Readers are advised that in view of The Copyright Revision Act of 1976, all Letters to the Editor submitted for publication must contain on the transmittal letter the following language: "The person(s) undersigned hereby grant the American Medical Association permission to publish this Letter and in addition, hereby assigns all copyright ownership therein to the AMA."

Publication of

Hypotheses

To the Editor.\p=m-\Youhave invited regard to the publication of hypotheses. A statistician once said that there is an infinity of hypotheses. Clearly, we have neither the paper to publish them all nor the desire to read them all. It would seem that space in the Archives should be reserved for those with data to present or those writing critical reviews. We have already had enough articles presenting hypotheses with the implication that it is up to others to support or refute the presented hypothesis. Please save valuable paper in the Archives for useful information. R. Arthur Gindin, MD Veterans Administration Hospital Augusta, GA 30904 comments in

Moyamoya and Hageman (Factor XII) Deficiency in

a

Factor

Black Adult

To the Editor.\p=m-\Wewish to add another case of moyamoya in a black adult to the cases described by Makoyo et al (Arch Neurol 34:130,

1977). A 42-year-old, right-handed, black woman was admitted to the Hospital of the Medical College of Pennsyl-

vania because of acute left-sided weakness. She had not been taking birth control pills. Four years earlier, the patient had experienced acute aphasia and right-sided weakness from which she recovered completely. On this present admission, cerebral angiography showed a moyamoya pattern, consisting of an extensive collateral vascular formation in both basal ganglia regions and bilateral stenosis of the terminal internal carotid arteries. Her prothrombin time was normal but the partial thromboplastin time was 69 seconds with a control time of 33 seconds. This

was

repeated

several times and was consistently twice that of the control. Assay of the coagulation factors was normal except for a 30% activity of factor XII. Results of hemoglobin electrophoresis were normal. Result of an antinuclear antibody test were positive at 1:20. Lupus erythematosus preparation and rheumatoid factor were negative. Complement levels of C3 and C4 were normal. The sedimentation rate was 33/hr; results of the direct and indi¬ rect Coombs' test were negative. Serum cholesterol, triglycérides, spi¬ nal fluid examination, and other stud¬ ies were unremarkable. Stenosis of the distal internal carot¬ id arteries with a collateral moyamoya pattern in the basal ganglia has been observed in children with sickle cell disease.1 The normal hemoglobin elec¬ trophoresis in our patient ruled out that entity. Taveras2 reported ten cases of moyamoya pattern under the term "multiple progressive intracranial ar¬ terial occlusions" and of his two black patients, one was a 16-year-old girl. A 50-year-old black man with moyamoya and subarachnoid hemorrhage has been described.3 With the exception of the article on sickle cell disease, the other two reports and the one by Makoyo et al did not mention any hématologie abnormalities. A defi¬ ciency of factor XII can go unnoticed unless a partial thromboplastin time is done. The deficiency is not usually clinically important. However, pa¬ tients with Hageman factor deficien¬ cy in whom myocardial infarction developed have been described.4 ä (Mr Hageman, himself, died of pulmonary

embolism.6)

In a black adult, the association of moyamoya and Hageman factor defi¬ ciency may be coincidental; however, since both entities are uncommon, we think this association should be docu¬ mented. Since very little is known about the cause of the terminal

carotid stenosis, a possible association with hématologie abnormalities should be further explored. V. P. Dhopesh, MD D. P. Dunn, MD Dept of Neurology Paul Schick, MD Dept of Medicine Medical College of Pennsylvania 3300 Henry Ave Philadelphia, PA 19129 1. Russell MO, Goldberg HI, Reis L, et al: Transfusion therapy for cerebrovascular abnormalities in sickle cell disease. J Pediatr 88:382\x=req-\ 387, 1976. 2. Taveras, JM: Multiple progressive intracranial arterial occlusions: A syndrome of children and young adults. Am J Roentgenol 106:235\x=req-\ 268, 1969. 3. Meriwether RP, Barnett HG, Echols DH: Moyamoya disease as a cause of subarachnoid hemorrhage in a Negro patient. J Neurosurg 44:620-622, 1976. 4. Hoak JC, Swanson LW, et al: Myocardial infarction associated with severe factor XII deficiency. Lancet 2:884-886, 1966. 5. Glueck HI, Roehill W Jr: Myocardial infarction in a patient with a Hageman (factor XII) defect. Ann Intern Med 64:390-396, 1966. 6. Ratnoff OD, Busse RJ Jr, Sheon, RP: The demise of John Hageman. N Engl J Med 279:760\x=req-\ 761, 1968.

Hemorrhagic Complications

of

Cerebral Arteritis

To the Editor.\p=m-\Thevalue of the arti-

cle, "Hemorrhagic Complications of Cerebral Arteritis" by Dr Keith Edwards in the Archives (34:549-552, 1977) is diminished by the absence of data, thus ruling out a bleeding

tendency in

the two patients described. Edwards' first case had subarachnoid hemorrhage, gross hematuria, and hematemesis. The coincidence of bleeding at multiple sites suggests a bleeding diasthesis; however, no laboratory data are given to rule in or out such a bleeding tendency as having contributed to the occurrence of subarachnoid hemorrhage after intravenous methamphetamine, nor is the possibility of a bleeding tendency discussed. Since reports of cerebral

hemorrhage complicating amphetamine abuse have been infrequent, it would seem important to rule out a bleeding tendency in patients in whom this complication develops. Edwards' second patient presumably had impaired clotting due to the use of intravenous heparin sodium for deep venous thrombophlebitis of the right leg. Since the author, on the basis of this case, discourages the use of anticoagulant agents in treating deep venous thrombophlebitis in pa¬ tients with known cerebral

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arteritis, it

would seem important to know wheth¬ er the partial thromboplastin time or clotting time was in the recognized therapeutic range when the intracerebral hemorrhage developed. It is well known that complications of anticoag¬ ulant therapy occur much more fre¬ quently when the partial thrombo¬ plastin time or the clotting time is excessively prolonged. This informa¬ tion is not provided in the article, and thus, the author's conclusion that the of anticoagulants should be use avoided in the presence of cerebral arteritis does not seem to be justified on the basis of the data given. Gordon J. Gilbert, MDPA 500 S Pasadena Ave St Petersburg, FL 33707

Reply.\p=m-\ Dr Gilbert's comments raise questions that should be considered in every case of subarachnoid hemorrhage. A coagulopathy, whether from a hematologic disorder or from excessive anticoagulation with heparin sodium or warfarin sodium, may precipitate a subarachnoid hemorrhage in certain cases. However, neither of these factors were present in the cases questioned by Dr Gilbert. Case 1 involved a woman in whom a necrotizing angiitis developed after amphetamine abuse. The urinary tract and GI tract bleeding that developed are a part of the clinical syndrome of necrotizing angiitis.1 Her complete blood cell count, prothrombin time, partial thromboplastin time, platelet count, and fibrinogen level were normal. Case 2 involved a young man who was receiving therapeutic doses of heparin sodium while his clotting function was monitored by frequent partial thromboplastin times. Although his partial thromboplastin times were in the usual therapeutic range, a possible contribution of the anticoagulant effect of heparin sodium toward the development of a subarachnoid hemorrhage in a patient with cerebral arteritis could not be excluded and was so discussed in the In

paper.

Keith R.

Edwards, MD Department of Neurology University of Vermont College of Medicine Burlington, VT 05401

1. Citron BP, Halpern M, McCarron M, et al: Necrotizing angiitis associated with drug abuse. N Engl J Med 283:1003-1011, 1970.

Remote

Neurological Effects of Primary Malignant Lymphoma of

a

Brain

To the Editor.\p=m-\Garofalo et al (Arch Neurol 35:50-52,1978) reported a polyneuropathy in association with a primary malignant lymphoma of the brain. Remote effects of primary brain neoplasm are distinctly rare. Relevant to the article is a previously reported case of remote neurological involvement associated with a primary malignant lymphoma of the brain.1 The case was that of a 42-year\x=req-\ old woman with recurrent cerebral infarcts in whom a primary unifocal reticulum cell sarcoma of the opposite

hemisphere subsequently developed. To my knowledge, these seem to be the only two cases of remote neurological manifestations secondary to primary

intracranial

plasms.

malignant

neo-

Pasquale F. Finnelli, MD Veterans Administration Davis Park Providence, RI 02908

Hospital

1. Finelli PF: Remote cerebral infarction as a manifestation of brain tumor: Primary reticulum cell sarcoma. Milit Med 141:548\x=req-\ 550, 1976.

presenting

Tuberculous Epidural Abscess Without Osteomyelitis To the Editor.\p=m-\We have

recently seen

of tuberculous epidural abscess without osteomyelitis. A search of the world's literature has shown only three such cases. a case

Report of a Case.\p=m-\A44-year-old

woman

admitted for intermittent fever and progressively severe left buttock and back pain radiating to the left leg. There had been no antecedent trauma or tuberculosis. Rectal temperature was 40.5\s=deg\C. Notice$able percussion tenderness was noted over the lower lumbar spine, without local mass or erythema. There was diminished sensation in the L5-S1 dermatome. Noticeable pain and spasm were evident on raising of the straight left leg. Hemogram and urinalysis were unrevealing; ESR rate was 100 mm/hr. Roentgenograms of chest and lumbosacral spine, with tomography, were normal. Intradermal testing, with tuberculin antigen test, with 5 tuberculin units, produced 15-mm induration. Examination of the spinal fluid was unrevealing. A scan of the lumbosacral spine was normal. Myelography disclosed an extradural filling defect at the left L5-S1 interspace. At laminectomy, 50 ml of purulent material was

evacuated from the epidural space, and smaller collection in the left paravertebral region was drained. Bone and disc space structures seemed normal. Acid-fast smears and cultures were positive for Mycobacterium tuberculosis, and the pa¬ tient was given conventional doses of isoniazid and ethambutol HC1. The patient is presently well. was

Comment—The clinical and radio¬

logical features of tuberculous spondylitis are well known; however, spinal tuberculosis may take a number of less common forms, including

intradural tuberculoma,1 intramedullary tuberculoma,2 and cord compres¬ sion syndromes simulating herniated disc3 or tumor.4 To our knowledge, only three prior instances of epidural tuberculous ab¬ scess were identified as of January I977.5-7 All reported patients were male, had back pain suggestive of disk herniation, and were not noted to have fever or pulmonary tuberculosis. One instance of concurrent tuberculous prostatitis was encountered.7 Tuber¬ culin testing and normal bone scan supported the diagnosis of extraosseous tuberculosis in this article. In view of the favorable prognosis offered by chemotherapy and surgical evacuation, early diagnosis is neces¬ sary to distinguish epidural tubercu¬ lous abscess from herniated spinal disc or tumor. Stephen A. Berger, MD Ira Mayer, MD Stuart Nelson, MD Division of Infectious Diseases Department of Medicine Metropolitan Hospital Center New York, NY 10029

Nonproprietary Name and Trademark of Drug Ethambutol

EO-Myambutol.

1. Slade

HW, Glazer N: Extramedullary spinal tuberculoma: Report of a case with unusual clinical and laboratory findings. J Pediatr 46:288-295,

1955. 2. Kupka E, Olsen RE: Tuberculoma of the lumbar spinal cord. Am Rev Tuberc 38:517-522, 1938. 3. Berris H: Tuberculous spondylitis simulating herniated disc. Neurology 4:710-712, 1954. 4. Kak VK, Pani KC, Chopra JS: Epidural spinal tuberculoma presenting as spinal tumor syndrome. Tubercle 53:139-142, 1972. 5. Decker HG, Shapiro SW, Porter HR: Epidural tuberculous abscess simulating herniated lumbar intervertebral disc. Ann Surg 149:294\x=req-\ 296, 1959. 6. Arct WA: Intraspinal, extradural tuberculous abscess with compression of nerve roots L5 and SI. Arch Orthop Unfallchir 80:13-19, 1974. 7. Chadduck WM: Intraspinal tuberculous abscess simulating lumbar disc disease. Va Med 99:968-971, 1972.

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Hemorrhagic complications of cerebral arteritis.

Readers are advised that in view of The Copyright Revision Act of 1976, all Letters to the Editor submitted for publication must contain on the transm...
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