Neuroradiologv
Neuror~digtogy 16, 22-23 (1978)
© by Springer-Verlag 1978
T h e F o l l o w - U p C T S c a n in C h i l d h o o d M e n i n g i t i s R. D. Snyder and J. Stovring Departments of Neurology, Radiology, and Pediatrics, University of New Mexico Medical Center, Albuquerque, New Mexico, USA
Summary. CT in childhood bacterial meningitis has indicated that bacterial meningitis is more than an inflammation o f the subarachnoid space; it is a disease process which often exerts a profound effect on the brain parenchyma. In some cases ventricular widening may be a reflection of loss o f brain substance rather than increased intracranial pressure. A vasculitis may occur in cerebral vessels with consequent ischemic infarct. The abnormalities found on CT during the acute illness are frequently persistent.
The use of antibiotics in the treatment of bacterial meningitis has reduced the mortality rate, but the incidence o f neurologic complications remains high [7]. The etiology of these complications is often unclear [9]. CT in bacterial meningitis has been a useful means of study [3] and may provide information regarding the pathogenesis of the neurologic complications which Occur.
Materials and Methods Between the years 1975-77, 44 children with bacterial meningitis were seen. Thirty-two of the children were under one year of age. Thirty-two of the infections were caused by Hemophilus influenzae, eight by Pneumococcus, and one by Streptococcus. The causative organism was not found in three cases. CT was performed when neurologic complications occurred. Twenty-one patients had one or more scans. The most frequent abnormality was ventricular widening (14 cases). Cerebral infarction occurred in six cases and subdural effusion in five. Ependymitis, cerebral swelling, and cortical necrosis also occurred. Only four children had normal scans. Follow-up CT is available on six patients. The duration of follow-up ranges from 1 month to 2 years. Three scans showed persistence of ventricular widening, one showed a persistent area of infarction, and one showed bilateral infarction not apparent on an earlier CT. One CT returned to normal after showing ventricular widening. An EMI Mark I scanner with 160 x 160 matrix was used in this study.
Discussion Previous reports have indicated that significant and lasting damage to brain parenchyma may be produced by bacterial meningitis [1, 4]. Our findings are confirmatory and may provide some insight into the pathogenesis of these complications. However, the precise pathological mechanisms remain incompletely understood. The CT has revealed a high incidence of brain infarcts. The infarcts are presumably produced by the infectious process with consequent vasculitis, spasm, and thrombosis occurring ill vessels as they cross the inflamed subarachnoid space [5, 6, 8]. On follow-up of one infarct the defect was persistent (Fig. l a) and in another case the infarct was first recognized on follow-up CT. Cerebrovascular complications appear to be one of the major factors in the pathogenesis o f the neurologic deficits produced by bacterial meningitis. The high incidence of vascular abnormalities suggests that the outcome of childhood bacterial meningitis could be improved if an appropriate anti-inflammatory and/or anticoagulant agent was available. Ventricular widening was an acute and chronic finding (Fig. lb). The ventricular widening appeared in some cases to result from loss o f brain tissue rather than from increased pressure within the ventricles. The loss of brain tissue was suggested by the CT findings (increased subarachnoid space, cortical atrophy, enlarged basilar cisterns, and increased size of interhemispheric fissure), and by the clinical findings (normal fontanel, no cranial suture spread). In the case represented by Figure lb, external ventricular drainage did not prevent progressive increase in ventricular size. On follow-up of four cases, the ventricular widening persisted in three. The etiology of ventricular widening in the absence of increased intraventricular pressure is unclear, although diffuse vasculitis produced by the bacteria or their products may lead to ischemia and general dissolution of brain substance [2]. The advent of the CT has led to a decrease in the frequency of subdural taps at our institution. The subdural
0028-3940/78/0016/0022/$ 01.00
R. D. Snyder and J. Stowing: Follow-Up CT in Meningitis
23
References
Fig. la. CT showing persistent right frontal infarct in a 3-yearold. Infarct noted at age 7 months followingH, influenzae meningitis complicated by seizures and left hemiparesis, b. CT showing ventricular widening in a 19-month-old. Ventrieular widening first noted at age 9 months following pneumococcal meningitis complicated by right focal seizures and early CT evidence of left parietal infarct. Head circumference not enlarged and intraventricular pressure normal
tap is n o t performed as a diagnostic test b u t only when an indication exists on CT of a significant subdural col, lection producing a shift in intracranial structures. The clinical significance of the subdural effusion m a y have been overemphasized in the past.
1. Adams, R. D., Kubik, C. S., Bonner, F. J.: The clinical and pathological aspects of influenzal meningitis. Arch. Pediatr. 6 5 , 3 5 4 - 3 8 0 , 4 0 8 - 4 5 9 (1948) 2. Buchan, G. C., Alvord, E. C.: Diffuse necrosis of subcortical white matter associated with bacterial meningitis. Neurology 19, 1-9 (1969) 3. Cockrill, H. H., Dreisbach, J., Lowe, B., Yamauchi, T.: Computed tomography in leptomeningeal infections. Am. J. Roentgenol. 130, 511-515 (1978) 4. Dodge, P. R., Swartz, M. N.: Bacterial meningitis - a review of selected aspects. N. Engl. J. Med. 272, 954-960, 10031010 (1965) 5. Gado, M., Axley, J., Appleton, D. B., Prensky, A. L.: Angiography in the acute and post-treatment phases of Hemophilus influenzae meningitis. Radiology 110, 439-444 (1974) 6. Headings, D. L., Glasgow, L. A.: Occlusion of the internal carotid artery complicating Hemophilus influenzae meningitis. Am. J. Dis. Child. 131,854-856 (1977) 7. Lindberg, J., Rosenhall, U., Nylen, O., Ringner, A.: Longterm outcome of Hemophilus influenzae meningitis related to antibiotic treatment. Pediatrics 60, 1-6 (1977) 8. Lyons, E. L., Leeds, N. E.: The angiographic demonstration of arterial vascular disease in purulent meningitis. Radiology 88, 935-938 (1967) 9. Smith, J. F., Landing, B. H.: Mechanism of brain damage in H. influenzae meningitis. J. Neuropathol. Exp. Neurol. 19, 248-265 (1960) R. D. Snyder, MD Department of Neurology and Pediatrics University of New Mexico Medical Center Albuquerque, NM 87131, USA
Neuror~digtogy 16, 22-23 (1978)
© by Springer-Verlag 1978
T h e F o l l o w - U p C T S c a n in C h i l d h o o d M e n i n g i t i s R. D. Snyder and J. Stovring Departments of Neurology, Radiology, and Pediatrics, University of New Mexico Medical Center, Albuquerque, New Mexico, USA
Summary. CT in childhood bacterial meningitis has indicated that bacterial meningitis is more than an inflammation o f the subarachnoid space; it is a disease process which often exerts a profound effect on the brain parenchyma. In some cases ventricular widening may be a reflection of loss o f brain substance rather than increased intracranial pressure. A vasculitis may occur in cerebral vessels with consequent ischemic infarct. The abnormalities found on CT during the acute illness are frequently persistent.
The use of antibiotics in the treatment of bacterial meningitis has reduced the mortality rate, but the incidence o f neurologic complications remains high [7]. The etiology of these complications is often unclear [9]. CT in bacterial meningitis has been a useful means of study [3] and may provide information regarding the pathogenesis of the neurologic complications which Occur.
Materials and Methods Between the years 1975-77, 44 children with bacterial meningitis were seen. Thirty-two of the children were under one year of age. Thirty-two of the infections were caused by Hemophilus influenzae, eight by Pneumococcus, and one by Streptococcus. The causative organism was not found in three cases. CT was performed when neurologic complications occurred. Twenty-one patients had one or more scans. The most frequent abnormality was ventricular widening (14 cases). Cerebral infarction occurred in six cases and subdural effusion in five. Ependymitis, cerebral swelling, and cortical necrosis also occurred. Only four children had normal scans. Follow-up CT is available on six patients. The duration of follow-up ranges from 1 month to 2 years. Three scans showed persistence of ventricular widening, one showed a persistent area of infarction, and one showed bilateral infarction not apparent on an earlier CT. One CT returned to normal after showing ventricular widening. An EMI Mark I scanner with 160 x 160 matrix was used in this study.
Discussion Previous reports have indicated that significant and lasting damage to brain parenchyma may be produced by bacterial meningitis [1, 4]. Our findings are confirmatory and may provide some insight into the pathogenesis of these complications. However, the precise pathological mechanisms remain incompletely understood. The CT has revealed a high incidence of brain infarcts. The infarcts are presumably produced by the infectious process with consequent vasculitis, spasm, and thrombosis occurring ill vessels as they cross the inflamed subarachnoid space [5, 6, 8]. On follow-up of one infarct the defect was persistent (Fig. l a) and in another case the infarct was first recognized on follow-up CT. Cerebrovascular complications appear to be one of the major factors in the pathogenesis o f the neurologic deficits produced by bacterial meningitis. The high incidence of vascular abnormalities suggests that the outcome of childhood bacterial meningitis could be improved if an appropriate anti-inflammatory and/or anticoagulant agent was available. Ventricular widening was an acute and chronic finding (Fig. lb). The ventricular widening appeared in some cases to result from loss o f brain tissue rather than from increased pressure within the ventricles. The loss of brain tissue was suggested by the CT findings (increased subarachnoid space, cortical atrophy, enlarged basilar cisterns, and increased size of interhemispheric fissure), and by the clinical findings (normal fontanel, no cranial suture spread). In the case represented by Figure lb, external ventricular drainage did not prevent progressive increase in ventricular size. On follow-up of four cases, the ventricular widening persisted in three. The etiology of ventricular widening in the absence of increased intraventricular pressure is unclear, although diffuse vasculitis produced by the bacteria or their products may lead to ischemia and general dissolution of brain substance [2]. The advent of the CT has led to a decrease in the frequency of subdural taps at our institution. The subdural
0028-3940/78/0016/0022/$ 01.00
R. D. Snyder and J. Stowing: Follow-Up CT in Meningitis
23
References
Fig. la. CT showing persistent right frontal infarct in a 3-yearold. Infarct noted at age 7 months followingH, influenzae meningitis complicated by seizures and left hemiparesis, b. CT showing ventricular widening in a 19-month-old. Ventrieular widening first noted at age 9 months following pneumococcal meningitis complicated by right focal seizures and early CT evidence of left parietal infarct. Head circumference not enlarged and intraventricular pressure normal
tap is n o t performed as a diagnostic test b u t only when an indication exists on CT of a significant subdural col, lection producing a shift in intracranial structures. The clinical significance of the subdural effusion m a y have been overemphasized in the past.
1. Adams, R. D., Kubik, C. S., Bonner, F. J.: The clinical and pathological aspects of influenzal meningitis. Arch. Pediatr. 6 5 , 3 5 4 - 3 8 0 , 4 0 8 - 4 5 9 (1948) 2. Buchan, G. C., Alvord, E. C.: Diffuse necrosis of subcortical white matter associated with bacterial meningitis. Neurology 19, 1-9 (1969) 3. Cockrill, H. H., Dreisbach, J., Lowe, B., Yamauchi, T.: Computed tomography in leptomeningeal infections. Am. J. Roentgenol. 130, 511-515 (1978) 4. Dodge, P. R., Swartz, M. N.: Bacterial meningitis - a review of selected aspects. N. Engl. J. Med. 272, 954-960, 10031010 (1965) 5. Gado, M., Axley, J., Appleton, D. B., Prensky, A. L.: Angiography in the acute and post-treatment phases of Hemophilus influenzae meningitis. Radiology 110, 439-444 (1974) 6. Headings, D. L., Glasgow, L. A.: Occlusion of the internal carotid artery complicating Hemophilus influenzae meningitis. Am. J. Dis. Child. 131,854-856 (1977) 7. Lindberg, J., Rosenhall, U., Nylen, O., Ringner, A.: Longterm outcome of Hemophilus influenzae meningitis related to antibiotic treatment. Pediatrics 60, 1-6 (1977) 8. Lyons, E. L., Leeds, N. E.: The angiographic demonstration of arterial vascular disease in purulent meningitis. Radiology 88, 935-938 (1967) 9. Smith, J. F., Landing, B. H.: Mechanism of brain damage in H. influenzae meningitis. J. Neuropathol. Exp. Neurol. 19, 248-265 (1960) R. D. Snyder, MD Department of Neurology and Pediatrics University of New Mexico Medical Center Albuquerque, NM 87131, USA
