Volume 86 Number 2
B r i e f clinical and laboratory observations
could contribute only 4-6 mg inorganic phosphorus/dt p l a s m a , i f c l e a v e d f r o m its t r i g l y c e r i d e m o i e t y . Lysosomal phospholipase C is the only enzyme in m a n which can cleave this bond, and it is not present in plasma] A nuclear magnetic resonance spectrum of phosphorus on a sample of serum obtained from patient No. 3, L. V., while h y p e r p h o s p h a t e m i c , showed a marked decrease in organically boufld phosphates and an increase in inorganic phosphates when compared w i t h his s e r u m v a l u e s while well. H o w e v e r , phospholipid electrophoresis on both of these serum samples produced normal results. Since prostaglandins may increase cyclic adenosine monophosphate concentrations in cultured fibroblasts, 8 we hypothesized that increased p r o s t a g l a n d i n prod u c t i o n m i g h t elevate intracellular phosphate concentrations, as phosphate is cleaved from adenosine triphosphate to produce cyclic adenosine monophosphate. We tested this by administering aspirin and diphenylhydramine to patient No. 3, L. V., to suppress prostaglandin synthesis. Although he lost the diurnal variations seen previously in his urine volume and excretion of urinary phosphorus, he did have a clinically attenuated attack of hyperphosphatemia (to 17.4 rag/ dl). All three children continue to have sporadic attacks of polyuria and occasionally of h y p e r p h o s p h a t e m i a . While these can be managed with intravenous saline and vasopressin for polyuria, and calcium gluconate for
Tuberculous arachnoiditis Joseph F. John, Jr., M.D., and R. Gordon Douglas,
Jr., M.D.,* Rochester, N. Y.
TUBERCULOSIS may involve the spinal cord and its associated s t r u c t u r e s at any level. T h e process may transgress all anatomic planes from bony vertebrae to the spinal cord proper, or be limited to any single discrete plane. 1The most c o m m o n clinical entity is tuberculous meningitis. Tuberculosis may also produce the myelographic picture of arachnoiditis w h i c h occurs much more rarely; it has been described by such terms as extradural spinal t u b e r c u l o u s g r a n u l o m a , spinal From the Infectious Disease Unit o f the Department o f Medicine, University o f Rochester School of Medicine and Den tistry. *Reprint address: 260 CrtttendenBlvd., Rochester, N.Y. 14642.
235
hypocalcemia, the mechanism and etiology of this disorder remains obscure. We thank Dr. Ella Cummins of Morristown, N.J., for referring these children to us. REFERENCES
1. Levitt M, Gessert C, and Finberg L: Inorganic phosphate (laxative) poisoning resulting in tetany in an infant, J PEDIATR82:479, 1973. 2. Smith MS, Feldman KW, and Furukawa CT: Coma in an infant due to hypertonic sodium phosphate medication, J PEDIATR82:481, 1973. 3. Armata J, and Depowska T: Letter to the editor, N Engl J Med 290:858, 1974. 4. Beutler E, and Srivastava SK: Composition of the erythrocyte, In Williams WJ, Beutler E, Ersler AJ, and Rundles RW, editors, Hematology, New York, 1972, McGraw-Hill Book Company, Inc. 5. Fredrickson DS, Gotto AM, and Levy RI: Familial lipoprotein deficiency, In Stanbury JB, Wyngaarden JB, and Fredrickson DS, editors: The metabolic basis of inherited disease, New York, 1972, McGraw-Hill Book Company, Inc. 6. Chen PS Jr, Toribara TY, and Warner H: Microdeterruination of phosphorus, Anal Chem 28:1756, 1956. 7. White A, Handler P, and Smith EL: Principles of biochemistry, ed 4, New York, 1968, McGraw-Hill Book Company, Inc. 8. Manganiello V, and Vaughn M: Prostaglandin E 1 effects on adenosine 3' :5' -cyclic monophosphate concentration and phosphodiesterase activity in fibroblasts, Proc Natl Acad Sci 69:269, 1972.
t u b e r c u l o m a , and t u b e r c u l o u s g r a n u l o m a t o u s leptomeningitis.1,2 We report a case of c u l t u r e - p o s i t i v e t u b e r c u l o u s arachnoiditis in a native American boy, who presented with minimal spinal dysfunction. Abbreviations used CSF: cerebrospinal fluid PPD: purified protein derivative CASE R E P O R T
A 16-year-old Caucasian boy was admitted to the hospital because of fever and stiff neck. Four days prior to admission, the patient began to experience malaise, anorexia, mild dysosmia, and dysgeusia, and a frontal pulsatile headache. Over the next 3 days symptoms worsened. His neck became more stiff and painful with movement. There was no weakness, numbness, or incontinence. The patient's father, age 51, had been treated 12 years earlier
236
Brief clinical and laboratory observations
The Journal of Pediatrics February 1975
Table I. Serial cerebrospinal fluid data Time after admission
Total cells
Neutrophils
1 day 8 days 12 days 16 days 16 days* 1 mo 4 mo 6 mo
175 722 379 939 11 350 120 0
3 77 65 10 100 6 0 0
(%)
Mononuclears
(%)
Protein (mg/dl)
Glucose (mg/dl)
95 8 35 90 0 88 100 0
528 5,200 5,500 5,100 55 5,100 3,900 1,020
25 20 12 21 27 7 54 60
Lactic dehydrogenase 112 682 344
Manometric response Minimal Absent Absent Absent Present Absent Present Low pressure
*Cisternal sample.
NORMAL - CSF
8.8
1:5.7
6.7
4.5
61.5
,4.9
PATIENT'S- CSF
19.8
7.8
9.8
5.8
58.8
0.0
Fig. 1. Cerebrospinal fluid protein electrophoresis. The total protein is 5.i gm/dl, and the various fractions of the patient's and previously published normal CSF 3 shown as percent of the tofa! protein. There is absence of a pre-albumin fraction, present in normal CSF, and an increase in both a- 2 atad y-globulins. for pulmonary tuberculosis. A brother, age 19, received isoniazid 2 years previously for conversion of a tuberculin skin test. The patient's tuberculin skin tests and chest films were negative at 4 89 4, and 2 years, respectively, prior to admission. On admission, blood pressure was 120/70 mm Hg, pulse 90 per minute and regular, respirations 18 and nonlabored, temperature 39.5~ C. The patient was experiencing intermittent rigors. No rash nor adenopathy was present. The lungs were clear to percussion and auscultatiori. Complete neurologic examination, including cranial nerve function, was normal except for stiffness of the neck and mild diffuse paravertebral tenderness. Initial laboratory data included a hemoglobin of 13.1 gm/dl, hematocrit 41%, total white blood cell count of 4,800/mm 3 with 61% neutrophils, 6% band cells, 20% lymphocytes, 13% monocytes, and normal red blood cell and platelet morphology.
Urinalysis showed clear, yellow urine with 2 to 6 white blood cells per high-power field and 5 to 7 red blood cells per highpower field. A chest film showed no abnormalities. An intermediate and second Strength PPD were negative. As shown in Table I, initial lumbar puncture revealed clear cerebrospinal fluid with 175 WBC/mm 3, protein 528 mg/dl, glucose 25 mg/dl. The blood sugar was 94 mg/dl. After repeat lumbar puncture on the eighth hospital day, because of suspected tuberculous meningitis and continuance of spiking fever to 40 ~ C, the patient wag placed on isoniazid, ethambutol, and streptomycin. Lumbar puncture on the twelfth hospital day showed no manometric response, and a CSF protein of 5.5 gm/dl. A CSF protein electrophoresis was performed to verify this abnormality (Fig. 1). These findings were also verified by repeated lumbar punctures (Table I). In contrast to these findings, CSF removed by cisternal puncture revealed normal protein concentration and manometrics, although hypoglycorrhagia was still present. Because of the protein abnormalities and persistence of spiking fever, a myelogram was done on the sixteenth hospital day, and showed a diffuse bizzare disarray of contrast material consistent with extensive arachnoiditis. The patient was started on 60 mg of prednisone per day and maintained on the antituberculosis drug regimen. Over the next two weeks, his fever gradually approached normal. Roentgenograms of the vertebral column revealed no abnormalities in the bony architecture. Multiple sputum and urine specimens cultured for mycobacteria were negative. A recent roentgenogram was unchanged. All CSF samples were submitted for mycobacterial culture. The cisternal sample grew Mycobacterium tuberculosis after 7 weeks, but the lumbar CSF samples remained sterile. This isolate was sensitive to streptomycin, isoniazid, and ethambutol. The patient gradually regained strength and was ambulatory on discharge one month after admission. One week after discharge, an intermediate PPD produced 22 mm of induration. On examination at this time, there were no positive findings except the inability to stand spontaneously from a sitting position, and absent ankle reflexes. These abnormalities improved and one month after discharge the patient could stand easily
Volume 86 Number 2
from a sitting position; however, deep tendon reflexes of the knees and ankles were decreased. Three months after discharge, prednisone was tapered to 10 mg every other day. Lumbar puncture at this time revealed normal manometric response and a decrease in total CSF protein. Over the next month, administration of prednisone was discontint~ed. Cerebrospinal fluid obtained 6 months after the onset of illness revealed a much lower protein concentration of 1,020 mg/dl. By that time, the patient was attending school and participating in physical education classes. DISCUSSION T u b e r c u l o u s arachnoiditis is very u n c o m m o n , especially in this country. 4 I n an Indian review, 15 of 74 patients with tuberculous paraplegia had arachnoiditis when examined by myelography, l All 15 had evidence of previous pulmonary tuberculosis and often other extrapulmonary tuberculosis. The isolated involvement of the leptomeninges with no extraspinal foci, and the lack of severe neurologic signs, is unusual,2 presenting a diagnostic dilemma as it did in the present case. Although the etiology of arachnoiditis was eventually proved by culture, early in the patient's course the diagnosis was not established. There are several readily notable causes of radiologically proved arachnoiditis, including intervertebral disc prolapse, intrathecal introduction of dyes, chemicals, or antibiotics, syphilis, spinal trauma, ruptured spinal hemangioma, syringomyelia, and other inflammatory conditions.5 It appears that a tentative diagnosis of tuberculous arachnoiditis can be made on clinical grounds, so that antituberculosis chemotherapy may be instituted. Wadia and Dastur 2 studied 70 cases of spinal arachnoiditis, 38 of which were proved to be due to tuberculosis. The authors devised a semiquantitati'Oe scoring method for diagnosis of idiopathic cases based on the presence of tuberculosis elsewhere; shortness of duration of the history of spinal involvement; onset of root pains and myelitis; myelopathy; myelographic changes; cell count, elevated protein and decreased glucose content of the CSF; failure to perform the lumbar puncture successfully; and response to antitiJberculosis therapy. Using these criteria, our patient obtains a score which in culture negative disease strongly suggests a tuberculous process. There are no controlled studies on the ideal mode or duration of therapy in patients with tuberculous spinal teptomeningitis. Since one of the histopathologic hallmarks of t u b e r c u l o u s l e p t o m e n i n g i t i s is a vasculitis with vascular necrosis, 6 it seems reasonable to utilize the a n t i - i n f l a m a t o r y properties of corticosteroids. A controlled study by O'Toole and associates 7 of steroid
Brief clinical and laboratory observations
237
therapy in tuberculous meningitis demonstrated that CSF protein decreased more ~n treated than in control patients. Whether this holds for patients with spinal block and loculated CSF compartments has not been studied. Several studies indicate favorable o u t c o m e s w h e n surgery is employed in c o n j u n c t i o n with c h e m o therapeutic agents. 8 Previously Slade and Glazer 9 reported a patient with similar myelographic findings as in our patient; the CSF protein concentration, at times exceeded 10 gm/dl. In this case, a preoperative diagnosis of tuberculous arachnoiditis with or without mass was confirmed at surgery more than 2 years later when a w e l l - c i r c u m s c r i b e d t u b e r c u l o m a c o m p r e s s i n g the spinal cord at T9.10 was excised inside the dura but above the arachnoid. Prior to surgery the CSF protein had remained above 5,0 gm/dl for nearly 3 years. Wadia and Dastur 2, 6 found that effective decompreSsion could not be accon~plished when involvement of the leptomeninges was extensive. In their later cases, when the diagnosis had been made clinically, surgery was not employed for therapeutic purposes, Improvem e n t in these patients treated medically was related to the (1) duration of the illness, (2) the extent of the myelopathy, (3) prompt initiation of antituberculosis therapy, and (4) prolonged treatment for 3 months to a year. This condition may be quite indolent, and tuberculous spinal leptomeningitis has a case fatality rate approximating 50%. REFERENCES
1. Dastur HM: A tuberculoma review with some personal experiences, Neurol India 20:127, 1972. 2. Wadia NH, and Dastur DK: Spinal meningitides with radiculomyelopathy. Part 1. Clinical and radiological features, J Neurol Sci 8:239, 1969. 3. Kaplan A, and Johnstone M: Concentration of cerebrospinal fluid proteins and their fractionation by cellulose acetate electrophoresis, Clin Chem 12:717, 1966. 4. Lepper MH, and Spies HW: The present status of the treatment of tuberculosis of the central nervous system, Ann NY Acad Sci 106:106, 1963. 5. Teng P, and Papatheodorou C: Myelographic findings in adhesive spinal arachnoiditis, Br J Radiol 40:201, 1967. 6. Dastur DK, and Wadia NH: Spinal meningitides with radiculomyelopathy. Part 2. Pathology and pathogenesis, J Neurol Sci 8:261, 1969. 7. O'Toole RD, Thornton GR, Mulherjee MK, and Nath RL: Dexamethasone in tuberculous meningitis. Relationship of cerebrospinal fluid effects to therapeutic efficacy, Ann Intern Med 70:39, 1969. 8. Benini A: Chronic circumscribed adhesive and cystic spinal leptomeningitis, Surg Neurol 1:223, 1973. 9. Slade HW, and Glazer N: Extramedullary spinal tuberculoma, J PEDIATR46:288, 1955.
B r i e f clinical and laboratory observations
could contribute only 4-6 mg inorganic phosphorus/dt p l a s m a , i f c l e a v e d f r o m its t r i g l y c e r i d e m o i e t y . Lysosomal phospholipase C is the only enzyme in m a n which can cleave this bond, and it is not present in plasma] A nuclear magnetic resonance spectrum of phosphorus on a sample of serum obtained from patient No. 3, L. V., while h y p e r p h o s p h a t e m i c , showed a marked decrease in organically boufld phosphates and an increase in inorganic phosphates when compared w i t h his s e r u m v a l u e s while well. H o w e v e r , phospholipid electrophoresis on both of these serum samples produced normal results. Since prostaglandins may increase cyclic adenosine monophosphate concentrations in cultured fibroblasts, 8 we hypothesized that increased p r o s t a g l a n d i n prod u c t i o n m i g h t elevate intracellular phosphate concentrations, as phosphate is cleaved from adenosine triphosphate to produce cyclic adenosine monophosphate. We tested this by administering aspirin and diphenylhydramine to patient No. 3, L. V., to suppress prostaglandin synthesis. Although he lost the diurnal variations seen previously in his urine volume and excretion of urinary phosphorus, he did have a clinically attenuated attack of hyperphosphatemia (to 17.4 rag/ dl). All three children continue to have sporadic attacks of polyuria and occasionally of h y p e r p h o s p h a t e m i a . While these can be managed with intravenous saline and vasopressin for polyuria, and calcium gluconate for
Tuberculous arachnoiditis Joseph F. John, Jr., M.D., and R. Gordon Douglas,
Jr., M.D.,* Rochester, N. Y.
TUBERCULOSIS may involve the spinal cord and its associated s t r u c t u r e s at any level. T h e process may transgress all anatomic planes from bony vertebrae to the spinal cord proper, or be limited to any single discrete plane. 1The most c o m m o n clinical entity is tuberculous meningitis. Tuberculosis may also produce the myelographic picture of arachnoiditis w h i c h occurs much more rarely; it has been described by such terms as extradural spinal t u b e r c u l o u s g r a n u l o m a , spinal From the Infectious Disease Unit o f the Department o f Medicine, University o f Rochester School of Medicine and Den tistry. *Reprint address: 260 CrtttendenBlvd., Rochester, N.Y. 14642.
235
hypocalcemia, the mechanism and etiology of this disorder remains obscure. We thank Dr. Ella Cummins of Morristown, N.J., for referring these children to us. REFERENCES
1. Levitt M, Gessert C, and Finberg L: Inorganic phosphate (laxative) poisoning resulting in tetany in an infant, J PEDIATR82:479, 1973. 2. Smith MS, Feldman KW, and Furukawa CT: Coma in an infant due to hypertonic sodium phosphate medication, J PEDIATR82:481, 1973. 3. Armata J, and Depowska T: Letter to the editor, N Engl J Med 290:858, 1974. 4. Beutler E, and Srivastava SK: Composition of the erythrocyte, In Williams WJ, Beutler E, Ersler AJ, and Rundles RW, editors, Hematology, New York, 1972, McGraw-Hill Book Company, Inc. 5. Fredrickson DS, Gotto AM, and Levy RI: Familial lipoprotein deficiency, In Stanbury JB, Wyngaarden JB, and Fredrickson DS, editors: The metabolic basis of inherited disease, New York, 1972, McGraw-Hill Book Company, Inc. 6. Chen PS Jr, Toribara TY, and Warner H: Microdeterruination of phosphorus, Anal Chem 28:1756, 1956. 7. White A, Handler P, and Smith EL: Principles of biochemistry, ed 4, New York, 1968, McGraw-Hill Book Company, Inc. 8. Manganiello V, and Vaughn M: Prostaglandin E 1 effects on adenosine 3' :5' -cyclic monophosphate concentration and phosphodiesterase activity in fibroblasts, Proc Natl Acad Sci 69:269, 1972.
t u b e r c u l o m a , and t u b e r c u l o u s g r a n u l o m a t o u s leptomeningitis.1,2 We report a case of c u l t u r e - p o s i t i v e t u b e r c u l o u s arachnoiditis in a native American boy, who presented with minimal spinal dysfunction. Abbreviations used CSF: cerebrospinal fluid PPD: purified protein derivative CASE R E P O R T
A 16-year-old Caucasian boy was admitted to the hospital because of fever and stiff neck. Four days prior to admission, the patient began to experience malaise, anorexia, mild dysosmia, and dysgeusia, and a frontal pulsatile headache. Over the next 3 days symptoms worsened. His neck became more stiff and painful with movement. There was no weakness, numbness, or incontinence. The patient's father, age 51, had been treated 12 years earlier
236
Brief clinical and laboratory observations
The Journal of Pediatrics February 1975
Table I. Serial cerebrospinal fluid data Time after admission
Total cells
Neutrophils
1 day 8 days 12 days 16 days 16 days* 1 mo 4 mo 6 mo
175 722 379 939 11 350 120 0
3 77 65 10 100 6 0 0
(%)
Mononuclears
(%)
Protein (mg/dl)
Glucose (mg/dl)
95 8 35 90 0 88 100 0
528 5,200 5,500 5,100 55 5,100 3,900 1,020
25 20 12 21 27 7 54 60
Lactic dehydrogenase 112 682 344
Manometric response Minimal Absent Absent Absent Present Absent Present Low pressure
*Cisternal sample.
NORMAL - CSF
8.8
1:5.7
6.7
4.5
61.5
,4.9
PATIENT'S- CSF
19.8
7.8
9.8
5.8
58.8
0.0
Fig. 1. Cerebrospinal fluid protein electrophoresis. The total protein is 5.i gm/dl, and the various fractions of the patient's and previously published normal CSF 3 shown as percent of the tofa! protein. There is absence of a pre-albumin fraction, present in normal CSF, and an increase in both a- 2 atad y-globulins. for pulmonary tuberculosis. A brother, age 19, received isoniazid 2 years previously for conversion of a tuberculin skin test. The patient's tuberculin skin tests and chest films were negative at 4 89 4, and 2 years, respectively, prior to admission. On admission, blood pressure was 120/70 mm Hg, pulse 90 per minute and regular, respirations 18 and nonlabored, temperature 39.5~ C. The patient was experiencing intermittent rigors. No rash nor adenopathy was present. The lungs were clear to percussion and auscultatiori. Complete neurologic examination, including cranial nerve function, was normal except for stiffness of the neck and mild diffuse paravertebral tenderness. Initial laboratory data included a hemoglobin of 13.1 gm/dl, hematocrit 41%, total white blood cell count of 4,800/mm 3 with 61% neutrophils, 6% band cells, 20% lymphocytes, 13% monocytes, and normal red blood cell and platelet morphology.
Urinalysis showed clear, yellow urine with 2 to 6 white blood cells per high-power field and 5 to 7 red blood cells per highpower field. A chest film showed no abnormalities. An intermediate and second Strength PPD were negative. As shown in Table I, initial lumbar puncture revealed clear cerebrospinal fluid with 175 WBC/mm 3, protein 528 mg/dl, glucose 25 mg/dl. The blood sugar was 94 mg/dl. After repeat lumbar puncture on the eighth hospital day, because of suspected tuberculous meningitis and continuance of spiking fever to 40 ~ C, the patient wag placed on isoniazid, ethambutol, and streptomycin. Lumbar puncture on the twelfth hospital day showed no manometric response, and a CSF protein of 5.5 gm/dl. A CSF protein electrophoresis was performed to verify this abnormality (Fig. 1). These findings were also verified by repeated lumbar punctures (Table I). In contrast to these findings, CSF removed by cisternal puncture revealed normal protein concentration and manometrics, although hypoglycorrhagia was still present. Because of the protein abnormalities and persistence of spiking fever, a myelogram was done on the sixteenth hospital day, and showed a diffuse bizzare disarray of contrast material consistent with extensive arachnoiditis. The patient was started on 60 mg of prednisone per day and maintained on the antituberculosis drug regimen. Over the next two weeks, his fever gradually approached normal. Roentgenograms of the vertebral column revealed no abnormalities in the bony architecture. Multiple sputum and urine specimens cultured for mycobacteria were negative. A recent roentgenogram was unchanged. All CSF samples were submitted for mycobacterial culture. The cisternal sample grew Mycobacterium tuberculosis after 7 weeks, but the lumbar CSF samples remained sterile. This isolate was sensitive to streptomycin, isoniazid, and ethambutol. The patient gradually regained strength and was ambulatory on discharge one month after admission. One week after discharge, an intermediate PPD produced 22 mm of induration. On examination at this time, there were no positive findings except the inability to stand spontaneously from a sitting position, and absent ankle reflexes. These abnormalities improved and one month after discharge the patient could stand easily
Volume 86 Number 2
from a sitting position; however, deep tendon reflexes of the knees and ankles were decreased. Three months after discharge, prednisone was tapered to 10 mg every other day. Lumbar puncture at this time revealed normal manometric response and a decrease in total CSF protein. Over the next month, administration of prednisone was discontint~ed. Cerebrospinal fluid obtained 6 months after the onset of illness revealed a much lower protein concentration of 1,020 mg/dl. By that time, the patient was attending school and participating in physical education classes. DISCUSSION T u b e r c u l o u s arachnoiditis is very u n c o m m o n , especially in this country. 4 I n an Indian review, 15 of 74 patients with tuberculous paraplegia had arachnoiditis when examined by myelography, l All 15 had evidence of previous pulmonary tuberculosis and often other extrapulmonary tuberculosis. The isolated involvement of the leptomeninges with no extraspinal foci, and the lack of severe neurologic signs, is unusual,2 presenting a diagnostic dilemma as it did in the present case. Although the etiology of arachnoiditis was eventually proved by culture, early in the patient's course the diagnosis was not established. There are several readily notable causes of radiologically proved arachnoiditis, including intervertebral disc prolapse, intrathecal introduction of dyes, chemicals, or antibiotics, syphilis, spinal trauma, ruptured spinal hemangioma, syringomyelia, and other inflammatory conditions.5 It appears that a tentative diagnosis of tuberculous arachnoiditis can be made on clinical grounds, so that antituberculosis chemotherapy may be instituted. Wadia and Dastur 2 studied 70 cases of spinal arachnoiditis, 38 of which were proved to be due to tuberculosis. The authors devised a semiquantitati'Oe scoring method for diagnosis of idiopathic cases based on the presence of tuberculosis elsewhere; shortness of duration of the history of spinal involvement; onset of root pains and myelitis; myelopathy; myelographic changes; cell count, elevated protein and decreased glucose content of the CSF; failure to perform the lumbar puncture successfully; and response to antitiJberculosis therapy. Using these criteria, our patient obtains a score which in culture negative disease strongly suggests a tuberculous process. There are no controlled studies on the ideal mode or duration of therapy in patients with tuberculous spinal teptomeningitis. Since one of the histopathologic hallmarks of t u b e r c u l o u s l e p t o m e n i n g i t i s is a vasculitis with vascular necrosis, 6 it seems reasonable to utilize the a n t i - i n f l a m a t o r y properties of corticosteroids. A controlled study by O'Toole and associates 7 of steroid
Brief clinical and laboratory observations
237
therapy in tuberculous meningitis demonstrated that CSF protein decreased more ~n treated than in control patients. Whether this holds for patients with spinal block and loculated CSF compartments has not been studied. Several studies indicate favorable o u t c o m e s w h e n surgery is employed in c o n j u n c t i o n with c h e m o therapeutic agents. 8 Previously Slade and Glazer 9 reported a patient with similar myelographic findings as in our patient; the CSF protein concentration, at times exceeded 10 gm/dl. In this case, a preoperative diagnosis of tuberculous arachnoiditis with or without mass was confirmed at surgery more than 2 years later when a w e l l - c i r c u m s c r i b e d t u b e r c u l o m a c o m p r e s s i n g the spinal cord at T9.10 was excised inside the dura but above the arachnoid. Prior to surgery the CSF protein had remained above 5,0 gm/dl for nearly 3 years. Wadia and Dastur 2, 6 found that effective decompreSsion could not be accon~plished when involvement of the leptomeninges was extensive. In their later cases, when the diagnosis had been made clinically, surgery was not employed for therapeutic purposes, Improvem e n t in these patients treated medically was related to the (1) duration of the illness, (2) the extent of the myelopathy, (3) prompt initiation of antituberculosis therapy, and (4) prolonged treatment for 3 months to a year. This condition may be quite indolent, and tuberculous spinal leptomeningitis has a case fatality rate approximating 50%. REFERENCES
1. Dastur HM: A tuberculoma review with some personal experiences, Neurol India 20:127, 1972. 2. Wadia NH, and Dastur DK: Spinal meningitides with radiculomyelopathy. Part 1. Clinical and radiological features, J Neurol Sci 8:239, 1969. 3. Kaplan A, and Johnstone M: Concentration of cerebrospinal fluid proteins and their fractionation by cellulose acetate electrophoresis, Clin Chem 12:717, 1966. 4. Lepper MH, and Spies HW: The present status of the treatment of tuberculosis of the central nervous system, Ann NY Acad Sci 106:106, 1963. 5. Teng P, and Papatheodorou C: Myelographic findings in adhesive spinal arachnoiditis, Br J Radiol 40:201, 1967. 6. Dastur DK, and Wadia NH: Spinal meningitides with radiculomyelopathy. Part 2. Pathology and pathogenesis, J Neurol Sci 8:261, 1969. 7. O'Toole RD, Thornton GR, Mulherjee MK, and Nath RL: Dexamethasone in tuberculous meningitis. Relationship of cerebrospinal fluid effects to therapeutic efficacy, Ann Intern Med 70:39, 1969. 8. Benini A: Chronic circumscribed adhesive and cystic spinal leptomeningitis, Surg Neurol 1:223, 1973. 9. Slade HW, and Glazer N: Extramedullary spinal tuberculoma, J PEDIATR46:288, 1955.
