Neuro
Neuroradiology (1992) 34:197-199
radiology 9 Springer-Verlag 1992
Locations of cerebral infarctions in tuberculous meningitis* E-Y. Hsieh 1, L.-G. Chia 1, and W.-C. Shen 2
Sections of ~ Neurology and 2 Neuroradiology, Taichung Veterans General Hospital, Taichung, Taiwan, Republic of China Received: 18 March 1991
Summary. The locations of cerebral infarctions were stu-
died in 14 patients with tuberculous meningitis (TBM) and 173 patients with noninflammatory ischemic stroke (IS). In patients with TBM, 75 % of infarctions occurred in the "TB zone" supplied by medial striate and thalamoperforating arteries; only 11% occurred in the "IS zone" supplied by lateral striate, anterior choroidal and thalamogeniculate arteries. In patients with IS, 29 % of infarctions occurred in the IS zone, 29 % in the subcortical white matter, and 24 % in (or involving) the cerebral cortex. Only 11% occurred in the TB zone. Bilaterally symmetrical infarctions of the TB zone were common with T B M (71%) but rare with IS (5 %). K e y words: Tuberculous meningitis - Ischemic stroke C o m p u t e d tomography
Previous papers have addressed the cerebral infarctions caused by tuberculous meningitis (TBM) [1-8]. However, specific analysis of the differences in the locations of cerebral infarctions resulting from T B M and from ischemic stroke (IS) has not been reported.
Materials and m e t h o d s
T B M was diagnosed on the basis of one or more of the following criteria: (1) demonstration of acid-fast bacilli by direct staining of cerebrospinal fluid (CSF); (2) positive culture of acid-fast bacilli from CSF (or sputum if miliary tuberculosis was present); (3) clinical and CSF responses to anti-tuberculous therapy [1]. Data from 40 patients with T B M admitted to our hospital from 1983 to 1988 were reviewed to select 14 patients with (1) evidence of cerebral infarctions on computed
* Presented at the 14th Scientific Meeting of the Neurological Society,R. O. C., held in Taiwan, 20-21 April 1990
tomography (CT) (Siemens Somatom D R III) and (2) no history of cerebral vascular disease, hypertension, diabetes mellitus, collagen disease, blood dyscrasia, or heart disease. Two patients with tuberculomas were excluded [2]. For comparison, CT studies were reviewed to select 173 patients admitted to our hospital from January to December 1984, with CT evidence of one or more noninflammatory IS, including lacunar infarctions. The locations of cerebral infarctions were determined by their geometric centers. However, an infarction extending from the cerebral cortex to the white matter, with or without involvement of the basal ganglia, was classified as an infarction involving the cerebral cortex. A small infarction with its center in the external capsule or claustrum was classified as an infarction of the subcortical white matter, because the blood supply of this zone arises from cortical branches [9]. To facilitate discussion, we defined a "TB zone" as the region supplied by medial striate, thalamotuberal and thalamoperforating arteries; that is, the heads of the caudate nuclei, the anteromedial thalami, the anterior limbs of the internal capsules and the genus of the internal capsules [10, 11]. Similarly, an "IS" zone was defined as the region supplied by the lateral striate, anterior choroidal and thalamogeniculate arteries; that is, the lenticular nuclei, the
Table 1. Locations of cerebral infarctions
Diagnosis
Numberof infarctions TBZ ISZ SWM (%) (%) (%) Tuberculous 27 4 1 Meningitis (75.0) (11.1) (2.8) Ischemic 48 128 127 Stroke (108) (29.0) (29.0) Pvalue* 0.0000 0.0343 0.0014
CC (%) 2 (5.5) 105 (23.8) 0.0205
BS (%) 1 (2.8) 20 (4.5) > 0.05
Cbl (%) 1 (2.8) 13 (2.9) > 0.05
Total (%) 36 (100) 441 (100)
* X2 test with Yates correction TBZ, Tuberculosis zone; SWM, subcortical white matter; BS, brain stem; ISZ, ischemic-stroke zone; CC, cerebral cortex; Cbl, cerebellum
198
Fig. L a Horizontal lines indicate the "tuberculosis zone." Vertical lines indicate the "ischemic-stroke zone" b, c Diagram of the distribution of infarcts in ischemic stroke (b, dots) and tuberculous meningitis (e, crosses) at a representative level
posterolateral thalami, and the posterior limbs of the internal capsules (Fig. i a) [10, 11]. The statistical significance of our data was evaluated by the chi-square test with Yates correction.
Results
Cerebral infarctions were found in 14 of the 40 TB patients (35 %). These patients were 38-74 years of age (mean age 57.9 years). The age distribution of the 137 with IS was 37-100 years, mean 64.1 years. The locations of the cerebral infarctions in T B M and in IS are summarized in Table 1. Infarctions caused by T B M occurred predominantly in the TB zone (75 % ), followed by the IS zone (11.1% ), the cerebral cortex (5.5 % ), subcortical white matter (2.8%), brain stem (2.8%), and cerebellum (2.8 %). Infarctions from IS occurred mainly in the IS zone (29 % ) and subcortical white matter (29 %), followed by the cerebral cortex (23.8%), TB zone (10.8 %), brain stem (4.5 %), and cerebellum (2.9 %).
Fig. 2 a-c. Computed tomography of patients with tuberculous men-
ingitis, a A 52-year-old man with two infarctions located at the genus of the internal capsules bilaterally, b A 51-year-old man with
T B M correlated with infarctions in the TB zone much better than did IS (Table 1, Fig. 1). IS correlated with infarctions in the IS zone, the subcortical white matter, and the cerebral cortex better than did T B M (Table 1). T B M and IS correlated with infarctions in the posterior fossa equally well (Table 1). Bilateral cerebral infarctions were observed in 7 of the 14 patients with T B M (50%) and 84 of the 137 patients with IS (61%). Symmetrical involvement of the TB zone correlated with T B M (5 of 7 patients) much better than with IS (4 of 84 patients) (P = 0.0000) (Fig. 2 a, b).
Discussion
In an autopsy study, Fisher [3] reported that 37 % of lacunar infarctions were situated in the lenticular nuclei, and only 10 % in the caudate nuclei. Similarly, in our series lesions of IS were more frequent in the IS zone (29.0 %) than in the TB zone (10.8 % ). In TBM, vessels that traverse the basal exudate develop vasculitis with inflammation, spasm, constriction,
five infarctions in the basal ganglia, internal capsules, and the left thalamus, c A 38-year-old man with an infarction at the anterior portion of the left thalamus
199 and eventual thrombosis that results in cerebral infarction [4]. In an autopsy study of TBM, Dastur et al. [5] reported that cerebral infarction due to vasculitis occurred in 43.6 % of children and 31.8 % of adult cases. In CT studies, 17 % - 5 3 % of patients with T B M show vascular lesions [1, 2, 6-8]. O u r study revealed cerebral infarctions in 35 9/0 of patients. The medial striate, thalamotuberal and thalamoperforating arteries are located medial to the lateral striate, anterior choroidal and thalamogeniculate arteries. Conceivably, the basal exudate of TB, which is usually most severe at the circle of Willis, m a y affect the m o r e medial TB zone vessels m o r e severely than the m o r e lateral IS zone vessels. This might explain why infarctions of T B M are frequently located in the TB zone and why they are so frequently symmetrical. We suggest that T B M should be considered first when imaging studies reveal multiple infarctions of about the same age situated symmetrically in the TB zone. A similar picture has not b e e n reported in other conditions.
3. Fisher CM (1965) Lacunes: small, deep cerebral infarcts. Neurology 15:774-784 4. Sheller JR, Des Prez RM (1986) CNS tuberculosis. Neurol Clin 4: 143-157 5. Dastur DK, Latitha VS, Udani PM, Parekh U (1970) The brain and meninges in tuberculous meningitis - gross pathology in 100 cases and pathogenesis Neurol Indian 18:86-100 6. Teoh R, Humphries MJ, Hoare RD, O'Mahony G (1989) Clinical correlation of CT changes in 64 CHinese patients with tuberculous meningitis. J Neuro1236:48-51 7. Bhargava S, Gupta AK, Tanon PN (1982) Tuberculous meningitis - a CT study. Br J Radio155:189-196 8. Kingsley DR Hendrickse WA, Kendall BE, Swash M, Singh V (1987) Tuberculous meningitis: role of CI" in management and prognosis. J Neurol Neurosurg Psychiatry 50:30-36 9. Takahashi S, Goto K, Fukasawa H, Kawata Y, Uemura K, Suzuki K (1985) Computed tomography of cerebral infarction along the distribution of the basal perforating arteries. I. Striate arterial group. Radiology 155:107-118 10. House EL, Pansky B, Siegel A (eds) (1979) A systemic approach to neuroscience, 3rd edn McGraw-Hill, New York, pp 58-72 11. Takahashi S, Goto K, Fukasawa H, Kawata Y, Uemura K, Yaguchi K (1985) Computed tomography of cerebral infarction along the distribution of the basal perforating arteries. II. Thalamic arterial group. Radiology 155:119-130
References 1. Bullock MRR, Welchman JM (1982) Diagnostic und prognostic features of tuberculous meningitis of CT scanning. J Neurol Neurosurg Psychiatry 45:1098-1101 2. Bonafe A, Manelfe C, Gomez MC, et al (1985) Tuberculous meningitis. J Neuroradio112: 302-316
E-Y. Hsieh, M. D. Section of Neurology Taichung Veterans General Hospital Taichung, Taiwan 40705 Republic of China
Neuroradiology (1992) 34:197-199
radiology 9 Springer-Verlag 1992
Locations of cerebral infarctions in tuberculous meningitis* E-Y. Hsieh 1, L.-G. Chia 1, and W.-C. Shen 2
Sections of ~ Neurology and 2 Neuroradiology, Taichung Veterans General Hospital, Taichung, Taiwan, Republic of China Received: 18 March 1991
Summary. The locations of cerebral infarctions were stu-
died in 14 patients with tuberculous meningitis (TBM) and 173 patients with noninflammatory ischemic stroke (IS). In patients with TBM, 75 % of infarctions occurred in the "TB zone" supplied by medial striate and thalamoperforating arteries; only 11% occurred in the "IS zone" supplied by lateral striate, anterior choroidal and thalamogeniculate arteries. In patients with IS, 29 % of infarctions occurred in the IS zone, 29 % in the subcortical white matter, and 24 % in (or involving) the cerebral cortex. Only 11% occurred in the TB zone. Bilaterally symmetrical infarctions of the TB zone were common with T B M (71%) but rare with IS (5 %). K e y words: Tuberculous meningitis - Ischemic stroke C o m p u t e d tomography
Previous papers have addressed the cerebral infarctions caused by tuberculous meningitis (TBM) [1-8]. However, specific analysis of the differences in the locations of cerebral infarctions resulting from T B M and from ischemic stroke (IS) has not been reported.
Materials and m e t h o d s
T B M was diagnosed on the basis of one or more of the following criteria: (1) demonstration of acid-fast bacilli by direct staining of cerebrospinal fluid (CSF); (2) positive culture of acid-fast bacilli from CSF (or sputum if miliary tuberculosis was present); (3) clinical and CSF responses to anti-tuberculous therapy [1]. Data from 40 patients with T B M admitted to our hospital from 1983 to 1988 were reviewed to select 14 patients with (1) evidence of cerebral infarctions on computed
* Presented at the 14th Scientific Meeting of the Neurological Society,R. O. C., held in Taiwan, 20-21 April 1990
tomography (CT) (Siemens Somatom D R III) and (2) no history of cerebral vascular disease, hypertension, diabetes mellitus, collagen disease, blood dyscrasia, or heart disease. Two patients with tuberculomas were excluded [2]. For comparison, CT studies were reviewed to select 173 patients admitted to our hospital from January to December 1984, with CT evidence of one or more noninflammatory IS, including lacunar infarctions. The locations of cerebral infarctions were determined by their geometric centers. However, an infarction extending from the cerebral cortex to the white matter, with or without involvement of the basal ganglia, was classified as an infarction involving the cerebral cortex. A small infarction with its center in the external capsule or claustrum was classified as an infarction of the subcortical white matter, because the blood supply of this zone arises from cortical branches [9]. To facilitate discussion, we defined a "TB zone" as the region supplied by medial striate, thalamotuberal and thalamoperforating arteries; that is, the heads of the caudate nuclei, the anteromedial thalami, the anterior limbs of the internal capsules and the genus of the internal capsules [10, 11]. Similarly, an "IS" zone was defined as the region supplied by the lateral striate, anterior choroidal and thalamogeniculate arteries; that is, the lenticular nuclei, the
Table 1. Locations of cerebral infarctions
Diagnosis
Numberof infarctions TBZ ISZ SWM (%) (%) (%) Tuberculous 27 4 1 Meningitis (75.0) (11.1) (2.8) Ischemic 48 128 127 Stroke (108) (29.0) (29.0) Pvalue* 0.0000 0.0343 0.0014
CC (%) 2 (5.5) 105 (23.8) 0.0205
BS (%) 1 (2.8) 20 (4.5) > 0.05
Cbl (%) 1 (2.8) 13 (2.9) > 0.05
Total (%) 36 (100) 441 (100)
* X2 test with Yates correction TBZ, Tuberculosis zone; SWM, subcortical white matter; BS, brain stem; ISZ, ischemic-stroke zone; CC, cerebral cortex; Cbl, cerebellum
198
Fig. L a Horizontal lines indicate the "tuberculosis zone." Vertical lines indicate the "ischemic-stroke zone" b, c Diagram of the distribution of infarcts in ischemic stroke (b, dots) and tuberculous meningitis (e, crosses) at a representative level
posterolateral thalami, and the posterior limbs of the internal capsules (Fig. i a) [10, 11]. The statistical significance of our data was evaluated by the chi-square test with Yates correction.
Results
Cerebral infarctions were found in 14 of the 40 TB patients (35 %). These patients were 38-74 years of age (mean age 57.9 years). The age distribution of the 137 with IS was 37-100 years, mean 64.1 years. The locations of the cerebral infarctions in T B M and in IS are summarized in Table 1. Infarctions caused by T B M occurred predominantly in the TB zone (75 % ), followed by the IS zone (11.1% ), the cerebral cortex (5.5 % ), subcortical white matter (2.8%), brain stem (2.8%), and cerebellum (2.8 %). Infarctions from IS occurred mainly in the IS zone (29 % ) and subcortical white matter (29 %), followed by the cerebral cortex (23.8%), TB zone (10.8 %), brain stem (4.5 %), and cerebellum (2.9 %).
Fig. 2 a-c. Computed tomography of patients with tuberculous men-
ingitis, a A 52-year-old man with two infarctions located at the genus of the internal capsules bilaterally, b A 51-year-old man with
T B M correlated with infarctions in the TB zone much better than did IS (Table 1, Fig. 1). IS correlated with infarctions in the IS zone, the subcortical white matter, and the cerebral cortex better than did T B M (Table 1). T B M and IS correlated with infarctions in the posterior fossa equally well (Table 1). Bilateral cerebral infarctions were observed in 7 of the 14 patients with T B M (50%) and 84 of the 137 patients with IS (61%). Symmetrical involvement of the TB zone correlated with T B M (5 of 7 patients) much better than with IS (4 of 84 patients) (P = 0.0000) (Fig. 2 a, b).
Discussion
In an autopsy study, Fisher [3] reported that 37 % of lacunar infarctions were situated in the lenticular nuclei, and only 10 % in the caudate nuclei. Similarly, in our series lesions of IS were more frequent in the IS zone (29.0 %) than in the TB zone (10.8 % ). In TBM, vessels that traverse the basal exudate develop vasculitis with inflammation, spasm, constriction,
five infarctions in the basal ganglia, internal capsules, and the left thalamus, c A 38-year-old man with an infarction at the anterior portion of the left thalamus
199 and eventual thrombosis that results in cerebral infarction [4]. In an autopsy study of TBM, Dastur et al. [5] reported that cerebral infarction due to vasculitis occurred in 43.6 % of children and 31.8 % of adult cases. In CT studies, 17 % - 5 3 % of patients with T B M show vascular lesions [1, 2, 6-8]. O u r study revealed cerebral infarctions in 35 9/0 of patients. The medial striate, thalamotuberal and thalamoperforating arteries are located medial to the lateral striate, anterior choroidal and thalamogeniculate arteries. Conceivably, the basal exudate of TB, which is usually most severe at the circle of Willis, m a y affect the m o r e medial TB zone vessels m o r e severely than the m o r e lateral IS zone vessels. This might explain why infarctions of T B M are frequently located in the TB zone and why they are so frequently symmetrical. We suggest that T B M should be considered first when imaging studies reveal multiple infarctions of about the same age situated symmetrically in the TB zone. A similar picture has not b e e n reported in other conditions.
3. Fisher CM (1965) Lacunes: small, deep cerebral infarcts. Neurology 15:774-784 4. Sheller JR, Des Prez RM (1986) CNS tuberculosis. Neurol Clin 4: 143-157 5. Dastur DK, Latitha VS, Udani PM, Parekh U (1970) The brain and meninges in tuberculous meningitis - gross pathology in 100 cases and pathogenesis Neurol Indian 18:86-100 6. Teoh R, Humphries MJ, Hoare RD, O'Mahony G (1989) Clinical correlation of CT changes in 64 CHinese patients with tuberculous meningitis. J Neuro1236:48-51 7. Bhargava S, Gupta AK, Tanon PN (1982) Tuberculous meningitis - a CT study. Br J Radio155:189-196 8. Kingsley DR Hendrickse WA, Kendall BE, Swash M, Singh V (1987) Tuberculous meningitis: role of CI" in management and prognosis. J Neurol Neurosurg Psychiatry 50:30-36 9. Takahashi S, Goto K, Fukasawa H, Kawata Y, Uemura K, Suzuki K (1985) Computed tomography of cerebral infarction along the distribution of the basal perforating arteries. I. Striate arterial group. Radiology 155:107-118 10. House EL, Pansky B, Siegel A (eds) (1979) A systemic approach to neuroscience, 3rd edn McGraw-Hill, New York, pp 58-72 11. Takahashi S, Goto K, Fukasawa H, Kawata Y, Uemura K, Yaguchi K (1985) Computed tomography of cerebral infarction along the distribution of the basal perforating arteries. II. Thalamic arterial group. Radiology 155:119-130
References 1. Bullock MRR, Welchman JM (1982) Diagnostic und prognostic features of tuberculous meningitis of CT scanning. J Neurol Neurosurg Psychiatry 45:1098-1101 2. Bonafe A, Manelfe C, Gomez MC, et al (1985) Tuberculous meningitis. J Neuroradio112: 302-316
E-Y. Hsieh, M. D. Section of Neurology Taichung Veterans General Hospital Taichung, Taiwan 40705 Republic of China
