620 AMERICAN JOURNAL OF EMERGENCY movement disorders. In Grossman AR, Sambrook MA (eds): Neural mechanisms in disorders of movement. London, England, Libbey, 1989, pp 17-27 23. Price KS, Farley IJ, Horny Kiavicz 0: Neurochemistry of Parkinson’s disease: Relation between striated and limbic dopamine. Adv Biochem Psychopharmacol 1978;19:293-300 24. Saris S: Chorea caused by caudate infarction. Arch Neurol 1983(Sept);40:590-591 25. Boles DM: Hemichorea-hemiballismus caused by lacunar infarcts in the basal ganglia. S Afr Med J 1983;64:154 (letter) 26. Graveland GA, Williams RS, Difiglia M: Evidence for degenerative and regenerative changes in neostriatal spring neurons in Huntington’s disease. Science 1985;227:770-773 27. Perry TL, Hansen S, Kloster M: Huntington’s chorea: Deficiency of gamma-aminobutyric acid in brain. New Engl J Med 1973;288:337-342 28. Gawin FH, Ellinwood EH Jr: Cocaine and other stimulants. New Engl J Med 1988;1318:1173-1182 29. Nicolaysen LC, Pan HT, Justice JB Jr: Extracellular cocaine and dopamine concentrations are linearly related in rat striatum. Brain Res 1988:456:317-328 30. Di-Chiara G, lmperato A: Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Proc Natl Acad Sci USA 1988 ;85 15274-5278 31. Martin JB, Gusella JF: Huntington’s disease: Pathogenesis and management. N Engl J Medj986;315:1267-1276 32. McDowell FH. Lee JE. Sweet RD: Extrapyramidal disease, in Baker AB, Baker LH (eds): Clinical Neurolbgy, vol 3. 1983, chapter 38 33. Bruyn GW: Huntington’s chorea: Historical, clinical, and laboratory synopsis, in Vinken PJ, Bruyn GW (ed): Handbook of Clinical Neurology, vol 6, 1968, pp 298-378 34. Bird ED: Chemical pathology of Huntington’s disease. Ann Rev Pharmacol Toxicol 1980;20:533-551 35. Scheinberg IH, Sternlieb: Wilson’s Disease. Philadelphia, PA, Saunders, 1984 36. Kelley WN, Wyngaarden JB: Clinical syndromes associated with hypoxanthine-guanine phosphoribosyltransferase deficiency, in Stanberry JB, Wyngaarden JB, Fredrickson DS, et al (eds): The Metabolic Basis of Inherited Disease (ed 5). New York, NY, McGraw-Hill, 1983 37. Vance JM, Pericak-Vance MA, Bowman MH, et al: Choreaacanthosis: A report of three new families and implications for aenetic counsellina. Am J Med Genet 1987:2:403-410 ” 38. Nausiada PA: Grossman BJ, Koller WC, et al: Sydenham’s chorea: An update. Neurology 1980;30:331-334 39. Paradise JL: Sydenham’s chorea without evidence of rheumatic fever. N Engl J Med 1960;263:625-629 40. Hamman KP, Henkel B, Erbel R, et al: Hemichorea associated with varicella-zoster reinfection and endocarditis: A case report. Eur Arch Psychiatry Neurol Sci 1985;234:404-407 41. Klawans HL: Chorea. Can J Neurol Sci 1987;14:536-540 (SUPPI) 42. Fishbeck LH, Layzer RB: Paroxysmal choreoathetosis associated with thyrotoxicosis. Ann Neurol 1979;6:453-454 43. Shahar E, Shapiro MS, Shenkman L, et al: Hyperthyroidinduced chorea. Case report and review of the literature. Israel J Med Sci 1988;24:264-266 44. McKinney AS: Idiopathic hyperparathyroidism presenting as chorea. Neurology 1962;12:485-491 45. Fonseca OA, Calverley JR: Neurologic manifestations of hypoparathyroidism. Arch Intern Med 1967;120:202-206 46. Groothins JR, Groothins DR, Mukhopadhyay D, et al: Lupus-associated chorea in childhood. Am J Dis Child 1977;131: 1131-1134 47. Hatron PY, Bouchez B, Wattel A, et al: Chorea systemic lupus erythematosus, circulating lupus anticoagulant. J Rheumatol 1986;13:991-993 (letter) 48. Bruyn GW, Padberg G: Chorea and polycythemia. Eur Neurol 1984;23:26-33 49. Crane GE: Tardive dyskinesias in patients treated with major neuroleptics. A review of the literature. Am J Psychiatry 1968;124:40-48 (suppl) MEDICINE n Volume 9, Number 6 w November 1991 50. Barbeau A: The clinical physiology of side effects of longterm L-dopa therapy. Adv Neurol 1974;5:347-365 51. Newman RP, Kinkel WR: Paroxysmal choreoathetosis due to hypoglycemia. Arch Neurol 1984;41:341-342 52. Bartolucci G, Pelletier JR: Glue sniffing and movement disorders. J Neurol Neurosurg Psychiatry 1984;47:1259 (letter) 53. Leys D, Bourgeois P, Destee A, et al: Acute choreic syndrome and psychotic state induced by an amphetaminic drug. Rev Neurol (Paris) 1985;141:499-500 54. Schwartz A, Hennerici M, Wegener OH: Delayed choreoathetosis following acute carbon monoxide poisoning. Neurology 1985;35:98-99 TRANSCORTICAL MOTOR APHASIA DUE TO A SUBDURAL HEMATOMA To the Editor:-Emergency physicians are well aware that acute or subacute aphasias typically result either from cerebral infarction or an intracerebral mass such as a tumor or hemorrhage.’ Wellcharacterized aphasia syndromes correlate well with distinct cortical lesions in the dominant hemisphere.” Wemicke’s and other fluent aphasias. characterized by well-articulated speech with abnormal content, usually localize to the parietal or temporal lobes. Nonfluent aphasias such as a Broca’s. typified by slow, incorrectly articulated words. are caused by frontal lesions.’ Rarely, aphasias can also be presenting symptoms of subdural hematomas (SDHS).‘-‘~ Here we describe a patient with a transcortical motor aphasia (TCMA) due to a SDH and then discuss its possible pathogenesis and implication in the management of aphasic patients in the emergency department. A 53-year-old right-handed man was evaluated in our emergency room for complaints of right-sided weakness and difficulty “getting the words out.” The patient stated his symptoms began 3 weeks earlier when he fell and struck his head. His appetite suffered, and his nephew brought the patient for a medical evaluation after he found him disheveled and “confused.” He had no headache. His past medical history was remarkable for hypertension, diabetes. gout, and alcoholism. On physical examination upon admission the patient had a blood pressure of 170/90 mm Hg and a pulse of 70 per minute, and he was afebrile. He was alert and attentive, though he spoke little spontaneously. His speech in response to questions was halting but without dysarthria or paraphasic errors. He was able to understand spoken as well as written words, and he could read aloud. Upon verbal command he was able to whistle, protrude his tongue, and pretend to blow out a match, but he had difftculty waving goodbye with either hand. He named a watch and a pen, but could not name the watch’s face, hands. or buckle, or the pen’s tip or cover. He was unable to write with either hand. However. he was able to repeat even a phrase as complex as “no ifs ands or buts.” His visual fields were full to confrontation, his optic discs were sharp, and his pupils and eye movements were normal. There were no sensory abnormalities. The right face, arm, and leg were mildly paretic. and the right brachioradiahs. biceps. and triceps reflexes were increased compared with the left. The ankle jerks were absent, and the right plantar reflex was extensor while the left was flexor. Computerized tomography (CT) of the head (Figure I) revealed a large left frontoparietal. extra-axial hypodense fluid collection containing scattered foci of hyperintensity. The fluid was lined by a convex hyperdense inner rim. Effacement of the left lateral ventricle accompanied left to right midline shift. The findings were thought to be consistent with a chronic SDH with an acute hemorrhagic component and significant mass effect. The patient underwent a left frontoparietal craniotomy and evacuation of a chronic SDH encapsulated by well-organized inner and outer membranes. The hematoma contained acute as well as old liquefied blood. Ten by eight-centimeter windows in both the inner and outer membranes were removed. Pathologic examination revealed fresh and organizing blood clot as well as hemosiderin depo- CORRESPONDENCE 621 FIGURE 1. Computed tomographic scan of the brain shows a large left frontoparietal hypodense fluid collection with scattered areas of hyperdensity consistent with a chronic subdural hematoma with acute components. The subdural hematoma caused a transcortical motor aphasia. sition and hemosiderin-containing macrophages, indicating old hemorrhage. By 2 days after surgery he had dramatically improved: his speech was fluent, he could write with only minor errors, and his hemiparesis was almost resolved. A follow-up CT on the third postoperative day demonstrated only mild residual fluid and little mass effect. The diagnosis of TCMA was established based upon his nonfluent spontaneous speech, agraphia, difficulty naming but intact auditory comprehension, reading, and repetition.2 His mild right hemiparesis, limb apraxia involving even the stronger arm, and normal sensory examination results and visual fields were also consistent with a TCMA.’ Patients with TCMA typically have lesions which involve either the supplementary motor area (SMA) or the subcortical white matter anterolateral to the frontal horn of the left lateral ventricle, thereby disconnecting fibers from the SMA to Broca’s area.2,14,15 The SMA, which lies anterior to the primary motor cortex on the medial surface of hemisphere, mediates the initiation and planning of movement and speech. I5 Intact repetition, the hallmark of transcortical aphasias, remains because the lateral inferior suprasylvian pathways are spared.r5 The resolution of our patient’s TCMA after evacuation of the SDH implies a causal relationship. The postoperative CT scan showed no other responsible cerebral infarction or mass lesion. To our knowledge, this association between a TCMA and a SDH has not been previously reported. Subdural hematomas, caused by hemorrhage from bridging veins between the dura and arachnoid, are almost always associated with head trauma. The blood typically lies over the convexity atop the frontal and parietal lobes, and in some cases is bilateral. Patients usually complain of a headache, and they may have mild mental status changes and a hemiparesis contralateral to the hematoma; aphasia is uncommon. Surgical evacuation is the treatment of choice.16 How could a SDH overlying the lateral aspect of the left frontal and parietal lobes cause a TCMA, which is usually associated with a deep white matter or a parasagittal cortical lesion? Subdural hematomas can cause epileptiform discharges; however, seizures involving language areas usually manifest themselves as speech arrest.” Daly et all8 suggested mass lesions can cause neurologic symptoms by mechanical stimulation of the cortex followed by a spreading depression of cerebral electrical activity,” but this effect would be too diffuse to cause a focal symptom. Direct compression or hemispheric pressure differences created by the SDH*” would also be too widespread. We cannot exclude the possibility that these diffuse processes may have induced the expression of an otherwise subclinical focal lesion. Vascular insufficiency, due either to compression of adjacent ce- 622 AMERICAN JOURNAL OF EMERGENCY or vascular displacement,6~” is a more plausible explanation for a focal deficit in our patient. Branches of the middle cerebral artery supply the white matter adjacent to the frontal horn of the lateral ventricle. The SMA lies in a division of the anterior cerebral artery, which may be compressed against the gyrus rectus proximally or the falx cerebri distally in cases of subfalcian hemiation.6 In three patients similar to ours with convexity SDHs complicated by midline shift, McLaurin angiographically demonstrated loss of flow in the anterior cerebral artery which subsequently returned after surgical drainage.6 Although CT scanning is already common in clinical practice, this case reinforces the importance of prompt cranial imaging studies in the emergency department evaluation of patients with aphasia and symptoms otherwise associated with focal lesions. Aphasic patients may be unable to give a history of head trauma, a fall, or a headache. Those with an SDH should receive immediate neurosurgical consultation. Like ours, such patients may respond dramatically to surgical evacuation of the hematoma. Emergency physicians should be keenly aware that in addition to strokes, intracerebral hemorrhages. and tumors, SDHs may lead to classic aphasia syndromes, perhaps as a result of vascular insufficiency. rebral vessels’.” GRANT T. Lru, MD MATTHEW R.MOORE, MD HAROLDGOLDMAN, MD Harvard Medical School Boston, MA Reterences 1. Mohr JP, Adams RD: Disorders of speech and language. In Braunwald E, lsselbacher KJ, Petersdorf FIG, et al (eds): Harrison’s Principles of Internal Medicine (ed 11). New York, NY, McGraw-Hill, 1987, pp 121-127 2. Benson DF, Geschwind N: Aphasia and related disorders: A clinical approach. In Mesulam MM (ed): Principles of Behavioral Neurology. Philadelphia, PA, Davis, 1985, pp 193-238 3. Groch SN, Hurwitz LJ, Wright IS, et al: intracranial lesions simulating cerebral thrombosis.-JAMA 1960;172:1469-1472 4. McKissock W. Richardson A, Bloom WH: Subdural haematoma. A review of 389 cases. Lancet 1960;1:1365-1369 5. Okihiro MM, Daly D, Yoss RE: Intermittent aphasia due to mass intracranial lesions. Mayo Clinic Proc 1961;36:525-529 6. McLaurin RL: Contributions of angiography to the pathophysiology of subdural hematomas. Neurology 1965;15:866-873 7. German WJ, Flanigan S, Davey LM: Remarks on subdural hematoma and aphasia. Clin Neurosurg 1964;12:344-350 8. Melamed E, Lavy S, Reches A, et al: Chronic subdural hematoma simulating transient ischemic attacks. J Neurosurg 1975;42:101-103 9. Robin JJ, Maxwell JA, Pitkethly DT: Chronic subdural hematoma simulating transient ischemic attacks. Ann Neurol 1978;4:154 10. Luxon LM, Harrison MJG: Chronic subdural haematoma. Q J Med 1979;189:43-53 11. Welsh JE, Tyson GW, Winn HR, et al: Chronic subdural hematoma presenting as transient neurologic deficits. Stroke 1979;10:564-567 12. Dell SO, Batson R, Kasdon DL, et al: Aphasia in subdural hematoma. Arch Neurol 1983;40:177-179 13. Moster ML, Johnston DE, Reinmuth OM: Chronic subdural hematoma with transient neurological deficits: A review of 15 cases. Ann Neurol 1983;14:539-542 14. Damasio AR, Kassel NF: Transcortical motor aphasia in relation to lesions of the supplementary motor area. Neurology 1978;28:396 15. Freedman M, Alexander MP, Naeser MA: Anatomic basis of transcortical motor aphasia. Neurology 1984;34:409-417 16. Sciarra D: Subdural hemorrhage. In Rowland LP (ed): Merritt’s Textbook of Neurology (ed 7). Philadelphia, PA, Lea & Febiger, 1984, pp 285290 17. Spiers PA, Schemer DL, Blume HW, et al: Temporolimbic MEDICINE n Volume 9, Number 6 n November 1991 epilepsy and behavior. ln Mesulam MM (ed): Principles of Behavioral Neurology. Philadelphia, PA, Davis, 1985, pp 289-326 18. Daly DD, Svien HJ, Yoss RE: Intermittent cerebral symptoms with meningiomas. Arch Neurol 1961;5:287-293 19. Leao AAP: Spreading depression of activity in the cerebral cortex. J Neurophysiol 1944;7:359-390 20. 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, Reivich M. et al (eds): Cerebral Circulation and Metabolism. New York, NY, SpringerVerlag, 1975, pp 235-237 LINGUAL TONSILLITIS: AN UNCOMMON CAUSE OF AIRWAY COMPROMISE RESPONSIVE TO EPINEPHRINE To the Ediror:-Lingual tonsillitis is a rare event that harbors a significant potential for airway compromise. The use of epinephrine for treatment of this airway compromise has not been previously reported. We report the case of an adult with lingual tonsillitis who developed respiratory distress responsive to parenteral epinephrine. A 35-year-old white woman presented to the emergency department with a 2-day history of progressive sore throat associated with increasing malaise, headache, and stiff neck. She noted a temperature of 38.3”C 24 hours prior to presentation and she had been having chills for 12 hours. She reported some nausea and photophobia. but denied vomiting. Over the preceding I? hours she noted a progression of the sore throat. Swallowing. even her own saliva, and speaking caused severe discomfort. She presented with a towel in her mouth, which she used to collect her saliva to keep it from going to the back of her throat. She denied cough. earache. chest pain. or diarrhea. Her past medical history was positive for primary hypothyroidism treated with synthroid. and mixed connective tissue disease treated with diflunisal. She had completed a course of steroids IO days prior to the onset of her symptoms for an exacerbation of her connective tissue disease. She stated she had not taken her usual medications for 24 hours due to her progressive sore throat. Physical examination revealed a well-nourished white female in obvious distress. with a small towel clenched in her mouth. The patient sat leaning forward and declined to lay back for examination. stating that she felt it was harder to breath when recumbent. Vital signs included a blood pressure of 108170mm Hg, pulse rate of 72 beats per minute. respirations of 20, and a temperature of 36.8”C. Head, eyes, ears. nose. and throat examination was pertinent for markedly dry mucous membranes, and a slightly erythematous pharynx with no obvious exudate. The neck was stiff and had shoddy anterior and posterior cervical adenopathy. The chest was clear to auscultation, and heart examination revealed a regular rate and rhythm without murmur. The abdomen was soft without organomegaly or masses, and was nontender. The skin was warm and dry without rash. The neurologic examination was intact. The diagnosis of acute epiglottitis was entertained and a soft tissue lateral cervical radiograph was obtained (Figure IA). As can be seen, the epiglottis is normal in appearance. with some scalloping of the anterior surface of the vallecula. Figure I B is a line drawing of the radiograph shown in Figure 1A highlighting the epiglottic area. Due to the abnormality noted on the lateral soft tissue cervical radiograph. an otolaryngology consultant was obtained and an oral endoscopic procedure performed. Only the edge of the epiglottis was viewed and it was normal. One gram of ceftriaxone was given intravenously. A computed tomographic scan of her head without contrast was obtained and was normal. A lumbar puncture revealed an opening pressure of 26 cm of water, and the cerebrospinal fluid was observed to be clear and colorless. immediately after the lumbar puncture, the patient sat upright and indicated that she was having trouble breathing. Significant respiratory distress associated with inspiratory and expiratory stridor was