ders in Children. Philadelphia, WB Saunders Co, 1972, pp 401-402. 3. Canter GJ: Observations on neurogenic stuttering: A contribution to differential diagnosis. Br J Disord Commun 1971;12:139-148. 4. Farmer A: Stuttering repetitions in aphasic and nonaphasic brain damaged adults. Cortex 1975;11:391-396. 5. Helm NA, Butler RB, Benson DF: Acquired stuttering. Neurology 1978;28:1159-1165. 6. Rosenfield DB: Stuttering and cerebral ischemia. N Engl J Med 1972;287:991. 7. Logemann JA, Fischer HB, Boshes B, et al: Frequency and co-occurrence of vocal tract dysfunction in the speech of a large sample of parkinsonian patients. J Speech Hear Disord 1978;53:47-57. 8. Nakano KK, Zubeixh H, Tyler HR: Speech defects of parkinsonian patients. Neurology 1973;23:865-870. 9. Netsell R, Daniel B, Celesia GC: Acceleration and weakness in parkinsonian dysarthria. J Speech Hear Disord 1975;50:170-178. 10. Canter GJ: Speech characteristic of patients with Parkinson's disease. J Speech Hear Disord 1963;28(pt 1):221-229. 11. Espir MLE, Rose FC: The Basic Neurology of Speech. Oxford, England, Blackwell Scientific Publications, 1970. 12. Bloodstein O: A Handbook on Stuttering. National Easter Seal Society for Crippled Children and Adults, 1969. Aphasia in Subdural Hematoma Stephen O. Dell, MD; Ramon Batson, MD; David L. Kasdon, MD; Thomas Peterson, MD \s=b\ The occurrence of aphasia as the only or dominant symptom of subdural hematoma (SDH) has not been emphasized in the literature. The possible confu- sion of traumatic aphasia with transient ischemic attacks or stroke has been the object of most recent investigations. Four patients with subacute SDH had aphasia as an initial symptom; the relevant pathophysiologic characteristics were noted in each. These patients had a rapid response to decompression with marked resolution of the aphasia irrespective of immediate or delayed drainage. (Arch Neurol 1983;40:177-179) phasia is known to occur with sub¬ dural hematoma (SDH), usually as part of a hemispheric syndrome.13 Several case reports have dealt with intermittent deficits in SDH that mimic stroke or transient ischemie attacks.49 We have recently treated four patients in whom language impairment was the predominant aspect of their occurrence; all of these patients suffered from subacute SDH. REPORT OF CASES Case 1.—A 52-year-old left-handed man fell, striking his right shoulder (a hyperabduction injury) and face. There was no loss of consciousness at the time, but a minimal dysnomic deficit was present. His right upper extremity, however, was immediate¬ ly rendered flaccid and areflexive, with severely impaired sensation. While hospi¬ talized for this presumed brachial plexus lesion, his aphasia cleared entirely. Twelve days after the injury, a sudden, severe aphasia was noted without other new neu¬ rologic deficits. His speech was nonfluent, comprehension was preserved only for the simplest commands, naming and repeti¬ tion were absent, and he was able to write only his name. A computed tomographic (CT) scan showed a 15-mm, right-sided frontoparietal SDH with a 12-mm rightto-left shift of the midiine. On drainage of a 60-mL acute collection of blood from the perisylvian region, no contusion of brain was noted. The patient's condition then improved dramatically. Within several days, his lan¬ guage deficits fully resolved, and CT dem¬ onstrated no residual collection or shift. Function of the right arm was not improved. Case 2.—A 58-year-old right-handed diabetic man fell, striking his left hip and head, without loss of consciousness. He suffered headache and neck ache without meningism for three days, when on the following day, an aphasia suddenly devel¬ oped. His speech was nonfluent, with occa¬ sional stereotypy ("yes yes"). He could not comprehend, repeat, name, or write. There was no papilledema. Minimal right hemiparesis was present. A CT scan showed a left-sided subdural collection, with a shift of the frontal horn of that ventricle and obliteration of its occipital horn. At operation, a thick perisylvian SDH (2 cm) was removed, as well as a similar frontal collection (0.5 cm). His deficits resolved in six days. A CT scan then dis¬ closed a small residual hematoma and a mild left-to-right shift, thought to be sec¬ ondary to cerebral edema. Aphasia did not ... recur. Accepted for publication May 8, 1982. From the Department of Neurosurgery, TuftsNew England Medical Center, Boston. Dr Dell is now with the Seacoast Neurosurgical Group, Dover, NH. Reprint requests to Seacoast Neurosurgical Group, Rollins Building, 787 Central Ave, Dover, NH 03820 (Dr Dell). Case 3.—A 66-year-old right-handed man fell without loss of consciousness but manifested slurred speech, retrograde amnesia for 30 minutes, and a right-sided facial paresis. A CT scan demonstrated a small bilateral almost isodense SDH, with¬ out shift. During the following two Downloaded From: http://archneur.jamanetwork.com/ by a University of Michigan User on 06/21/2015 13. Rosenbek JC, Collins M, Massert B: Cortical stuttering. Read before the American Speech and Hearing Association, Washington, DC, Nov, 1975. 14. Rigrodsky S, Morrison EB: Speech changes in parkinsonism during L-dopa therapy. J Am Geriatr Soc 1971;18:142-151. 15. Perry AR, Dast PK: Speech assessment in Parkinson's disease, in Rose FC, Capildeo R (eds): Research in Parkinson's Disease. London, Pitman Publisher Ltd, 1980, pp 373-384. 16. Sarno M: Speech impairment in Parkinson's disease. Arch Phys Med Rehabil 1968; 49:269-273. months, he demonstrated increasing forgetfulness, gross swings of mood and affect, intermittent slurring of speech, and a persistent mild right hemiparesis. A second scan demonstrated the right-sided SDH to be unchanged, while that on the left side had enlarged. He was alert but confused. Speech was fluent and dysnomic, with gross impairment of comprehension but relative sparing of repetition. There was minimal right hemiparesis and a slightly hemiparetic gait, with inconstant sensory extinction to double simultaneous stimulation. After drainage of the left-sided collec¬ tion, the patient demonstrated a dramatic resolution of all language, motor, and sen¬ sory deficits. 74-year-old right-handed fell, striking his head without imme¬ diate symptoms. Five weeks later, he suf¬ fered the abrupt onset of confusion, apha¬ sia, and a right spastic hemiparesis that spared the face. His aphasia was fluent with perseveration and paraphasic errors. Case 4.—A man He was severely dysnomic and demon¬ strated moderate impairment of compre¬ hension and repetition. A CT scan showed a left-sided temporoparietal collection (20 mm), with a shift to the right side of 15 mm. The patient under¬ went craniotomy with evacuation of a large chronic SDH, with an acute compo¬ nent beneath the inner membrane. There was significant cerebral atrophy. The post¬ operative course was complicated. The hematoma required redrainage, but ulti¬ mately, he made a dramatic recovery from his aphasia. A mild right hemiparesis remained, and there were now newer or unmasked parietal deficits (Gerstmann's syndrome). At that time, a CT scan dis¬ closed a small, resolving residual SDH. The course was marked by worsening confu¬ sion, recurrent episodes of dysphasia simi¬ lar to that originally described, and a persistent mild hemiparesis and parietal deficits. Serial CT scans showed a reaccumulated SDH. The patient's speech distur¬ bance was similar to that of his initial condition but with worsened comprehen¬ sion and repetition. Dramatic recovery of language function occurred after a second drainage proce¬ dure. Ultimately, full recovery occurred with the exception of a minimal right arm pronation. Aphasia Typology Dominant Hemisphere Lesion Location Aphasia Type Fluency Comprehension Repetition No Partial No No Broca's 50- to 60-mL collection, associated brachial plexus No No No No Global Minimal associated R Partial Partial Isolation Bilateral chronic subdural hematoma, chronic cognitive and mood changes No Partial Wernicke's Intermittent course, episodes of mild hemiparesis and parietal deficit R side, Naming frontoparietal Comment injury L side, perisylvian hemiparesis Bilateral temporoparietal L side, temporoparietal COMMENT possible pathophysiologic theories for Of the major clinical reports con¬ cerning SDH, many include no men¬ tion of language dysfunction in detailed descriptions of clinical ap¬ pearance.1026 (In total, these represent more than 1,434 consecutive patients.) Other studies refer to dysphasia in SDH as a rarity.27'29 Only two large studies report apha¬ sia in a significant percentage of SDH. McKissock30 described 389 patients, of whom 26 (7%) had unspe¬ cified speech symptoms and 39 (10% ) had signs. These were approximately equally distributed between acute, subacute, and chronic cases. Few fur¬ ther details are given. Jamieson and Yelland31 classified their data as sim¬ ple or complicated SDH according to whether a surface lesion (contusion or laceration) was present. Aphasia (type undescribed) was seen in 10% (24/249) of the former and 6% (14/224) of the latter groups, although language function often was difficult to evaluate among the more severely injured patients. Eight of these patients had coexistent seizures, mak¬ ing the cause of the dysphasia unclear. No patient in either series had an isolated language deficit. Isolated speech deficits have been reported in several reviews of SDH 4.6,27,32,33 The incidence of aphasia in these more recent studies is consid¬ erably less (approximately 1%), but this may reflect different patient pop¬ ulations or attention to the problem. There have been eight patients described with symptoms similar to transient ischemie attacks, secondary to SDH.1-5'9 Of these, only one patient demonstrated an isolated language deficit. In all, to our knowledge, only three cases of isolated language defi¬ cits secondary to SDH (two perma¬ nent and one transient) have been reported.4·27·32 Perlmutter22 has suggested several the effects of SDH that may relate to dysphasia. These include (1) large but reversible local pressure gradients,34 (2) secondary local tissue hypoperfusion as with mass lesions,35·36 (3) alter¬ ations in oxygen availability in the face of normal partial pressure for oxygen (Pa02) (R. Morowitz, MD, oral communication, February 1982), and (4) irritative (epileptiform) dis¬ charges (more dubious). Types of aphasia varied in our small series, as they were both fluent and nonfluent in type. One example each was noted of Broca's, global, isolation, and Wernicke's aphasia (Table). This dispersion is similar to that in the literature of closed or missile head injury.3743 A variety of dysarthrias and sensory and motor dysphasias have also been described, reflecting the direction of the compressive or destructive vector. By contrast, is¬ chemie aphasias of thrombotic or embolie origin are far more stereo¬ typed in appearance and evalua¬ tion.1'3 The conclusions that emerge from this study are largely clinical. Apha¬ sia in SDH appears from hours to weeks after injury or bleeding. This subacute period may be analogous to the "lucid interval" that is more fre¬ quently ascribed to epidural hemato¬ mas. When deterioration in language function occurs, it proceeds rapidly; there seems to be a critical threshold for compression of cortical speech areas. Such aphasias are probably more than usually recognized. Global deterioration in mental state or frank herniation may easily mask them. Unlike other deficits of SDH, there is dramatic resolution function¬ ally with decompression. Thus, re¬ markable results are seen even when treatment is delayed as long as two weeks. Nonetheless, prompt treat¬ ment is obviously indicated when the common Downloaded From: http://archneur.jamanetwork.com/ by a University of Michigan User on 06/21/2015 problem is recognized. To our knowl¬ edge, the rapid deterioration and equally dramatic response to decom¬ pression have not previously been reported in the literature. Because aphasia of sudden onset (either as a reversible neurologic deficit or fixed deficit) is usually ascribed to ischemie vascular disease and an adequate his¬ tory of trauma may not be forthcom¬ ing, such reversible condition a deserves consideration in the exami¬ nation of the patient with transient ischemie attacks or stroke. References 1. Benson DF, Geschwind NN: The aphasias and related disturbances, in Baker AB, Baker LH: Clinical Neurology. Hagerstown, Md, Harper & Row Publishers Inc, 1976, vol 1, pp 1-28. 2. Geschwind N: Current concepts: Aphasia. N Engl J Med 1971;284:654-656. 3. Lhermitte F, Gautier JC: Aphasia, in Vinken PJ, Bruyn GW, Braakman R (eds): Handbook of Clinical Neurology. New York, Elsevier North Holland Inc, 1969, vol 4: Disorders of Speech, Perception, and Symbolic Behavior, pp 84-104. 4. Groch SN, Hurwitz LJ, Wright IS: Intracranial lesion simulating cerebral thrombosis. JAMA 1960;172:1469-1472. 5. Melamed E, Lavy S, Reches A, et al: Chronic subdural hematoma stimulating transient cerebral ischemic attacks: Case report. J Neurosurg 1975;42:101-103. 6. Okihiro MM, Daly D, Yoss RE: Intermittent aphasia due to mass intracranial lesions. Mayo Clinic Proc 1961;36:525-529. 7. Plenge KL, Sonntag VKH: Chronic subdural hematoma causing 'transient ischemic attacks' in a young woman. Ann Neurol 1979;6:279. 8. Robin JJ, Maxwell JA, Pirkethly DT: Chronic subdural hematoma simulating transient ischemic attacks. Ann Neurol 1978;4:154. 9. Welsh JE, Tyson GW, Winn HR, et al: Chronic subdural hematoma presenting as transient neurologic deficits. Stroke 1979;10:564-567. 10. Arseni C, Stanciu M: Particular clinical aspects of chronic subdural hematoma in adults. Eur Neurol 1969;2:109-122. 11. Davies FL: Mental abnormalities following subdural hematoma. Lancet 1960;1:1369-1370. 12. Echlin F: Traumatic subdural hematoma\p=m-\ acute, subacute and chronic: An analysis of 70 operated cases. J Neurosurg 1949;6:294-303. 13. Fell DA, Fitzgerald S, Moiel RH, et al: Acute subdural hematomas: Review of 144 cases. J Neurosurg 1975;42:37-42. 14. Fogelholm R, Heiskanen O, Waltimo O: Chronic subdural hematoma in adults: Influence of patient's age on symptoms, signs, and thick- ness of hematoma. J Neurosurg 1975;42:43-46. 15. Gardner WJ: Traumatic subdural hematoma with particular reference to the latent interval. Arch Neurol 1932;27:847-858. 16. Kretschmer H: Subdurale h\l=a"\matome,in Kretschmer H (ed): Neurotraumatologie. Stuttgart, West Germany, Georg Thieme Verlag, 1978, pp 71-75. 25. Schisano G, Bruzaco J: Acute and subacute subdural hematomas. Acta Chir Scand 1964; 128:471-482. 26. Talalla A, Morin MA: Acute traumatic subdural hematoma: A review of 100 consecutive cases. J Trauma 1971;11:771-777. 27. Bender MB, Christoff N: Nonsurgical treatment of subdural hematomas. Arch Neurol 17. Laudig GH, Browder EJ, Watson RA: Subdural hematoma: A study of 143 cases encountered during a five-year period. Ann Surg- 1974;31:73-79. 1941;113:170-191. 10:305-307. 29. Loew F, Kivelitz R: Chronic subdural haematomas, in Vinken PJ, Bruyn GW, Braakman R (eds): Handbook of Clinical Neurology. New York, Elsevier North Holland Inc, 1976, vol 24: Injuries of the Brain and Skull, pp 297-328. 30. McKissock W: Subdural hematoma: A review of 389 cases. Lancet 1960;1:1365-1369. 31. Jamieson KG, Yelland JDN: Surgically traumatic subdural hematomas. J Neurosurg 18. McLaurin RL, Tutor FT: Acute subdural hematoma: Review of 90 cases. J Neurosurg 1961;18:61-67. 19. Miller D, Bleasel KF: Study of subdural haematoma. Med J Aust 1960;47:1034-1037. 20. Moiel RH, Caram PC: Acute subdural hematomas: A review of 84 cases, a six-year evaluation. J Trauma 1967;7:660-666. 21. Northcroft GB: Some experiences in the management of subdural hematoma and spontaneous intracerebral hemorrhage. Postgrad Med J 1962;38:409-416. 22. Perlmutter I: Subdural hematoma in older patients. JAMA 1961;176:212-214. 23. Ramamurthi B: Acute subdural haematoma, in Vinken PJ, Bruyn GW, Braakman R (eds): Handbook of Clinical Neurology. New York, Elsevier North Holland Inc, 1976, vol 24: Injuries of the Brain and Skull, pp 275-296. 24. Rosenbluth PR, Arias B, Quartetti EV, et al: Current management of subdural hematoma: An analysis of 100 consecutive cases. JAMA 1962;179:759-762. 28. Endtz LJ: Historical article: Posttraumatic hygroma in the 18th century. Surg Neurol 1978; 1972;37:137-149. 32. Cameron MM: Chronic subdural haematoA review of 114 cases. J Neurol Neurosurg ma: Psychiatry 1978;41:834-839. 33. Heilman KM, Safran A, Geschwind N: Closed head trauma and aphasia. J Neurol Neurosurg Psychiatry 1971;34:265-269. 34. Symon L, Pasztor E, Dorsch NWC, et al: Differential pressures recorded in acute epidural expanding lesions: Correlation with local cerebral blood flow by hydrogen clearance in baboons, in Langfitt TW, McHenry LC Jr, Reivich M, et al (eds): Cerebral Circulation and Metabolism. New York, Springer-Verlag, 1975, pp Meningeal Sarcomatosis and Multiple Astrocytomas Steven A. Lukes, MD; Robert Wollmann, MD, PhD; Kari Stefannson, MD 235-237. 35. Daly DD, Svien HJ, Yoss RE: Intermittent cerebral symptoms with meningiomas. Arch Neurol 1961;5:287-293. 36. Weisberg LA, Nice CN: Intracranial tumors simulating the presentation of cerebrovascular syndromes: Early detection with cerebral computed tomography. Am J Med 1977; 63:517-524. 37. Groher M: Language and memory disorders following closed head trauma. J Speech Hear Res 1977;20:212-223. 38. Levin HS, Grossman RG, Kelly PJ: Aphasic disorder in patients with closed head injury. J Neurol Neurosurg Psychiatry 1976;39:1062\x=req-\ 1070. 39. Levin HS, Grossman RG: Behavorial sequelae of closed head injury: A quantitative study. Arch Neurol 1978;35:720-727. 40. Mohr JP, Weiss GH, Caveness WF, et al: Language and motor disorders after penetrating head injury in Vietnam. Neurology 1980;30:1273\x=req-\ 1279. 41. Sarno MT: The nature of verbal impairment after closed head injury. J Nerv Ment Dis 1980;168:685-692. 42. Thomsen IV: Evaluation and outcome of aphasia in patients with severe closed head injury. J Neurol Neurosurg Psychiatry 1975;38:713\x=req-\ 718. 43. Thomsen IV, Skinhoj E: Regressive language and severe head injury. Acta Neurol Scand 1976;54:219-226. gag reflex was diminished on the left, and the tongue protruded to the left. The gait unsteady. There was modest weakness of the right leg. There was no limb ataxia. Sensation was normal. Tendon reflexes were brisk bilaterally, and sustained clonus was present at the right ankle. The right plantar response was was broad based and extensor. \s=b\ We report the clinical course and the pathological findings in a 28-year-old in whom a chronic, progressive "meningitis" was caused by extensive invasion of the meninges by a primary sarcoma. The patient was also found to have two anatomically and histologically distinct astrocytomas. (Arch Neurol 1983;40:179-182) woman sarcomatosis is a rare /Teningeal condition in which the meninges and Virchow-Robin spaces are dif¬ fusely invaded by sarcoma, with little or no invasion of the parenchyma of the CNS. The tumor may encase the CNS, producing the clinical picture of chronic meningitis. We report a case Accepted for publication May 20, 1982. From the Departments of Neurology (Dr Lukes) and Pathology (Neuropathology) (Drs Wollmann and Stefannson), University of Chicago Hospitals. Dr Lukes is now with the Department of Neurology, Memorial Sloan-Kettering Cancer Center, New York. Reprint requests to Department of Neurology, Memorial Sloan-Kettering Cancer Center, 1275 York Ave, New York, NY 10021 (Dr Lukes). in which a primary sarcoma invaded the meninges of the brain stem and spinal cord, manifesting as a progres¬ sive meningitis resembling invasion of the meninges by metastatic cancer. In addition, the patient was found to have two anatomically and histologi¬ cally distinct astrocytomas. REPORT OF A CASE A 28-year-old woman was admitted to the University of Chicago Hospital in December 1977 with a two-month history of increasingly severe generalized head¬ ache and diplopia on left lateral gaze. During the month before admission, she had had photophobia and a stiff neck. On admission, she was drowsy and appeared to be chronically ill. The vital signs and physical findings were normal. There were no stigmata of phakomatosis. There were striking Kernig's and Brudzinski's signs. Visual fields were full and the acuity was normal. Both pupils were 4 mm in diame¬ ter, but the left reacted sluggishly to light. The ocular fundi were normal. There was weakness of abduction of the left eye and bilateral facial weakness, with modest sensorineural hearing loss on the right. The Downloaded From: http://archneur.jamanetwork.com/ by a University of Michigan User on 06/21/2015 A lumbar puncture disclosed an opening pressure of 170 mm of water. There were no cells in the fluid. The protein concentra¬ tion was 117 mg/dL, and the glucose con¬ centration 24 mg/dL. Cultures were sterile, and cryptococcal antigen was not found. A computed tomographic (CT) scan demon¬ strated an enhancing density in the left quadrigeminal cistern and enlargement of Fig 1.—Computed tomographic scan demon¬ density in left quadrigeminal cistern and enlargement of third and lateral ventri¬ strates cles.