A Treatable Cause of Cerebral Palsy: Brain Abscess Masquerading as Cerebral Palsy
Corresponding Author: Vykuntaraju K Gowda, Department of Pediatric Neurology, Indira Gandhi Institute of Child Health, Bengaluru, Karnataka, India, Phone: +91 9535212556, e-mail: firstname.lastname@example.org
Received on: 31 October 2021; Accepted on: 16 October 2022; Published on: 30 June 2023
Introduction: A brain abscess is an intraparenchymal collection of pus in the brain. Cerebral palsy (CP) is a static encephalopathy due to injury to the developing brain. CP is a group of disorders due to multiple etiologies. We are reporting a rare cause of brain abscess presenting as CP.
Case description: A 12-month-old boy presented with a developmental delay with perinatal depression. He had attained only partial head control. On examination, head size was 42.5 cm between –2SD and –3SD, and tone was increased in both spasticity and dystonia with exaggerated deep tendon reflexes. On investigations, complete blood count, liver function test, and renal function test were normal. Magnetic resonance imaging (MRI) of the brain showed two ring-enhancing lesions in the left frontal and right temporoparietal lobe. The cerebrospinal fluid (CSF) showed two lymphocytes, protein of 32 mg/dL, and glucose of 60.1 mg/dL. Due to nonreduction in size of the abscess on repeat MRI of the brain after 4 weeks of intravenous antibiotics, the child underwent burr hole aspiration of abscess in the left frontal lobe. The intravenous antibiotics continued for another 4 weeks. On follow-up, computed tomography (CT) of the brain showed a reduction in the size of brain abscesses with calcification. The child attained a social smile, reached for objects, and his tone was improved.
Conclusion: For any child presenting with developmental delay with perinatal history of hypoxic–ischemic encephalopathy (HIE), neuroimaging should be done as it gives important clues for etiology and helps in specific management and prognosis.
How to cite this article: Gowda VK, Mohanty SB, Dhananjaya KVN. A Treatable Cause of Cerebral Palsy: Brain Abscess Masquerading as Cerebral Palsy. Pediatr Inf Dis 2023;5(2):52-55.
Source of support: Nil
Conflict of interest: None
Patient consent statement: The author(s) have obtained written informed consent from the patient’s parents/legal guardians for publication of the case report details and related images.
Keywords: Brain abscesses, Cerebral palsy, Hypoxic–ischemic encephalopathy, Infant.
A brain abscess is an intraparenchymal collection of pus in the brain. The incidence of brain abscess among intracranial masses varies from 1 to 2% in the western countries, to about 8% in developing countries.1 CP describes a group of permanent disorders of the development of movement and posture, causing activity limitations that are attributed to nonprogressive disturbances that occurred in the developing fetal or infant brain. There are various risk factors and causes of CP; in India, perinatal HIE is still the major cause. CP has been reported in 4% following neonatal sepsis, 8% following pyogenic meningitis, and 2% following tubercular meningitis.2 We report a case of multiple brain abscesses in an infant presented with CP.
A 12-month-old male child presented with developmental delay. The term baby was delivered through normal vaginal delivery with delayed cry after birth. The baby had respiratory distress requiring mechanical ventilation for 3 days. The baby was discharged after 7 days. After discharge, the baby had decreased activity and difficulty in feeding. On the 25th day of life, the child had an excessive cry with decreased feeding for that he was readmitted for 4 days and received intravenous antibiotics (cefotaxime and amikacin). At 4 months of age, the child had one episode of right focal seizure. Developmentally attained partial neck control at 5 months of age. On examination, head circumference was 42.5 cm (–2SD to –3SD), strabismus, tone increased both spasticity and dystonia, brisk deep tendon reflexes, and extensor plantar response (Fig. 1A). Clinical possibility of CP secondary to perinatal HIE was considered as the child had a global developmental delay with tone abnormalities with the static course.
On investigations, hemoglobin was 12 mg/dL, total leukocyte count was 7200 cells/µL, and platelet count was 3,77,000 cell/µL. Serum electrolytes and renal and liver function tests were normal. MRI of the brain (Figs 1B to F) showed two well-defined lesions in bilateral frontal deep white matter region with diffusion restriction (Fig. 1B) and corresponding low signal on apparent diffusion coefficient map (Fig. 1C). Coronal section showed well-defined isointense lesions with peripheral hypointense rim on T2 weighted image (Fig. 1D), and peripheral rim enhancing isointense lesions in bilateral frontal deep white matter in T1 weighted image (Fig. 1E). Hypointense nodular lesions in the right frontal and left parietal subcortical white matter region on susceptibility-weighted imaging were suggestive of calcification (Fig. 1F). Magnetic resonance spectroscopy with voxel selected at the peripheral enhancing rim of the right frontal lobe lesion showed normal levels of N-acetyl aspartate (NAA), Cho, and Cr metabolites suggesting a nonneoplastic lesion (Fig. 2A). Contrast-enhanced CT of the brain was done to confirm calcification seen in the MRI of the brain showing peripheral enhancing hypodense lesions in bilateral frontal lobe deep white matter with calcifications seen in the peripheral rim of the lesions (Fig. 2B). Blood culture showed no growth. CSF showed two lymphocytes, glucose 60.1 mg/dL, and protein 32 mg/dL. The CSF gram staining, fungal stain (India ink), and acid-fast bacilli staining were normal. The CSF culture was sterile. He was treated with intravenous ceftriaxone, gentamicin, and oral levetiracetam. Antibodies against toxoplasma and human immunodeficiency virus (for the mother) were found to be negative. Chest X-ray, echocardiography, abdominal ultrasonography, and otologic examination did not reveal any occult source of infection. The immunoglobulin profile was normal. After 4 weeks of intravenous antibiotics, a repeat MRI of the brain did not show a reduction in the size of abscesses. The child underwent a left frontal burr hole and aspiration of a left lobe abscess with antibiotic infusion. Analysis of aspiration from brain abscess showed gram-positive cocci in pairs but no motile trophozoite and fungal elements were seen. Pus culture shows no bacterial growth. The child was discharged after 8 weeks of intravenous antibiotics. Postoperative contrast-enhanced CT brain showed persistent shrunken abscesses with peripheral wall calcifications and pneumocephalus in the left frontal region (Fig. 2C). Calcified nodular lesions in bilateral frontal and parietal subcortical white matter regions and atrophic changes in bilateral frontal lobes during follow-up of the child after 2 months of surgery were seen (Fig. 2D). Development was improved with improvement in head control, response to names, and reaching for objects. Clinical photos showed significant improvement in tone ability to stand with support with good eye contact after 6 months of surgical intervention (Fig. 2E). Parents gave consent to take photographs of their child.
We report a case of global developmental delay with quadriparesis initially diagnosed as CP secondary to suspected HIE who had multiple brain abscesses successfully treated with surgical aspiration of the abscesses and intravenous antibiotics. We initially diagnosed the child with CP who had a developmental delay with static course with birth insult and tone abnormalities, however, after neuroimaging, we later diagnosed it as brain abscess. Atypical feature for brain abscesses is absence of fever in this case which may be due to infantile age and previous treatment with antibiotics.
The neuroinfection is predominantly dissemination from an endogenous reservoir such as the gastrointestinal tract, the urinary and respiratory tracts, as well as surgical sites and burn wounds, hence, we consider our case to be due to unrecognized bacteremia from the sepsis and partially treated meningitis during neonatal period causing multiple abscesses in the brain. However, generally, the nonpredisposed brain is remarkably resistant to bacterial and fungal infections despite occult bacteremia due to its relatively impermeable blood–brain barrier. Even experimental brain abscess models often need direct inoculation of organisms into the animal’s brain for abscess induction.3 Bacteria enter the brain through contiguous spreading in about one-half of brain abscess cases, and through hematogenous dissemination in about one-third of the cases, while 25–35% of the remaining cases reveal unknown mechanisms in which no obvious source can be identified.4 Streptococcus and Staphylococcus are the most common etiological organisms of brain abscesses in children.4,5 In this case, gram-positive cocci in pairs are found in the pus of brain abscesses which are rarely seen nowadays in the newborn period.
Characteristic MRI features that help in the recognition of a “pyogenic abscess” include a peripherally enhancing T2-isointense wall composed of a well-defined rim of collagen and inflammatory cells (which is thinner than in tuberculous abscesses) and a central area of liquefaction which shows T1-hypointensity, T2-hyperintensity, and diffusion restriction. The lesion is invariably surrounded by vasogenic edema appearing as finger-like hyperintensity on T2 and fluid-attenuated inversion recovery images.6 However, it must be differentiated from other causes such as hematoma, metastasis, and granuloma which have an appropriate clinical background and specific imaging appearances.6 Bacterial abscesses are completely necrotic lesions and normal brain metabolites such as NAA, a neuronal and axonal marker; choline, a constituent metabolite of cell membrane and myelin; and creatine, a marker of energy metabolism, are absent. The presence of amino acids AAs and lipid/lactate, along with acetate and/or succinate, is considered specific for a brain abscess on in vivo magnetic resonance spectroscopy,7,8 and based on the presence of these metabolites, an etiologic characterization of the brain abscess has been diagnosed.9
Magnetic resonance spectroscopy shows a marked reduction of NAA in a deep-seated abscess in this child. The pus culture shows no growth after 48 hours of incubation, probably due to injectable antibiotics given 4 weeks before surgical aspiration.
O’Connor et al.10 reported a 28-month-old male, previously known case of CP with epileptic spasms due to antenatal middle cerebral artery (MCA) infarct diagnosed as having multiple brain abscesses with encephalomalacia. The complicating organism Neisseria meningitidis was detected in a polymerase chain reaction both in CSF and pus. The culture CSF and pus of brain abscesses do not show any growth of the organism. The study hypothesizes that areas of encephalomalacia in the left MCA distribution may have facilitated the development of multiple meningococcal abscess cavities in the posterior left frontal, left parietal, and left temporal lobes following an initial period of cerebritis and meningitis. This is like our case, the child with the global developmental delay with a birth history of perinatal insult with a neonatal intensive care unit stay. Neuroimaging suggestive of multiple brain abscesses might be due to sepsis or partially treated meningitis in the newborn period detected at 12 months of age. The cystic encephalomalacia due to HIE may be the predisposing factor.
A child with a global developmental delay with perinatal depression and encephalopathy presented with CP diagnosed as multiple brain abscesses. Early evaluation and neuroimaging are important for any child with suspected CP due to perinatal depression as timely specific management like surgical intervention of brain abscesses and intravenous antibiotics have a good outcome like in this case.
Vykuntaraju K Gowda https://orcid.org/0000-0001-7244-0492
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6. Luthra G, Parihar A, Nath K, et al. Comparative evaluation of fungal, tubercular, and pyogenic brain abscesses with conventional and diffusion MR imaging and proton MR spectroscopy. AJNR Am J Neuroradiol 2007;28(7):1332–1338. DOI: 10.3174/ajnr.A0548
7. Gupta RK, Nath K, Prasad A, et al. In vivo demonstration of neuroinflammatory molecule expression in brain abscess with diffusion tensor imaging. AJNR Am J Neuroradiol 2008;29(2):326–332. DOI: 10.3174/ajnr.A0826
8. Mishra AM, Gupta RK, Jaggi RS, et al. Role of diffusion-weighted imaging and in vivo proton magnetic resonance spectroscopy in the differential diagnosis of ring-enhancing intracranial cystic mass lesions. J Comput Assist Tomogr 2004;28(4):540–547. DOI: 10.1097/00004728-200407000-00017
10. O’Connor C, Collins A, Twomey E, et al. A case report of multiple cerebral abscess formation complicating serogroup B Neisseria meningitidis meningitis. BMC Infect Dis 2019;19(1):863. DOI: 10.1186/s12879-019-4509-y
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