and hypointense. This appearance is due to vascular channels which are immediately adjacent to each other without interspersed normal brain tissue, containing blood products in different stages of degradation. An axial gradient echo MRI (right) shows that the lesion is hypointense, again due to blood products. Figure 33-33. A developmental venous anomaly (DVA) and its collecting vein in the left cerebellum on a T1-weighted MRI with contrast. Figure 33-34. Axial susceptibility-weighted MR images from a 65-year-old man with cerebral amyloid angiopathy. The left image shows innumerable cortical and subcortical microhemorrhages. The right panel shows cortical gyriform hemosiderosis, with additional cortical and subcortical microhemorrhages.


Neurology_Adams

Neurology_Adams. Figure 33-35. Hypertensive encephalopathy. Axial T2-FLAIR images showing fairly symmetric abnormal hyperintensity predominately in the parietooccipital lobes. The lesion affects the cortex and subcortical white matter and there is little mass effect. In severe cases, there may be hemorrhage and heterogeneous infarction in the cerebral cortex. The same imaging findings may occur in eclampsia (see also Chap. 41). Figure 33-36. Reversible cerebral vasoconstriction syndrome. Axial (left) and sagittal (right) CT angiogram showing segmental narrowing of the middle and anterior cerebral artery branches (arrows). Figure 33-37. Granulomatous angiitis of the brain. Cerebral arteriogram from a common carotid artery injection, lateral projection, demonstrating numerous areas of irregular narrowing (arrows) and, in some areas, contiguous slight dilatation (“beading”), particularly in the anterior cerebral artery.


Neurology_Adams

Neurology_Adams. Figure 33-38. Typical lesions of Susac syndrome in the central portion of the corpus callosum shown in a sagittal T-2 FLAIR MRI. These abnormal areas may show restriction of diffusion. Figure 33-39. Venous sinus thrombosis. Coronal (left) and sagittal (center) magnetic resonance venogram demonstrating absence of flow in the superior sagittal and left transverse sinuses (arrows). Note that the straight sinus and right transverse sinuses remain patent. Axial T2-FLAIR MRI shows left otomastoiditis, which was the cause of the extensive thrombosis. The clot can be seen in the MRI (right) (arrow).


Neurology_Adams

Neurology_Adams. Among the vast array of neurologic diseases, cerebral trauma ranks high in order of frequency and gravity. In the United States, trauma is the leading cause of death in persons younger than 45 years of age and more than half of these deaths are a result of head injuries. According to the American Trauma Society, an estimated 500,000 Americans are admitted to hospitals yearly following cerebral trauma; of these, 75,000 to 90,000 die and even larger numbers, most of them young and otherwise healthy, are left permanently disabled. Among adults over age 40, approximately 20 percent recall having had a head injury of any severity in their lifetimes (NHANES-Schneider A).


Neurology_Adams

Neurology_Adams. The basic problem in craniocerebral trauma is at once both simple and complex: simple because there is usually no difficulty in determining causation, namely, a blow to the head or in some cases a percussion wave from explosion, and complex because of a number of immediate and delayed effects to the brain and cranium that complicate the injury. As for the trauma itself, little can be done, for it is finished before the physician or others arrive on the scene. At most there can be an assessment of the full extent of the immediate cerebral injury, an evaluation of factors conducive to complications and further lesions, and the institution of measures to avoid additional problems. Specifically, the neck can be stabilized and adequate perfusion and particularly, oxygenation can be secured. New techniques of cellular biology are exposing phenomena that are set in motion by traumatic injury of nerve cells and glia. Some of these changes may be reversible, but at the moment, despite a large


Neurology_Adams

Neurology_Adams. techniques of cellular biology are exposing phenomena that are set in motion by traumatic injury of nerve cells and glia. Some of these changes may be reversible, but at the moment, despite a large body of animal experimentation such knowledge is limited.


Neurology_Adams

Neurology_Adams. It is a common misconception that craniocerebral injuries are matters that concern only the neurosurgeon and not the general physician or neurologist. Actually, 80 percent of head injuries are first seen by a physician in an emergency department, and fewer than 20 percent ever require neurosurgical intervention of any kind, and even this number is decreasing. The neurologist must be familiar with the clinical manifestations and the natural course of primary brain injury and its complications and have a grasp of the underlying physiologic mechanisms. Such knowledge must also relate to the interpretation of CT and MRI, both of which have enhanced our ability to deal with traumatic brain injury. The present chapter reviews the salient facts concerning craniocerebral injuries and outlines a clinical approach that the authors have found useful over the years. Matters pertaining to spinal injuries, often coexistent with head trauma, are considered in Chap. 42.


Neurology_Adams

Neurology_Adams. The very language that one uses to discuss certain types of head injuries divulges a number of misconceptions inherited from previous generations of physicians. Certain terms have crept into the medical vocabulary and have been retained long after the ideas for which they stood have been refuted, attesting to the disadvantage of premature adoption of explanatory terms rather than descriptive ones. The word concussion, for example, implies a violent shaking or jarring of the brain and a resulting transient functional impairment. Yet despite numerous postulates of physical changes within nerve cells, axons, or myelin sheaths (vibration effects, formation of intracellular vacuoles) that putatively occur with concussion, confirmation of their existence has proved difficult in humans and experimental animals.


Neurology_Adams

Neurology_Adams. In all attempts to analyze the mechanisms of closed, or blunt (nonpenetrating), head injury, one fact is preeminent: there must be the sudden application of a physical force of considerable magnitude to the head. Unless the head is struck, the brain suffers no injury except in the rare instances of violent flexion–extension (whiplash) of the neck and possibly in explosion-blast injury with a sudden extreme increase of atmospheric pressure. In military medical practice, blast injuries assume great importance and in theory, challenge many concepts of loss of consciousness in closed head injury; that is, there is no contact with, or sudden acceleration or deceleration of the cranium. The mechanical factors of importance in brain injury are the differential mobility of the head on the neck, and of the brain within the cranium, the tethering of the upper brainstem that allows movement of the cerebral hemispheres around that vertex, and the striking of parts of the brain on dural septa and


Neurology_Adams

Neurology_Adams. of the brain within the cranium, the tethering of the upper brainstem that allows movement of the cerebral hemispheres around that vertex, and the striking of parts of the brain on dural septa and bony prominences. As to concussive injuries, it is useful to point out that concussions usually involve a physical force that imparts motion to the stationary head or more commonly, a hard surface that arrests the motion of a moving head, that is, concussion does not occur if the head remains entirely stationary. This sudden deceleration or acceleration of the cranium is the mechanism of most civilian head injuries, and they are notable in two respects: they may induce at least a temporary loss of consciousness, and the brain may suffer gross damage even though the skull is not penetrated, that is, contusion, laceration, hemorrhage, and swelling. In the past few decades, the definition of concussion has been expanded to include any neurological phenomenon that follows a strike to the head,


Neurology_Adams

Neurology_Adams. is, contusion, laceration, hemorrhage, and swelling. In the past few decades, the definition of concussion has been expanded to include any neurological phenomenon that follows a strike to the head, as discussed further on, and there has been renewed interest in the degenerative brain changes that follow especially repeated concussion by years or decades. A theory that brings coherence to all of these physical and gross neuropathologic changes and their relation to concussion and coma has not been formulated. As mentioned in alter parts of the chapter, several degenerative neurological disorders have been attributed to repeated traumatic brain injury, the most prevalent of which seems to be “chronic traumatic encephalopathy” due to deposition of tau in the cortex. However, epidemiologic studies have been conflicting on whether other conditions are associated with prior head injury, for example, the report by Crane et al on 3 large prospective cohorts, in which only Lewy body disease


Neurology_Adams

Neurology_Adams. studies have been conflicting on whether other conditions are associated with prior head injury, for example, the report by Crane et al on 3 large prospective cohorts, in which only Lewy body disease and progression of


Neurology_Adams

Neurology_Adams. Parkinson disease were found to be associated. Other similar surveys came to different conclusions. In contrast to closed head injury, high-velocity missiles penetrate the skull and cranial cavity, or rarely, the skull may be compressed between two converging forces that crush the brain without causing significant displacement of the head or the brain. In these circumstances, the patient may suffer severe and even fatal injury without preceding loss of consciousness. Hemorrhage, destruction of brain tissue, and, if the patient survives for a time, meningitis or abscess are the principal pathologic changes created by injuries of these types. They offer little difficulty to our understanding. Figure 34-1 illustrates these various types of head injuries.


Neurology_Adams

Neurology_Adams. The relation of skull fracture to brain injury has been viewed in changing perspective throughout the history of the subject. In the first half of the last century, fractures dominated the thinking of the medical profession, and cerebral lesions were regarded as secondary. Later, it became clear that the skull, although rigid, is still flexible enough to yield to a blow that injures the brain without causing fracture. Therefore, the presence of a fracture, although a rough measure of the force to which the brain has been exposed, is not an infallible index of the presence of cerebral injury (see further on in discussion of predictive features for imaging abnormalities with concussion). Even in immediately fatal head injuries, autopsy reveals an intact skull in 20 to 30 percent of cases. Of course, many patients suffer skull fractures without serious or prolonged disorder of cerebral function, partly because the energy of a blow is dissipated in the fracture. Indeed, this diffusion of


Neurology_Adams

Neurology_Adams. course, many patients suffer skull fractures without serious or prolonged disorder of cerebral function, partly because the energy of a blow is dissipated in the fracture. Indeed, this diffusion of the impact might be expected to reduce underlying brain damage.


Neurology_Adams

Neurology_Adams. Nevertheless, fractures cannot be dismissed without further comment for several reasons. Overall, brain injury is estimated to be 5 to 10 times more frequent with skull fractures than without them and perhaps 20 times more frequent with severe and multiple fractures. Fractures assume further importance in providing an explanation for cranial-nerve palsies, and in creating potential pathways for the ingress of bacteria and air or the egress of cerebrospinal fluid (CSF leak). In these respects, fractures through the base of the skull are of special significance, and are considered below.


Neurology_Adams

Neurology_Adams. Figure 34-2 illustrates the major sites and directions of basilar skull fractures. One can readily perceive the possibilities of injury to cranial nerves. Fractures of the base are difficult to detect in plain skull films and may be missed by other imaging techniques, but their presence should be suspected in the presence of any one of a number of characteristic clinical signs. Fracture of the petrous pyramid often deforms the external auditory canal or tears the tympanic membrane, with resultant leakage of CSF (otorrhea); or, blood may collect behind an intact tympanic membrane and discolor it. If the fracture extends more posteriorly, damaging the sigmoid sinus, the tissue behind the ear and over the mastoid process becomes boggy and discolored (Battle sign). Basal fracture of the anterior skull may also cause blood to leak into the periorbital tissues, imparting a characteristic “raccoon” or “panda bear” appearance. The presence of any of these signs calls for CT scanning of the


Neurology_Adams

Neurology_Adams. skull may also cause blood to leak into the periorbital tissues, imparting a characteristic “raccoon” or “panda bear” appearance. The presence of any of these signs calls for CT scanning of the skull base using bone window settings to detect a fracture.


Neurology_Adams

Neurology_Adams. The existence of a basal fracture is also indicated by signs of cranial nerve damage. The olfactory, facial, and auditory nerves are the ones most liable to injury, but any one, including the 12th, may be damaged. Anosmia and an apparent loss of taste (actually a loss of perception of aromatic flavors, as the elementary modalities of taste are unimpaired) are frequent sequelae of head injury, especially with falls on the back of the head. In the majority of cases the anosmia is permanent. If unilateral, it will not be noticed by the patient. However, mechanism of these disturbances is thought to be a displacement of the brain and tearing of the olfactory nerve filaments in or near the cribriform plate, through which they course, rather than being attributable to a fracture. A fracture in or near the sella may tear the stalk of the pituitary gland with resulting diabetes insipidus. Rarely, such a fracture may cause bleeding from a preexisting pituitary adenoma and produce the syndrome


Neurology_Adams

Neurology_Adams. or near the sella may tear the stalk of the pituitary gland with resulting diabetes insipidus. Rarely, such a fracture may cause bleeding from a preexisting pituitary adenoma and produce the syndrome of pituitary apoplexy (see Chap. 30). A fracture of the sphenoid bone may lacerate the optic nerve, with blindness from the beginning. The pupil is unreactive to a direct light stimulus but still reacts to a light stimulus to the opposite eye (consensual reflex). The optic disc becomes pale, that is, atrophic, after an interval of several weeks. Partial injuries of the optic nerve result in scotomas and a troublesome blurring of vision.


Neurology_Adams

Neurology_Adams. Complete oculomotor nerve injury is characterized by ptosis and diplopia, a divergence of the globes with the affected eye resting in an abducted and slightly depressed position, loss of medial and most of the vertical movements of the eye, and a fixed, dilated pupil, as described in Chap. 12. The most common symptom is diplopia that is worse on looking down and compensatory tilting of the head indicating a trochlear nerve injury. In a series of 60 patients with head injury, Lepore confirmed that fourth-nerve palsy was the most common cause of diplopia, occurring unilaterally twice as often as bilaterally, followed in frequency by damage to one or both third nerves, then, least often, unilateral or bilateral sixth-nerve palsy. Five of his patients had palsies that reflected damage to more than one nerve and seven had supranuclear disorders of convergence. The long, circumferential subarachnoid course of the fourth nerve is usually given as the explanation for its frequent injury, but


Neurology_Adams

Neurology_Adams. than one nerve and seven had supranuclear disorders of convergence. The long, circumferential subarachnoid course of the fourth nerve is usually given as the explanation for its frequent injury, but this mechanism has never been validated. These optic and ocular motor nerve disorders must be distinguished from those caused by displacement of the globe or entrapment of an extraocular muscle as a result of direct injury to the orbit.


Neurology_Adams

Neurology_Adams. Injury to the ophthalmic and maxillary divisions of the trigeminal nerve may be the result of either a basal fracture across the middle cranial fossa or a direct extracranial injury to the branches of the nerves. Numbness and paresthesia of the skin supplied by the nerve branch or chronic neuralgia can be troublesome sequelae of these injuries. The facial nerve may be involved in one of two ways. In the first type of injury, associated with transverse fractures through the petrous bone, there is an immediate facial palsy, probably caused by contusion or transection of the nerve. Surgical anastomosis has sometimes been successful in restoring function in this circumstance. The second, more common type, is associated with longitudinal fractures of the petrous bone, the facial palsy then often being delayed for several days, a sequence that may be misinterpreted as progression of the intracranial traumatic lesion. This latter type is usually transitory, and its mechanism is not known.


Neurology_Adams

Neurology_Adams. Injury to the eighth cranial nerve because of petrous fractures results in a loss of hearing or in postural vertigo and nystagmus coming on immediately after the trauma. Deafness as a result of nerve injury must be distinguished from the high-tone hearing loss due to cochlear injury and from deafness caused by bleeding into the middle ear and disruption of the ossicular chain (conduction deafness). Also, vertigo must be distinguished from the very common symptom of posttraumatic dizziness discussed in a later section. The rare condition of fracture through the hypoglossal canal causes weakness of one side of the tongue. It should be kept in mind that blows to the upper neck may also cause lower cranial-nerve palsies, either by direct injury to their peripheral extensions or as a result of carotid artery dissection in the cervical segment of the artery.


Neurology_Adams

Neurology_Adams. A basal fracture through the sphenoid bone may lacerate the internal carotid artery or one of its intracavernous branches where it lies in the cavernous sinus. Within hours or a day or two, a disfiguring pulsating exophthalmos develops as arterial blood enters the sinus and distends the superior and inferior ophthalmic veins that empty into the sinus. The orbit feels tight and painful, and the eye may become partially or completely immobile because of pressure on the ocular nerves traversing the sinus (see Fig. 13-5). The sixth nerve is affected most often, and the third and fourth nerves less often. Also, there may be a loss of vision as a result of ischemia of the optic nerve and retina, although the mechanism has not been entirely clear; congestion of the retinal veins and glaucoma are potential factors in the visual failure. There is usually an easily audible bruit over the eye. Some 5 to 10 percent of fistulas resolve spontaneously, but the remainder must be obliterated by


Neurology_Adams

Neurology_Adams. are potential factors in the visual failure. There is usually an easily audible bruit over the eye. Some 5 to 10 percent of fistulas resolve spontaneously, but the remainder must be obliterated by interventional radiologic means, usually a detachable balloon, or by a direct surgical repair of the fistula (see Stern).


Neurology_Adams

Neurology_Adams. Not all carotid–cavernous fistulas are traumatic. They may occasionally occur with rupture of an intracavernous saccular aneurysm or in Ehlers-Danlos disease, where the connective tissue is defective; or the cause may be unexplained. Occasionally, a dural-based arteriovenous fistula opens in the region of the cavernous sinus after an injury and they cause fewer signs such as orbital swelling than a carotid–cavernous fistula. Pneumocephalus, Aerocele, and Rhinorrhea (Cerebrospinal Fluid Leak)


Neurology_Adams

Neurology_Adams. If the skin over a skull fracture is lacerated and the underlying meninges are torn, or if the fracture passes through the inner wall of a paranasal sinus, bacteria may enter the cranial cavity, with resulting meningitis or abscess formation. CSF that leaks into the sinus presents as a watery discharge from the nose (CSF rhinorrhea). The nasal discharge can be identified as CSF by testing it for glucose with diabetic test tape (mucus has no glucose) or by the presence of fluorescein or radionuclide-labeled dye that is injected into the lumbar subarachnoid space and then absorbed by pledgets placed in the nasal cavity. Mucus, when absorbed onto a handkerchief and allowed to dry, will leave the material stiff, whereas CSF, will not. A more elaborate test is to detect tau protein in the discharge; it is present only in CSF and not in mucus or blood. Most cases of acute CSF rhinorrhea heal by themselves. An indwelling lumbar drain for a few days may aid the process but this approach has


Neurology_Adams

Neurology_Adams. it is present only in CSF and not in mucus or blood. Most cases of acute CSF rhinorrhea heal by themselves. An indwelling lumbar drain for a few days may aid the process but this approach has only been tested in small trials such as the one by Albu and colleagues, in which the leak persisted for 2 fewer days but meningitis was not avoided. If the condition is persistent or is complicated by an episode of meningitis, surgical repair of the torn dura is indicated and this is sometimes possible through endoscopic methods. The prophylactic use of antibiotics to prevent meningitis in cases of nasal CSF leak is controversial, but many neurosurgeons continue this practice, particularly in children.


Neurology_Adams

Neurology_Adams. A collection of air in the cranial cavity (aerocele) is a common occurrence following skull fracture or any extended neurosurgical procedure. The pocket of air is apparent by CT scan in the epidural or subdural space over the cerebral convexities or between the hemispheres, and serves only to warn of a potential route for the entry of bacteria into the cranium. Small collections of air are usually absorbed without incident, but a large volume may act as a mass and cause clinical deterioration after injury (tension pneumocranium; Fig. 34-3). Inhalation of 100 percent oxygen has a slight salutary effect, but aspiration of the air is required if the collection is causing clinical signs. Depressed skull fractures are of significance only if the underlying dura is lacerated or the brain is compressed by indentation of bone. They then are surgically elevated, preferably within the first 24 to 48 h.


Neurology_Adams

Neurology_Adams. Much has been written about the mechanisms of concussion in closed head injury and its definition has undergone serial revision. In the past, a transient loss of consciousness and amnesia after a blow to the head had been considered necessary to qualify as concussion but lesser degrees of mild confusion, incoordination, or even symptoms such as headache and fatigue that follow mild head injury are now encompassed under the term. Whether all these problems derive from the same mechanism cannot be stated with confidence.


Neurology_Adams

Neurology_Adams. History of concepts of concussion The mechanism of concussive “cerebral paralysis” has been interpreted in various ways throughout medical history in light of the state of knowledge at a particular period of time. The favored hypotheses for the better part of a century were “vasoparalysis” (suggested by Fischer in 1870) or an arrest of circulation by an instantaneous rise in intracranial pressure (ICP) (proposed by Strohmeyer in 1864 and popularized by Trotter in 1932). Jefferson, in his essay on the nature of concussion (1944), convincingly refuted these vascular hypotheses. Later, Shatsky and coworkers, by the use of high-speed cineangiography, showed displacement of vessels but no arrest of circulation immediately after impact.


Neurology_Adams

Neurology_Adams. Beginning with the work of Denny-Brown and Russell in 1941, the physical factors involved in head and brain injuries were subjected to careful analysis. These investigators demonstrated that in monkey and cat the concussion resulted when the freely moving head was struck by a heavy mass. If the head was prevented from moving at the moment of impact, the same degree of force invariably failed to produce concussion. The importance of head motion was verified by Gennarelli and colleagues, who were able to induce concussion in primates by rapid acceleration of the freely moving head without impact, a condition that rarely occurs in humans.


Neurology_Adams

Neurology_Adams. Holbourn, a Cambridge physicist, from a study of gelatin models under conditions simulating head trauma, deduced that when the head is struck, movement of the partly tethered but suspended brain always lags (because of inertia), but inevitably the brain moves also, and when it does it must rotate in an arc because of attachment to the neck. Ommaya and Gennarelli (1974) proved the correctness of this assumption by photographing the brain through a transparent calvarium at the moment of impact. The brain was thus subjected to stresses set up by rotational forces mainly in the sagittal plane, centered at its point of tethering in the high midbrain. The torque at the level of the upper reticular formation would explain the immediate loss of consciousness, as described later. An extensive and scholarly review of the pathophysiology of concussion was done by Shaw (although we are uncertain of the validity of his view of a seizure-concussive mechanism).


Neurology_Adams

Neurology_Adams. Mechanism of concussion The core features of loss of consciousness or confusion are notable for being immediate after trauma (not delayed even by seconds) and for being largely reversible. This is the sense in which concussion was used to mean a reversible traumatic paralysis of nervous function and any physiologic explanation of the syndrome would have to incorporate this temporal sequence. However, the effects of concussion on brain function may last for a variable time (seconds, minutes, hours, or longer) and to set arbitrary limits on the duration of loss of symptoms, that is, to consider a brief loss as indicative of concussion and a prolonged loss as indicative of contusion or other traumatic cerebral lesion, is unsound physiologically. As pointed out by Symonds, any such difference is quantitative, not qualitative. It is true that in the more prolonged states of stupor or coma, there is a far greater chance of finding brain hemorrhage and contusion, which undoubtedly contribute


Neurology_Adams

Neurology_Adams. is quantitative, not qualitative. It is true that in the more prolonged states of stupor or coma, there is a far greater chance of finding brain hemorrhage and contusion, which undoubtedly contribute to the persistence of coma and the likelihood of irreversible change. Finally, the optimal condition for the production of concussion, demonstrated originally by Denny-Brown and Russell, is a sudden change in the momentum of the head; that is, either movement is imparted to the stationary head by a blow or movement of the head is arrested by a hard, unyielding surface.


Neurology_Adams

Neurology_Adams. Rotational movements of the brain also provide a reasonable explanation for the occurrence of surface injuries in specific locations, that is, where the swirling brain comes into contact with bony prominences on the inner surface of the skull (petrous and orbital ridges, sphenoid wings), and of injuries to the corpus callosum, which is flung against the falx. Not well explained by any of these mechanisms are concussions after blast injuries, a serious problem in military medicine. This syndrome possibly resurrects the notion that a shock wave travels through the brain and disrupts neural function throughout the cerebral hemispheres or in the reticular formation of the midbrain.


Neurology_Adams

Neurology_Adams. These views on the site and mechanism of concussion are not fully accepted but have been supported by a number of additional physiologic observations. Foltz and Schmidt, in 1956, suggested that the reticular formation of the upper brainstem was the anatomic site of concussive injury. They showed that in the concussed monkey, lemniscal sensory transmission through the brainstem was unaltered, but its effect in activating the reticular formation was blocked and that the electrical activity of the medial reticular formation was depressed for a longer time and more severely than that of the cerebral cortex.


Neurology_Adams

Neurology_Adams. What was further noteworthy in most of these cases, and in those reported by Jellinger and Seitelberger, was the presence of additional lesions in the region of the reticular activating system and small hemorrhagic softenings in the corpus callosum, superior cerebellar peduncles, and dorsolateral tegmentum of the midbrain. As discussed further on, Strich (1956) interpreted the extensive white matter lesions, both in the hemispheres and in the upper brainstem, to represent a degeneration of nerve fibers that had been stretched or torn by the shear stresses set up during rotational acceleration of the head, as had been postulated earlier by Holbourn. She suggested that if nerve fibers are stretched rather than torn, the lesions may be reversible and may play a part in the mechanism of concussion. Symonds elaborated on this view and saw in the shearing stresses, which are maximal at the point where the cerebral hemispheres rotate on the relatively fixed upper brainstem, the explanation


Neurology_Adams

Neurology_Adams. Symonds elaborated on this view and saw in the shearing stresses, which are maximal at the point where the cerebral hemispheres rotate on the relatively fixed upper brainstem, the explanation of concussion.


Neurology_Adams

Neurology_Adams. How these mechanical factors relate directly to the transient confusion, ataxia, or visual impairment of concussion or to the later headache and difficulty with concentration that follow some concussions is not clear. Nor is it known how repeated concussion leads in some individuals to the deposition of tau and degenerative changes subsumed under the term “chronic traumatic encephalopathy” (see below). Clinical Manifestations of Concussion


Neurology_Adams

Neurology_Adams. Clinical Manifestations of Concussion In its fullest form, the characteristic clinical signs of concussive brain injury are the immediate abolition of consciousness, suppression of supportive reflexes (falling to the ground if standing), transient arrest of respiration, a brief period of bradycardia, and fall in blood pressure following a momentary rise at the time of impact. Rarely, if these abnormalities are sufficiently intense, death may occur at the moment of impact, presumably from respiratory arrest. In its mildest form, there is no apparent loss of consciousness or collapse, only a brief period of stunned disorientation, staggering, and amnesia during which the individual appears outwardly normal. The vital signs usually return to normal and stabilize within a few seconds even if the patient remains unconscious.


Neurology_Adams

Neurology_Adams. Brief tonic extension of the limbs, clonic convulsive movements lasting up to approximately 20 s, and other peculiar movements may occur immediately after the loss of consciousness. These “concussive convulsions” are probably of little prognostic significance and have not been shown to confer an increased risk of later seizures. McCrory and Berkovic noted an association between motor and convulsive movements and facial impact, and we have seen this feature several times in teenagers who collided while pursuing a ball.


Neurology_Adams

Neurology_Adams. In the period during which the patient is unconscious and for a few moments afterward, the plantar reflexes are extensor. After a variable period of time, the patient begins to stir and opens his eyes. Corneal, pharyngeal, and cutaneous reflexes, originally depressed, return, and the limbs withdraw from painful stimuli. Gradually, contact is made with the environment and the patient begins to obey simple commands and respond slowly to questions. Memories are not formed during this period; the patient may even carry on a conversation, which he cannot later recall. This aspect of the syndrome closely simulates transient global amnesia, a disorder of obscure cause, discussed in Chap. 20. Finally, there is ostensibly full neurologic recovery corresponding to the time when the patient can form consecutive memories of current experiences.


Neurology_Adams

Neurology_Adams. The time required for the patient to pass through these stages of recovery may be only a few seconds or minutes, several hours, or possibly a limited number of days; but again, between these extremes there seem to be only quantitative differences. To the observer, such patients are unresponsive only from the moment of injury until they open their eyes and begin to speak; however, for the patient, the period of unconsciousness in one limited perspective extends from a point before the injury occurred (retrograde amnesia) until the time when he is able to form consecutive memories at the end of the period of anterograde amnesia. The duration of the amnesic period, particularly of anterograde amnesia, is but one index of the severity of the concussive injury. Although momentary “stunning” without loss of consciousness represents the mildest degree of concussion, as mentioned earlier, it is not known if it shares the same mechanism as overt loss of consciousness. The aftereffects of


Neurology_Adams

Neurology_Adams. without loss of consciousness represents the mildest degree of concussion, as mentioned earlier, it is not known if it shares the same mechanism as overt loss of consciousness. The aftereffects of concussion in causing anxiety, sleep disturbance, mental fogginess and cognitive difficulty, and dizziness are common to both and are discussed further on.


Neurology_Adams

Neurology_Adams. This is a topic of current interest and various guidelines regarding return to play have been published. A summary from the American Academy of Neurology can be consulted (authored by Giza and colleagues) and as can an often cited consensus statement of the International Conference on Concussion (McCrory et al, 2009). The later-life development of dementia and other neurodegenerative conditions in professional athletes is also discussed further on. Many useful observations have emerged from study of athletes after head injury. Foremost among these observations is that athletes who have had concussion are more likely than other players to have another concussion in the same playing season (Guskiewicz et al); whether this is a reflection of incoordination or the person’s style of play, or another factor, is not known. Second, most prospective studies show a decline in reaction time and in other neuropsychologic tests after concussion, which returns to baseline over several days or


Neurology_Adams

Neurology_Adams. or another factor, is not known. Second, most prospective studies show a decline in reaction time and in other neuropsychologic tests after concussion, which returns to baseline over several days or weeks. Third, there is an indication from several series of concussions in National Collegiate Athletic Association and National Football League players that the number of recollected concussions is proportional to the degree of impairment on neuropsychologic tests (McCrea et al, 2003). Similar results have been found in other pursuits such as jockeying (Wall et al), but there are few adequate prospective studies.


Neurology_Adams

Neurology_Adams. The appropriate duration of removal from play has been the subject of numerous and largely arbitrary systems. The duration of loss of the initial symptoms of concussion and of amnesia was formerly a major component of the decision about return to play. Current guidelines focus instead on slowness in answering questions, uncertainty about plays or game assignments, slowed motor skills, and clumsiness, with or without loss of consciousness or amnesia. All such players are removed from the game. The basis of most rules has been an appropriate conservatism that requires the absence of cerebral symptoms both at rest and under graduated increased physical stress testing such as running or repetitive squatting. After medical evaluation, which may include imaging and neuropsychologic testing, a program of physical and cognitive “rest” is followed by graduated physical and mental activity under observation and a return to a lower level if symptoms occur (McCrory et al, 2003). Specifically,


Neurology_Adams

Neurology_Adams. a program of physical and cognitive “rest” is followed by graduated physical and mental activity under observation and a return to a lower level if symptoms occur (McCrory et al, 2003). Specifically, light aerobic exercise is followed by sport-specific training and noncontact, then contact, drills.


Neurology_Adams

Neurology_Adams. In contrast to concussion, in cases of traumatic brain injury that are fatal or very serious, the brain is contused, swollen, or lacerated, and there are hemorrhages, both meningeal and intracerebral, as well as hypoxic-ischemic lesions. A majority of patients who remain in a coma for more than 24 h after a head injury are found to have intracerebral hematomas and contusions. Of these lesions, the most frequent are contusions of the surface of the brain beneath the point of impact (coup lesion) and the sometimes more extensive lacerations and contusions on the side opposite the site of impact (contrecoup lesion), as shown in


Neurology_Adams

Neurology_Adams. Fig. 34-4. Blows to the front of the head may produce mainly coup lesions, whereas blows to the back of the head may cause mainly contrecoup lesions. Blows to the side of the head produce either coup or contrecoup lesions, or both. Irrespective of the site of the impact, the common sites of cerebral contusions are in the frontal and temporal lobes, as illustrated in Figs. 34-4 and 34-5. The inertia of the malleable brain—which causes it to be flung against the side of the skull that is struck, to be pulled away from the contralateral side, and to be impelled against bony promontories within the cranial cavity, explains these coup–contrecoup patterns. Relative sparing of the occipital lobes in coup–contrecoup injury has been explained by the smooth inner surface of the occipital bones and subadjacent tentorium, as pointed out by Courville.


Neurology_Adams

Neurology_Adams. The contused cortex is diffusely swollen and hemorrhagic, most of the blood being found around parenchymal vessels. On CT, the lesions appear as edematous regions of cortex and subcortical white matter admixed with areas of increased density representing leaked blood (Fig. 34-6). The bleeding points may coalesce and give the appearance of a unitary clot in the cortex and immediately adjacent white matter. The predilection of these lesions for the crowns of convolutions attests to their traumatic origin (being thrown against the overlying skull) and distinguishes them from cerebrovascular and other types of cerebral lesions. There may be ball hemorrhages within the hemispheres that are independent of contusions as discussed below. Not surprisingly, such deep areas of bleeding are common in patients receiving anticoagulant or antiplatelet medications.


Neurology_Adams

Neurology_Adams. Of equal importance are axonal lesions that occur at the time of impact or evolve soon afterward. Strich (1961) described the neuropathologic findings in patients who died months after severe closed head injuries that had caused immediate and protracted coma. In all of her cases, in which there were no signs of skull fracture, raised ICP, or gross subarachnoid hemorrhage, she observed an uneven but diffuse degeneration of the cerebral white matter that has become the basis of all subsequent work on diffuse axonal shearing (diffuse axonal injury, DAI). In cases of shorter survival (up to 6 weeks), she observed ballooning and interruption of axis cylinders. These findings were subsequently confirmed and expanded by Nevin, by Adams and colleagues (1982), and by Gennarelli and coworkers, the last of these groups also working with monkeys.


Neurology_Adams

Neurology_Adams. The extension of Strich’s concept, that postulates diffuse axonal injury throughout the cerebral white matter as the main cause of persistent unconsciousness, has been widely adopted. In relation to concussion, shearing lesions are also seen in the midbrain and lower thalamus in severe injury, providing some evidence for neuronal dysfunction in these regions as the cause of concussion rather than diffuse white matter injury as commented below. The matter has not been settled and the two types of injury can occur together.


Neurology_Adams

Neurology_Adams. In most cases of severe head injury, there is damage to the corpus callosum by impact with the falx; necrosis and hemorrhage are sometimes visible by CT and can be seen to spread bilaterally to adjacent white matter (Fig. 34-7). There may also be scattered hemorrhages in the white matter along lines of force from the point of impact to the contralateral side. The degeneration of white matter from diffuse axonal injury can be remarkably diffuse, with no apparent relationship to focal destructive lesions, although differentiating it from secondary wallerian change that originates in a surface or callosal contusion can be difficult. Investigations using MRI, such as the series by Kampfl and colleagues, suggest that diffuse axonal injury may be the substrate of the persistent vegetative state. However, in most cases of severe cranial injury and protracted coma, there have been major sites of injury in the midbrain and subthalamus, that is, in the zones subjected to the greatest torque,


Neurology_Adams

Neurology_Adams. However, in most cases of severe cranial injury and protracted coma, there have been major sites of injury in the midbrain and subthalamus, that is, in the zones subjected to the greatest torque, and these latter lesions may be the critical ones in persistent coma and vegetative state (Adams et al, 2000; Ropper and Miller). This was true of the cases of persistent coma described by Jellinger and Seitelberger. Notable, again, was that these deep lesions coincided with the postulated locus of reversible concussive paralysis.


Neurology_Adams

Neurology_Adams. Primary brainstem hemorrhages due to torsion and tearing of tissue at the time of impact are distinguished from the secondary hemorrhages that are a result of the effects of downward displacement of the brainstem. Duret originally emphasized the medullary location of these secondary hemorrhages, but the term “Duret hemorrhage” has come to signify all brainstem hemorrhages when there is mass effect that distorts the brainstem.


Neurology_Adams

Neurology_Adams. In addition to contusions and extradural, subdural, subarachnoid, and intracerebral hemorrhages, closed head injury induces variable degrees of vasogenic edema that increases during the first 24 to 48 h and sometimes, small zones of infarction that have been attributed to vascular spasm caused by subarachnoid blood surrounding basal vessels. The frequency and importance of this type of secondary cerebral infarction have been debated. A retrospective imaging study by Marino and colleagues found that 17 of 89 patients had regions of stroke after moderate or severe head injury, a feature that had been pointed out by Adams and colleagues. Most were in the distribution of a major branch or penetrating cerebral vessel or in a watershed territory.


Neurology_Adams

Neurology_Adams. The presence of intracranial hypertension has also been associated with a higher incidence of infarction. Marmarou and colleagues demonstrated that brain swelling after head injury is essentially the result of edema and not of an increase in cerebral blood volume, as has long been postulated. In children, and in some cases in adults, the cerebral edema may be massive and lead to secondary brainstem compression.


Neurology_Adams

Neurology_Adams. With fractures of large bones, particularly the femur, with or without head injury, after 24 to 72 h there may be an acute onset of pulmonary symptoms (dyspnea and hyperpnea) followed by coma with or without focal signs or seizures. This sequence is a result of systemic fat embolism, first of the lungs and then of the brain. Cranial trauma is not required. In some cases the onset of pulmonary symptoms is associated with a petechial rash over the thorax, especially in the axillae and also in the conjunctivea and 1 in 3 cases is said to show fat globules in the urine. The specificity of the last of these findings has been questioned. Respiratory distress is the most important and often the only feature of the fat embolism syndrome, evident in the chest film as fluffy infiltrates in both lungs; however, cases have been reported without respiratory involvement.


Neurology_Adams

Neurology_Adams. In the brain, multiple small fat emboli cause widespread petechial hemorrhages and small infarctions, involving both white and gray matter and a few larger infarcts. Most patients with fat embolism recover spontaneously in 3 or 4 days, although a mortality rate of up to 10 percent is cited, usually related to underlying systemic and bony injuries. Treatment, aside from respiratory support, is supportive. Heparin, which had been used in the past, is not considered effective.


Neurology_Adams

Neurology_Adams. The physician first called on to examine a patient who has had a closed head injury will generally find one of three clinical conditions as indicated by the headings below, each of which is dealt with differently. It is usually possible to categorize the patient by assessing the mental and neurologic status when first seen and at intervals after the accident. The Glasgow Coma Scale has been used for almost 50 years as a rapid reference to accomplish this purpose (Table 34-1) but does not substitute for a fuller neurologic examination. The scale registers three aspects of neurologic function: eye opening, verbal response, and motor response to various stimuli. The scale uses a summed score from 3 to 15; a score of 7 or less is considered to reflect severe trauma and a poor clinical state, 8 to 12, moderate injury, and higher scores, mild injury. The scores provided by this scale correspond roughly with the outcome of the head injury as discussed further on, but its main utility is in


Neurology_Adams

Neurology_Adams. 8 to 12, moderate injury, and higher scores, mild injury. The scores provided by this scale correspond roughly with the outcome of the head injury as discussed further on, but its main utility is in recording sequential changes in the patient’s clinical state with an easily learned and reproducible tool.


Neurology_Adams

Neurology_Adams. This is the most frequently encountered clinical situation. Roughly, two degrees of disturbed function can be recognized within this category. In one, the patient only stunned momentarily, “saw stars,” or was briefly disoriented. This injury is insignificant when judged in terms of life or death and brain damage, although, as we point out further on there is still the small possibility of a skull fracture or the later development of an epidural or subdural hematoma. Moreover, some patients are liable to a troublesome posttraumatic syndrome consisting of various combinations of headache, giddiness, lack of mental clarity, fatigability, insomnia, and nervousness that can appear soon after or within a few days of the injury. This problem is discussed in a later section. In the instance of consciousness that was temporarily abolished for a few seconds or minutes, recovery may already be complete or the patient may be in one of the stages of partial recovery described earlier when first


Neurology_Adams

Neurology_Adams. consciousness that was temporarily abolished for a few seconds or minutes, recovery may already be complete or the patient may be in one of the stages of partial recovery described earlier when first encountered by the physician. Even though mentally clear, there is amnesia for events immediately preceding and following the injury. The latter produces a circumscribed confusional state that is usually confined to inattention and may be ongoing when the patient is first examined. It is characterized by a dazed appearance and repetitive questions from the patient about the circumstances that led to his being found.


Neurology_Adams

Neurology_Adams. In most such mild cases, a brief assessment for mental clarity, weakness, ocular abnormalities, and Babinski signs is appropriate, but there is little need of extensive neurologic consultation and hospitalization is not required, provided that a responsible family member is available to report any change in the clinical state. In only a small group of these patients, mainly in those who are slow in regaining consciousness or who have severe headache, vomiting, or a skull fracture, is there significant risk of intracerebral hemorrhage or other delayed complications. There should also be caution if there is any chance of neck injury.


Neurology_Adams

Neurology_Adams. Whether to obtain imaging of the head routinely in such patients is an unresolved problem. In our litigious society, the physician is inclined to obtain a CT scan. If imaging shows no subarachnoid blood (a common finding) or intraparenchymal clot or contusion, and the patient is mentally clear there is little chance of developing an extradural hemorrhage. The presence of a fracture may increase these odds but most studies, such as the one by Lloyd and colleagues, have found that the presence of a skull fracture in children proves to be a relatively poor indicator of intracranial injury. The exception is a fracture through the squamous bone and the groove of the middle meningeal artery, which represents a risk for arterial bleeding and epidural hemorrhage.


Neurology_Adams

Neurology_Adams. With the current focus on the cost-effective use of ancillary studies, criteria that justify obtaining a cranial CT following minor forms of head trauma have been developed as discussed in the next paragraph. We have generally advised a CT in cases of head injury that was associated with loss of consciousness (more than 1 min), severe and persisting headache, nausea and vomiting, a confusional state, and any new, objective neurologic signs, but these are admittedly arbitrary criteria. The CT scan may be particularly important in elderly patients with minor head trauma, in whom the presence of an intracranial lesion (mainly subdural hematoma) may not be predicted by clinical signs and, of course, imaging may be advisable if the patient is taking anticoagulants or antiplatelet agents of any type beyond small doses of aspirin. In children, it may be advisable to perform the scans more liberally. This is underscored by the results of a study of 215 children with minor head trauma


Neurology_Adams

Neurology_Adams. of any type beyond small doses of aspirin. In children, it may be advisable to perform the scans more liberally. This is underscored by the results of a study of 215 children with minor head trauma conducted by Simon and colleagues: 34 children with no known loss of consciousness and a Glasgow Coma Scale score of 15 nonetheless displayed intracranial lesions, 3 of whom required surgery.


Neurology_Adams

Neurology_Adams. Several studies in adults have given broad guidance in choosing which patients to image (“New Orleans Criteria” and “Canadian CT Head Rule”; Table 34-2). They include features that are sensitive but not specific for intracranial injury, such as age above 60 years, intoxication, more than 30 min of retrograde amnesia, suspected skull fracture, seizure, anticoagulation, and dangerous mechanism of injury (see Smits et al and Stiell et al). These two validated schemes for assisting in the determination of need for CT scanning in the emergency department are included for the reader’s reference but they should be viewed as guidelines with fairly high sensitivity for important lesions on the CT, but low specificity so that most CT scans done under these advisories can be expected to be normal. These issues were addressed in a review by Ropper and Gorson.


Neurology_Adams

Neurology_Adams. Minor and seemingly trivial head injuries may sometimes be followed by a number of puzzling and worrisome clinical phenomena, some insignificant, others serious and indicative of a pathologic process other than concussion. The latter are described below. When they occur, a neurologic or neurosurgical evaluation is indicated.


Neurology_Adams

Neurology_Adams. Drowsiness, headache, and confusion These symptoms occur most often in children, who, minutes or hours after a concussive head injury, seem not to be themselves. They lie down, are drowsy, complain of headache, and may vomit—symptoms that suggest the presence of an intracranial hemorrhage. Mild focal edema near the point of impact may be seen on MRI. There is usually no skull fracture but, as Nee and colleagues point out, vomiting is associated with an increase in the incidence of skull fracture and the New Orleans and Canadian CT rules found vomiting to be a factor associated with intracranial bleeding (see Table 34-2). The symptoms subside after a few hours, attesting to the benign nature of the condition in most cases but some form of cerebral imaging is required.


Neurology_Adams

Neurology_Adams. Transient paraplegia, blindness, and migrainous phenomena With falls or blows on top of the head, both legs may become temporarily weak and numb, with wavering bilateral Babinski signs and sometimes with sphincteric incontinence. Impact over the occiput may cause temporary blindness. The symptoms disappear after a few hours. It seems possible that these transient symptoms represent a direct localized concussive effect, caused either by indentation of the skull or by impact on these parts of the brain against the inner table of the skull, but a vascular mechanism cannot be excluded. The blindness and paraplegia are usually followed by a throbbing, vascular type of headache. Transient migrainous visual phenomena, aphasia, or hemiparesis, followed by a headache, are observed sometimes after minimal concussion in athletes who participate in contact sports. Possibly all of these phenomena are the result of an attack of migraine induced by a blow to the head. These focal syndromes can be


Neurology_Adams

Neurology_Adams. minimal concussion in athletes who participate in contact sports. Possibly all of these phenomena are the result of an attack of migraine induced by a blow to the head. These focal syndromes can be perplexing and very worrisome for a few hours, especially if it is the first such attack of migraine in a child. Possibilities to be remembered, particularly in cases of acute quadriplegia, is traumatic cord compression or the rarer cartilaginous embolism of the cervical cord (see “Fibrocartilaginous Embolism” in Chap. 42). A concussion of the cervical portion of the spinal cord is another potential mechanism of transient paraplegia.


Neurology_Adams

Neurology_Adams. Episodes of transient global amnesia (TGA) after minor head injury have been described by Haas and Ross, as mentioned in Chap. 20 but the difficulty differentiating concussive amnesia from TGA has been mentioned. They share the sign of repetitive stereotyped questioning regarding orientation that is common to both processes. A duration of 2 to 24 h for TGA and the feature of repetitive querying were suggested by Haas and Ross as differentiating the two conditions but the separation on this basis is not compelling. Delayed hemiplegia The main causes of delayed hemiplegia are a late-evolving epidural or subdural hematoma and, in more severe injuries, an intracerebral hemorrhage. Most of these are associated with a diminution in the level of consciousness from the outset but there are exceptions.


Neurology_Adams

Neurology_Adams. Dissection of the internal carotid artery should also be considered in cases of delayed hemiplegia. The dissection may occur in the extracranial or the intracranial portion of the carotid artery and should be sought by vascular imaging study if the hemiparesis has no other explanation. In other instances, the hemiplegia has no clear explanation other than the blow to the head, perhaps related to the migraine phenomenon described earlier.


Neurology_Adams

Neurology_Adams. This group is smaller than the other two but is of importance because it includes a disproportionate number of patients who are in urgent need of surgical treatment. The initial loss of consciousness from concussion may have lasted only a few minutes or, exceptionally, there may have been no period of unresponsiveness at all, in which instance one might wrongly conclude that there was no concussion and little possibility of traumatic hemorrhage or other type of brain injury. Patients who display this sequence of events, in the past referred to vividly as “talk and die” by Marshall and associates (1983), have late deterioration because of the expansion of a subdural hematoma, worsening brain edema around a contusion, or the delayed appearance of an epidural clot. Among 34 such patients in the Traumatic Coma Data Bank who had this type of lucid interval, the majority showed substantial degrees of midline shift on the initial CT scan, reflecting the presence of early brain edema and


Neurology_Adams

Neurology_Adams. in the Traumatic Coma Data Bank who had this type of lucid interval, the majority showed substantial degrees of midline shift on the initial CT scan, reflecting the presence of early brain edema and contusion (Marshall et al, 1983). A somewhat related condition of delayed intracerebral hematoma (spät apoplexie), discussed further on, is a feature of a more severe initial head injury that usually produces coma from the onset. The problem of cerebral fat embolism, mentioned earlier, should be considered in these cases of delayed deterioration, especially if there is interposed respiratory failure.


Neurology_Adams

Neurology_Adams. Patients Who Remain Comatose From the Time of Head Injury


Neurology_Adams

Neurology_Adams. Here, the central problem, set forth by Symonds, is the relationship between concussion and contusion and other forms of persisting structural brain damage. Because consciousness is abolished at the moment of injury, one can hardly doubt the existence of concussion in such cases; but when hours pass without consciousness being regained, the second half of the usual definition of concussion—that the disruption of cerebral function be transitory—is not satisfied. Pathologic examination of such cases usually discloses evidence of increased ICP and of cerebral contusions, subarachnoid hemorrhage, zones of infarction, and scattered intracerebral hemorrhages both at the point of injury (coup) and on the opposite side (contrecoup), in the corpus callosum, and between these points, along the line of force of the impact. In some patients, the diffuse axonal type of injury is prominent or, as mentioned, there are separate but strategically placed ischemic and hemorrhagic lesions in the upper


Neurology_Adams

Neurology_Adams. of force of the impact. In some patients, the diffuse axonal type of injury is prominent or, as mentioned, there are separate but strategically placed ischemic and hemorrhagic lesions in the upper midbrain and lower thalamic region. Varying amounts of blood in the subarachnoid and subdural spaces are present. Displacement of the thalamus and midbrain may be present, with compression of the opposite cerebral peduncle against the free margin of the tentorium as well as secondary midbrain hemorrhages and zones of necrosis; in some cases, there is transtentorial herniation.


Neurology_Adams

Neurology_Adams. Severe head injury is often associated with an immediate arrest of respiration and sometimes with bradyarrhythmia and cardiac arrest. The immediate effects on the brain of these systemic changes may in themselves be sufficiently profound to cause coma. Intracranial pressure is almost always elevated and imaging of the brain shows various degrees of brain swelling, ventricular compression, and displacement of midline structure. Also, head injury often complicates alcohol and drug ingestion, so the possibility of a toxic or metabolic encephalopathy as the cause (or a contributing cause) of stupor must always be considered.


Neurology_Adams

Neurology_Adams. In all of these patients, following the initial period of stabilization, the matter of interest is the clinical and imaging assessment, with the purpose of uncovering a surgically remediable lesion, namely a subdural or epidural hematoma or a treatable, well-defined, intraparenchymal hematoma that is not simply a contusion. In most cases, the discovery of such a mass lesion leads to surgical removal. But unless it is the only lesion, the procedure often proves to be insufficient and coma is likely to persist because of the associated cerebral damage. The recognition and management of these hematomas are described further on.


Neurology_Adams

Neurology_Adams. In the Traumatic Coma Data Bank, which included 1,030 gravely injured patients with Glasgow Coma Scale scores of 8 or less, 21 percent had subdural hematomas, 11 percent had intracerebral clots, and 5 percent had epidural hematomas. Notable, however, half the patients had no mass lesions on the CT scan. On this basis, these patients were thought to have diffuse axonal injury. However, in 50 consecutive autopsies of severely injured patients, summarized in an earlier era by Rowbotham, all but 2 showed macroscopic changes, suggesting the relative unreliability of CT analysis. The lesions in these cases consisted of surface contusions (48 percent), lacerations of the cerebral cortex (28 percent), subarachnoid hemorrhage (72 percent), subdural hematoma (15 percent), extradural hemorrhage (20 percent), and skull fractures (72 percent). As these figures indicate, several pathologic entities were found in the same patient.


Neurology_Adams

Neurology_Adams. There is that relatively small, distressing group of severely brain-injured patients in whom the vital signs become normal but who never regain full consciousness. As the weeks pass, the prospects become bleaker. Such a patient, especially if a child, may still emerge from coma after 6 to 12 weeks or longer and make a relatively good, although usually incomplete, recovery. Some of those who survive for long periods open their eyes and move their heads and eyes from side to side but betray no evidence of seeing or recognizing even the closest members of their families. They do not speak and are capable of only primitive postural or reflex withdrawal movements. Jennett and Plum referred to this as the “persistent vegetative state” (see Chap. 16 for a full discussion of this subject). Fourteen percent of the patients in the Traumatic Coma Data Bank remained in this state. Hemiplegia or quadriplegia with varying degrees of decerebrate or decorticate posturing are usually present. Life is


Neurology_Adams

Neurology_Adams. percent of the patients in the Traumatic Coma Data Bank remained in this state. Hemiplegia or quadriplegia with varying degrees of decerebrate or decorticate posturing are usually present. Life is sometimes terminated after several months or years by some medical complication but may patients have survived for decades. Our colleague R.D. Adams examined the brains of 14 patients who remained in coma and in vegetative states from 1 to 14 years. All showed extensive zones of necrosis and hemorrhage in the upper brainstem. Among patients who survived and remained vegetative until death, J.H. Adams and colleagues (2000) found that 80 percent had thalamic damage and 71 percent had findings of diffuse axonal injury. Moreover, trauma of extracranial organs and tissues is frequent and obviously contributes to the fatal outcome. Recent functional studies have shown that a limited proportion of patients who are in a vegetative or minimally conscious state can be trained to purposefully engage


Neurology_Adams

Neurology_Adams. contributes to the fatal outcome. Recent functional studies have shown that a limited proportion of patients who are in a vegetative or minimally conscious state can be trained to purposefully engage parts of the cerebrum.


Neurology_Adams

Neurology_Adams. In generalizing about this category of head injury, the effects of contusion, hemorrhage, and brain swelling often become evident within 18 to 36 h after the injury and then may progress for several days. If a patient survives this period, his chances of dying from complications of these effects are greatly reduced. The mortality rate of those who reach the hospital in coma is approximately 20 percent, and most of the deaths occur in the first 12 to 24 h as a result of direct injury to the brain in combination with other nonneurologic injuries. Of those alive at 24 h, the overall mortality falls to 7 to 8 percent; after 48 h, only 1 to 2 percent of patients succumb. There is some evidence that transfer of such patients to an intensive care unit, where personnel experienced in the handling of head injury can monitor them, improves the chances for survival (see further on).


Neurology_Adams

Neurology_Adams. One modest advance in the medical treatment of traumatic unresponsiveness has come from a randomized trial by Giacino and colleagues showing that amantadine accelerated slightly the emergence from the vegetative or minimally conscious state; it was given for 4 weeks between the fourth and twelfth weeks after injury, 100 mg twice per day and increasing to 200 mg twice per day. The effects were less evident by 6 weeks but this and other activating agents seems like a promising approach that has gone in and out of favor over the years. In cases of longer standing, deep brain stimulation of thalamic nuclei has been explored in past decades and has had some successes. Claims for other types of behavioral activation programs have not been validated.


Neurology_Adams

Neurology_Adams. The following lesions are considered in all cases of serious cranial injury. They each have characteristic clinical and imaging features but they may be admixed and the contribution of each to the clinical state must be assessed before deciding on a course of action.