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NEUROIMAGE
Year : 2020  |  Volume : 68  |  Issue : 5  |  Page : 1267-1268

Superficial Cerebral Hemosiderosis and the Neurosurgical Informed Consent


Department of Neurosurgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India

Date of Web Publication27-Oct-2020

Correspondence Address:
Dr. Mathew Abraham
Department of Neurosurgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.299170

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How to cite this article:
Jamaluddin MA, Gohil JA, Abraham M. Superficial Cerebral Hemosiderosis and the Neurosurgical Informed Consent. Neurol India 2020;68:1267-8

How to cite this URL:
Jamaluddin MA, Gohil JA, Abraham M. Superficial Cerebral Hemosiderosis and the Neurosurgical Informed Consent. Neurol India [serial online] 2020 [cited 2020 Dec 4];68:1267-8. Available from: https://www.neurologyindia.com/text.asp?2020/68/5/1267/299170




Microglia and Bergmann cells in the cerebellum produce ferritin to counteract any rise in the harmful CSF free iron levels.[1],[2],[3] In cases where repeated subarachnoid microbleeds occur, beyond the capacity of the Bergmann cells, iron is released from ferritin due to oxidative stresses.[1],[2],[3] Superficial cortical layers and structures exposed in the cisternal space get permanently destroyed by free radical damage and lipid peroxidation catalyzed by free iron.[1],[2],[3] Common sites of injury in superficial cerebral hemosiderosis (SCH) include the cerebellum and the vestibulocochlear nerve.[2],[3],[4] Patients usually present with gradually progressive hearing loss with gait ataxia and a distinctive pattern of socio-cognitive decline.[2],[3]

Early identification and removal of the inciting factor are essential.[2],[3] Role of chelating factors is not proven. Once damage to the cortex is done, eradication of the underlying cause will not reverse the clinical deficits due to SCH.[3] It is also not clear whether removing the source of bleed will halt the progression of the damage.[2] Guarded prognosis needs to be explained prior to surgical intervention in such cases. Cognitive dysfunction, gait ataxia, and vestibulocochlear symptoms are not expected to improve even when the patient recovers from the primary condition (such as a bled intracranial neoplasm or vascular abnormality) without any deficits.

A 49-year-old male patient, with history of repeated episodes of moderate to severe holocranial headache associated with vomiting for past seven years, had presented with gait disturbance of 1-year duration and behavioral disturbance for past one week. The patient was disoriented in time and person, significant cognitive dysfunction with bilateral cerebellar signs and gait ataxia. The clinico-radiological picture was suggestive of SCH [Figure 1], [Figure 2], [Figure 3]. Histopathology of the inciting lesion was Astrocytoma Grade III.
Figure 1: Axial T2-weighted brain MR Imaging showing signal hypointensity due to hemosiderin deposition (a) around the medulla, (b) around the midbrain and cerebellar vermis as well as along the Sylvian fissure and (c) along the cerebral convexities. A pineal region lesion is also seen with fluid level suggestive of bleed

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Figure 2: (a) Sagittal T2 weighted brain MR Imaging showing signal hypointensity along the brainstem and cord with severe cerebellar atrophy (b and c). Axial gradient-echo MR imaging showing areas corresponding to the such as around the midbrain and along the cerebellar folia as well as along the Sylvian fissure, cortical sulci, and interhemispheric fissure. Hypointensities are also noted on the ventricular surface. The causative lesion can also be seen

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Figure 3: Intraoperative photograph of the cortical surface showing hemosiderin deposition along the cortical sulci (arrow)

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Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
River Y, Honigman S, Gomori JM, Reches A. Superficial hemosiderosis of the central nervous system. Mov Disord 1994;9:559-62.  Back to cited text no. 1
    
2.
Rodriguez FR, Srinivasan A. Superficial Siderosis of the CNS. Am J Roentgenol 2011;197:W149-52.  Back to cited text no. 2
    
3.
Kumar N. Superficial Siderosis: Associations and Therapeutic Implications. Arch Neurol 2007;64:491.  Back to cited text no. 3
    
4.
Messori A. The importance of suspecting superficial siderosis of the central nervous system in clinical practice. J Neurol Neurosurg Psychiatry 2004;75:188-90.  Back to cited text no. 4
    


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