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Table of Contents    
Year : 2015  |  Volume : 63  |  Issue : 5  |  Page : 771-772

Basal ganglia infarction due to mild trauma in a case of mineralizing angiopathy: A rare entity

1 Department of Radiology and Imageology, Nizam's Institute of Medical Sciences, Punjagutta, Hyderabad, Telangana, India
2 Department of Neurology, Nizam's Institute of Medical Sciences, Punjagutta, Hyderabad, Telangana, India

Date of Web Publication6-Oct-2015

Correspondence Address:
Abhishek J Arora
Department of Radiology and Imageology, Nizam's Institute of Medical Sciences, Punjagutta, Hyderabad, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.166566

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How to cite this article:
Arora AJ, Bolla H, Arora R, Kaul S, Yarlagadda J. Basal ganglia infarction due to mild trauma in a case of mineralizing angiopathy: A rare entity. Neurol India 2015;63:771-2

How to cite this URL:
Arora AJ, Bolla H, Arora R, Kaul S, Yarlagadda J. Basal ganglia infarction due to mild trauma in a case of mineralizing angiopathy: A rare entity. Neurol India [serial online] 2015 [cited 2021 Jan 25];63:771-2. Available from:


Basal ganglia infarction and hemorrhage in infants after mild trauma has been reported earlier; however, their association with mineralizing angiopathy is often not referred to. Mineralization along the lenticulostriate arteries demonstrable on computed tomography scans and termed as “mineralizing angiopathy” was proposed by Lingappa et al., in their original article, in order to differentiate it from sonographic vasculopathy. It is believed that even minor trauma to arteries at a particular stage of mineralization predisposes to thrombus formation within their lumen thus leading to stroke in the territory supplied by them.

An 18-month-old female child presented in October 2014 with left upper limb tonic posturing associated with deviation of the eye. There was history of the patient falling from a bench 4 days ago, which was followed by a transient loss of consciousness. There was left-sided hemiparesis noticed after a few hours of the fall; the tonic posturing of the left upper limb was an associated feature that hastened the visit of the child to the hospital.

The patient underwent a head computed tomography (CT) and a magnetic resonance (MR) scan. On the CT scan, there were punctate to linear calcifications in bilateral basal ganglia and in the subcortical white matter of both cerebral hemispheres. The linear calcifications in the basal ganglia region have been documented in earlier cases, but the prolific nature of subcortical linear mineralization was unique to our case. There was also a well-defined hypodense lesion of approximately 2.5 cm × 2 cm in the right basal ganglia involving the head and proximal body of the caudate nucleus suggestive of an infarct [Figure 1]. On MR imaging, the T2-weighted, and fluid-attenuated inversion recovery sequences showed an increased signal intensity in the right basal ganglia involving the lentiform nucleus and the body of right caudate nucleus [Figure 2]. On MR angiography, no abnormality pertaining to the intracranial vasculature was noticed.
Figure 1: Axial non-contrast CT sections of the brain show punctate to linear calcifications in bilateral basal ganglia and the subcortical white matter. There is also a well-defined hypodense lesion seen in the right basal ganglia involving the posterior aspect of the head and body of the right caudate nucleus suggestive of an infarct

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Figure 2: Axial magnetic resonance imaging, T2 (above row), and fluid-attenuated inversion recovery (second row) images of brain show a well-defined hyperintense lesion in the region of basal ganglia involving the body of the right caudate nucleus, corresponding to the infarct seen on the computed tomography images

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Other investigations, such as the echocardiography, the sickling test, and the vasculitic profile were normal. Cerebrospinal fluid (CSF) examination showed increased red blood corpuscles (350 per cubic mm) and white blood cells (30 per cu mm ) consistent with the history of trauma. The CSF analysis for herpes simplex, herpes zoster, and TORCH group of viruses yielded a negative result. Other investigations related to parathyroid hormone and vitamin D were also within normal limits.

Basal ganglia infarctions in infants below the age of 18 months occur in less than 2% of all childhood strokes and constitute a rare entity. Basal ganglia strokes in infants after minor trauma have been reported previously; however, awareness regarding their co-existence with mineralizing angiopathy has recently been established.[1],[2],[3] Very few case series and studies have documented the association of stroke with the basal ganglia calcification/vascular mineralization. Some authors have stated that basal ganglia calcification and cytomegalovirus infection are the potential risk factors, whereas others have attributed the infarct to vascular mineralization.[3],[4],[5] Investigations into the causes of mineralization and stroke are often not conclusive, and specific causes of mineralization of the lenticulostriate arteries are not definitively known.

Affected patients usually present with facial paresis and hemiparesis soon after the fall. Children show rapid neurological deficits leading to hemidystonia typically within 4 days, which usually subsides within a day, as was seen in our case. However, our patient had a more extensive subcortical small vessel mineralization involving the subcortical vessels apart from the lenticulostriate arterial mineralization.

In a previous case series, Lingappa et al., had recommended aspirin as a treatment for the patients, adding cilostazol after the recurrence of stroke in one of their patients. Yang et al., however, gave no additional drugs to their patients and continued them on a conservative management. Most of the patients of basal ganglia infarct with mineralizing angiopathy show a good prognosis, recovering from the symptoms without any residual neurological deficits, although some patients who have recurrent strokes have a poor prognosis in the form of persistent residual weakness and dysarthria.[3],[4] Our patient had a full recovery without any neurological deficit.

Through this report, we would like to draw the attention of treating physicians as well as radiologists towards the association of mineralizing angiopathy with basal ganglia infarct after a mild trauma that may lead to gross but often reversible motor symptoms.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Ishihara C, Sawada K, Tateno A. Bilateral basal ganglia infarction after mild head trauma. Pediatr Int 2009;51:829-31.  Back to cited text no. 1
Seçkin H, Demirci AY, Degerliyurt A, Dagli M, Bavbek M. Posttraumatic infarction in the basal ganglia after a minor head injury in a child: Case report. Turk Neurosurg 2008;18:415-9.  Back to cited text no. 2
Yang FH, Wang H, Zhang JM, Liang HY. Clinical features and risk factors of cerebral infarction after mild head trauma under 18 months of age. Pediatr Neurol 2013;48:220-6.  Back to cited text no. 3
Lingappa L, Varma RD, Siddaiahgari S, Konanki R. Mineralizing angiopathy with infantile basal ganglia stroke after minor trauma. Dev Med Child Neurol 2014;56:78-84.  Back to cited text no. 4
Sobani ZA, Ali A. Pediatric traumatic putaminal strokes: Mechanisms and prognosis. Surg Neurol Int 2011;2:51.  Back to cited text no. 5


  [Figure 1], [Figure 2]

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