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| LETTERS TO EDITOR |
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| Year : 2016 | Volume
: 64
| Issue : 1 | Page : 174-175 |
Brain studded with bright spots: The unusual cause
Mandeep Singh Ghuman1, Shabdeep Kaur2, Sushanta K Sahoo3, Kavita Saggar4, Archana Ahluwalia4, Gagandeep Singh5
1 Department of Radiodiagnosis, Post-graduate Institute of Medical Education and Research, Chandigarh, Punjab and Haryana, India
2 Department of Radiodiagnosis, Indira Gandhi Medical College, Shimla, Punjab, India
3 Department of Neurosurgery, Post-graduate Institute of Medical Education and Research, Chandigarh, Punjab and Haryana, India
4 Department of Radiodiagnosis, Dayanand Medical College and Hospital, Ludhiana, Punjab, India
5 Department of Neurology, Dayanand Medical College and Hospital, Ludhiana, Punjab, India
| Date of Web Publication | 11-Jan-2016 |
Correspondence Address:
Mandeep Singh Ghuman
Department of Radiodiagnosis, Post-graduate Institute of Medical Education and Research, Chandigarh, Punjab and Haryana
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.173647
How to cite this article:
Ghuman MS, Kaur S, Sahoo SK, Saggar K, Ahluwalia A, Singh G. Brain studded with bright spots: The unusual cause. Neurol India 2016;64:174-5 |
Sir,
A 23-year-old young man, without any previous medical or drug history, was admitted to the emergency room after a road-side accident. He was found to have comminuted fractures of the left tibia and fibula, and the right femur. There was no external evidence of head injury. At admission, he was alert and conscious. Next morning, the patient had a generalised tonic–clonic seizure followed by altered sensorium. He became restless, confused, and unresponsive to verbal stimuli. He developed dyspnea, tachypnea, and tachycardia and was found to have thrombocytopenia and anemia. Cranial computed tomography (CT) was essentially unremarkable. Subsequently, brain magnetic resonance imaging (MRI) was performed, which revealed innumerable, punctuate, T2-hyperintense foci diffusely scattered within both the cerebral and the cerebellar hemispheres [Figure 1]a and [Figure 2]. Diffusion-weighted (DW) MR images showed a bright signal consistent with restricted diffusion in almost all of these lesions [Figure 1]b. | Figure 1: Axial T2-weighted MR images (a) and diffusion-weighted images (b) show small, innumerable, discrete, high-signal foci scattered in subcortical and deep white matter of bilateral cerebral hemispheres, including corpus callosum and deep grey nuclei. Diffusion bright lesions resemble a “starfield” pattern
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 | Figure 2: Axial T2-weighted MR image depicts similar multiple, small high-signal lesions in bilateral cerebellar hemispheres
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The differential diagnoses of disseminated hyperintense lesions on T2-weighted scans include vastly different pathologies such as chronic ischemic or gliotic foci, acute thromboembolic infarcts, septic emboli, foci of vasogenic edema, demyelinating disease, diffuse axonal injury, and cerebral fat embolism.[1],[2] Diffusion restriction narrowed down the differential to acute conditions producing cytotoxic edema. DW imaging had a typical “starfield” pattern of scattered bright spots against the dark background consistent with acute cerebral microinfarcts due to multiple fat emboli.[1] Brain MRI constitutes an important step in determining the cause of altered mental status in patients who have suffered a traumatic brain injury but have a negative CT scan as it may distinguish between cerebral fat embolism and diffuse axonal injury.[2],[3]
The exact pathogenesis of brain lesions in fat embolism syndrome is still debated; suggested mechanisms include generation of white matter lesions as a result of venous congestion and edema due to cortical emboli,[1] direct occlusion of cerebral microvasculature by fat microemboli,[4] and activation of the inflammation cascade caused by release of free fatty acids.[5] Some form of fat embolism accompanies almost all long-bone fractures; however, the clinically significant fat embolism syndrome occurs in only 0.9%–2.2% of cases.[1],[4] Rarely, nontraumatic causes, for example, diabetes, pancreatitis, sickle-cell disease, decompression sickness, and liposuction, have been found to be associated with fat embolism syndrome.[6] The clinical triad of fat embolism syndrome consists of pulmonary symptoms, neurological impairment, and petechial skin rash.[2],[3],[5]
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| » References | |  |
| 1. | Parizel PM, Demey HE, Veeckmans G, Verstreken F, Cras P, Jorens PG, et al. Early diagnosis of cerebral fat embolism syndrome by diffusion-weighted MRI (starfield pattern). Stroke 2001;32:2942-4.  |
| 2. | Simon AD, Ulmer JL, Strottmann JM. Contrast-enhanced MR imaging of cerebral fat embolism: Case report and review of the literature. AJNR Am J Neuroradiol 2003;24:97-101. |
| 3. | Kumar S, Gupta V, Aggarwal S, Singh P, Khandelwal N. Fat embolism syndrome mimicker of diffuse axonal injury on magnetic resonance imaging. Neurol India 2012;60:100-2. [ PUBMED]  |
| 4. | Aravapalli A, Fox J, Lazaridis C. Cerebral fat embolism and the “starfield” pattern: A case report. Cases J 2009;2:212. |
| 5. | Butteriss DJ, Mahad D, Soh C, Walls T, Weir D, Birchall D. Reversible cytotoxic cerebral edema in cerebral fat embolism. AJNR Am J Neuroradiol 2006;27:620-3. |
| 6. | Ten Duis HJ. The fat embolism syndrome. Injury 1997;28:77-85. |
[Figure 1], [Figure 2]
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