Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 59, Num. 2, 2011, pp. 270-272

Neurology India, Vol. 59, No. 2, March-April, 2011, pp. 270-272

Case Report

Magnetic resonance imaging findings in a fatal case of Salmonella typhi-associated encephalopathy: A case report and literature review

Munawwar Ahmed¹, Jyoti Sureka¹, Vivek Mathew², Ravi Kanth Jakkani¹, K. P. P. Abhilash³

¹ Department of Radiology, Christian Medical College & Hospital, Vellore, Tamil Nadu, India
² Department of Neurological Sciences, Neurology Unit, Christian Medical College & Hospital, Vellore, Tamil Nadu, India
³ Department of Medicine, Christian Medical College & Hospital, Vellore, Tamil Nadu, India

Correspondence Address: Munawwar Ahmed, Assistant Professor, Department of Radiology, CMC Hospital, Vellore, TN , India, munawwarahmned19@yahoo.co.in

Date of Submission: 16-Dec-2010
Date of Decision: 05-Jan-2011
Date of Acceptance: 06-Jan-2011

Code Number: ni11072

PMID: 21483131

DOI: 10.4103/0028-3886.79145

Abstract

Keywords: Salmonella associated encephalopathy, demyelination, magnetic resonance imagaing

Introduction

Non-infectious neurological complications of Salmonella typhi infection occur in 3-35% of patients, mostly in pediatric age group. Very few reports have described the imaging findings of Salmonella-associated encephalopathy (SAE). ^[1],[2] We describe magnetic resonance imaging (MRI) findings in a fatal case of SAE due to S. typhi. This is probably the first case report describing the bilateral diffuse symmetrical MRI brain findings in a fatal case of culture proven SAE.

Case Report

A 17-year-old female presented to the Emergency Department with high-grade fever of 3 days duration and altered mental status and seizures of 1 day duration. She had an episode of 1 day fever followed by papulo-vesicular rashes all over the body 12 days back which regressed spontaneously leaving scars and hyperpigmentation. She did not have any other history of prior co-morbidities. On examination, the patient was febrile, drowsy and disoriented, with a Glasgow Coma Scale (GCS) score of 13/15. There was increased tone in both the lower limbs with exaggerated deep tendon reflexes and extensor plantar response. Rest of the neurological examination was normal. A diagnostic possibility of varicella encephalitis was considered and she was started on intravenous (IV) acyclovir and dexamethasone empirically.

Laboratory tests showed the following: white blood cell count 4700 (neutrophils 81%, lymphocytes 17%, monocytes 2%); hemoglobin 10.9 g%; erythrocyte sedimentation rate (ESR) 5 mm first hour; platelet count 81,000/mm ³ ; and normal liver functions. Cerebrospinal fluid (CSF) showed cells 8 lymphocytes/mm ³ , protein level of 27 mg/dl, and glucose of 94 mg/dl. CSF gram stain and culture was negative for bacterial growth. CSF polymerase chain reaction (PCR) for varicella virus, cytomegalovirus, Epstein-Barr virus, herpes simplex 1 and 2 and adenovirus was negative. Serum rapid HIV Elisa test was negative. Tests for all the vasculitis markers were negative.

Blood culture taken at admission grew S. typhi on day 6 of hospitalization, with susceptibility to ciprofloxacin, co-trimoxazole, ampicillin and chloramphenicol and resistance to nalidixic acid. She was then treated with oral gatifloxacin, high dose of dexamethasone and mannitol. Her fever settled down but sensorium did not improve and she had further few episodes of seizures. Considering the possibility of SAE, MRI of brain was done on day 7 of her hospitalization. MRI revealed bilateral diffuse symmetrical hyperintense signal on long TR sequences involving the centrum semiovale, periventricular and deep white matter (WM) and splenium of corpus callosum (CC) with minimal subcortical and deep cerebellar WM involvement [Figure - 1]a-c. Diffusion-weighted imaging (DWI) revealed central area of diffusion restriction in the involved areas [Figure - 2]a and b. No abnormal enhancement was seen on post gadolinium study [Figure - 3]. Considering the diagnosis of postinfectious demyelinating process, she was started on high doses of IV methylprednisolone. However, she continued to deteriorate and died on day 13 of her hospitalization.

Discussion

A wide spectrum of non-infectious neurological complications of typhoid fever include encephalopathy, neuropsychiatric disorder, cerebral edema, cerebellar ataxia, Parkinsonism, acute disseminated encephalomyelitis and brainstem encephalitis. Exact pathophysiology of these complications is not clear. Of the various mechanisms that have been proposed, immune mediated process and endotoxemia are the most widely accepted mechanisms. Early SAE is an uncommon and potentially fatal neurological complication. Pathologic findings in SAE are nonspecific and include cerebral edema, minimal ischemia, vasculitis, perivenous demyelination and cellular infiltrates. ^[3],[4]

The literature on imaging findings of SAE and other neurological complications is sparse. MRI findings include multifocal cerebellar subcortical WM hyperintense lesions in a case of acute cerebellar ataxia post typhoid fever ^[1] and focal areas of reversible restricted diffusion in the splenium of the CC and bilateral parietal subcortical WM in a patient with Salmonella enteridis-associated encephalopathy (non-typhoid fever). ^[2] These findings were attributed to cytotoxic edema. ^[2] Case reports with normal MRI brain and abnormal EEG ^[5],[6] and CT showing diffuse vasogenic cerebral edema have been reported. ^[7],[8] Bilateral symmetrical WM hypodensity with minimal gyral enhancement and no significant mass effect was described in a case of S. typhi-associated cerebritis. ^[9] All these patients had a good clinical recovery with treatment. In a series of eight patients with non-typhoidal SAE, MRI and CT showed diffuse cerebral edema without any focal lesion. ^[3] There were three fatalities in this series. These observations suggest that abnormal findings on MRI may not have any prognostic significance.

In the present patient, the MRI lesions were suggestive of demyelinating process. ^[10] However, we could not confirm it on histopathology or follow-up. We believe endotoxemia and/or sepsis may be the possible mechanisms in our patient as the temporal evolution of clinical features does not support the immune mediated mechanism. Mechanism of brain injury in sepsis-associated encephalopathy includes both inflammatory and non-inflammatory processes that induce blood-brain barrier breakdown, dysfunction of intracellular metabolism and brain cell death. ^[11] In conclusion, SAE can be of multiple pathophysiological mechanisms, and accordingly, the MRI findings can range from normal to diffuse white matter involvement including CC as in the present case.

References

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