Diabetic Striatopathy
A 33-year-old male patient was admitted to the hospital with a 1-month history of polydipsia and polyuria, followed by unconsciousness for 1 day. The patient had polydipsia and polyuria 1 month ago and was found syncope by the roadside 1 day before admission. Upon the regaining consciousness, the patient was apathetic and unresponsive, presenting with blurred vision, bilateral hearing loss, involuntary movements of the right limb, and urinary incontinence. Physical examination revealed anarthria and choreic involuntary movements affecting the right limb. Auxiliary examination showed that the blood glucose was 63.93 mmol/L. Blood gas analysis: pH 7.293, carbon dioxide partial pressure 23.7 mmHg, bicarbonate concentration 14, standard alkali residual -15.10 mmol/L, lactate concentration 2.20 mmol/L. Bicarbonate 9.6 mmol/L. β-Hydroxybutyric acid 4.61 mmol/L. Cranial CT: Increased density of bilateral putamen nucleus, thalamus, globus pallidus, and right caudate nucleus [Figure 1]. Cranial MRI revealed abnormal signals of bilateral putamen nucleus, thalamus, globus pallidus, and right caudate nucleus [Figure 2]. The SWI sequence demonstrates multiple microhemorrhage in the bilateral basal ganglia [Figure 2d]. Diabetic striatopathy is a basal ganglia lesion that occurs in the context of acute glucose metabolism disorders, such as severe hyperglycemic hyperosmolar or diabetic ketoacidosis.[1,2] Patients often present with involuntary movements, such as chorea-like movements of the affected limb.[1,2] Although diabetic striatopathy has previously been described in patients with diabetic nonketotic hyperglycemic hyperosmolarity,[3] it can also occur in patients with diabetic ketosis.[1] Its occurrence is closely related to dyslipidemia, insulin resistance, and long-term irregular glycemic control. Its characteristic imaging findings include high density in the striatum on CT scans or hyperintensity on T1WI, with variable T2WI signals that may be associated with microhemorrhage.[2,3] Chronic micro hemorrhagic lesions in the striatum may be the common pathological mechanism of diabetic striatopathy on DTI and MRS.[4]Figure 1: CT changes in patients with diabetic striatopathyFigure 2: MRI changes in patients with diabetic striatopathyDeclaration 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 General Program Sponsored by Basic Research Fund in Shenzhen Natural Science Foundation (JCYJ20240813153011015). Conflicts of interest There are no conflicts of interest.
Authors
- Han Luo
- Shanshan Li (ORCID: https://orcid.org/0000-0002-9021-8470)
- Bo Liu (ORCID: https://orcid.org/0000-0002-6235-1573)
Institutions
- Longgang Central Hospital (CN)
Publication Details
- Journal
- Neurology India
- Published
- 2025-09-01
- DOI
- https://doi.org/10.4103/neurol-india.neurol-india-d-25-00478
- Citations
- 1
- Primary Topic
- Neurological and metabolic disorders
- Type
- article
- Field-Weighted Citation Impact
- 1.29