Background: Diabetic striatopathy (DS), coined as a generic term, has been defined as a hyperglycemic condition associated with either one of the two following conditions: chorea/ballism or striatal hyperdensity on computed tomography or striatal hyperintensity on T1-weighted magnetic resonance imaging. This review highlights those “gray areas,” which need further exploration to understand better hyperglycemia-induced striatal changes and diverse movement disorder phenotypes associated with these changes. Results and Discussion: We searched in PubMed and Google Scholar the terms “diabetes mellitus,” “movement disorders,” “diabetic striatopathy,” “chorea,” “hemichorea,” “ballism,” “hemichorea-hemiballism,” and “neuroradiology” in various combinations (time range from 1980 to March 2022). We selected the publications about our topic of discussion. Summary: Hemichorea-hemiballismus is the most commonly associated movement disorder in DS, and the putamen is the most frequently affected anatomical region. The exact pathophysiological mechanisms remain elusive. Clinical-radiological discordance is not rare. Complete reversal of symptoms with the resolution of the imaging findings is the most prevalent outcome in patients with DS. Dramatic improvement of chorea can be achieved by either insulin monotherapy or combination therapy of insulin and D2-blocker or, in some cases, even spontaneously. Conclusion: The term “diabetic striatopathy” is ambiguous and controversial. Pathological mechanisms behind clinical-radiological discordance in hyperglycemia-induced striatopathy need further exploration through well-designed studies. We propose a classification of DS that includes symptomatic DS (striatal neuroimaging lesions in association with a clinically evident movement disorder and hyperglycemia), clinically isolated DS (clinically evident movement disorders without striatal changes in neuroimaging), and radiologically isolated DS.

The term “diabetic striatopathy” (DS) was coined as a generic term to refer to a hyperglycemic condition associated with either chorea/ballism or striatal hyperdensity on computed tomography or striatal hyperintensity on T1-weighted (T1-WI) magnetic resonance imaging (MRI) (Fig. 1) [1]. Although hemichorea-hemiballismus is the most commonly identified movement disorder in DS [1], many involuntary movements are increasingly recognized [1-5]. However, the anatomic localization, exact pathophysiological mechanisms, radiological correlates, and the probable explanation for clinical-radiological discordance remain elusive. In this paper, we highlight those “gray areas” which need further exploration to understand better hyperglycemia-induced striatal changes and diverse movement disorder phenotypes associated with the changes.

Fig. 1.

MRI of the brain revealing increased signal intensity on T1-WI imaging in the right caudate, putamen, and globus pallidus, suggestive of striatopathy.

Fig. 1.

MRI of the brain revealing increased signal intensity on T1-WI imaging in the right caudate, putamen, and globus pallidus, suggestive of striatopathy.

Close modal

We searched in PubMed and Google Scholar the terms “diabetes mellitus,” “movement disorders,” “diabetic striatopathy,” “chorea,” “hemichorea,” “ballism,” “hemichorea-hemiballism,” and “neuroradiology” in various combinations (time range from 1980 to March 2022). We selected the publications about our topic of discussion.

Data Statement

The data used to support the findings of this study are included in the article.

The Classic Concept of DS

Hyperintense signal in contralateral (to the side of the abnormal movements) putamen on T1-WI without surrounding edema or mass effect, along with hyperglycemia and choreiform movements, is pathognomonic of DS [1, 6]. For detection of DS, brain MRI has higher sensitivity than CT [1, 5]. Overall, isolated putaminal involvement is the most common finding, followed by combined involvement of the caudate nucleus and putamen and, in some cases, the concomitant affliction of all three striatal components (putamen, caudate, and globus pallidus) [1, 5].

A hyperglycemic state results in hyperosmolarity leading to reduced cerebral blood flow and may cause ischemic insult to the astrocytes of basal ganglia [1]. Petechial hemorrhage, causing accumulation of methemoglobin and a breakdown of the blood-brain barrier, has been considered the cause of striatal hyperintensity on T1-WI and hyperdensity on CT scan in these patients [1]. Mineral deposition, myelinolysis, gemistocytopathy, cytotoxic edema, and atrophy are proposed pathological mechanisms [1, 6, 7]. Furthermore, magnetic resonance spectroscopy studies have found neuronal damage, gliosis, and mild ischemia in the basal ganglia during the episodes of abnormal movements [8].

DS – Current Controversies and Proposed Pragmatism

We will discuss sequentially current controversies of this entity and a proposal to classify DS based on MRI.

Anatomical Perspective – Basal Ganglia and Hyperglycemic Movement Disorders

The lesion behind chorea-ballismus is usually described in the sub-thalamic nucleus, caudate nucleus, and putamen [1]. The meta-analysis by Chua et al. [1] showed that hemichorea-hemiballismus was most frequently associated with a lesion in the putamen (∼94% lesion on MRI), with caudate nucleus and globus pallidus being affected in a significantly lesser number of patients. Very few cases of DS have been reported where neuroimaging findings were positive but without putamen involvement (only caudate was involved in those cases) [1]. Among other striatum regions, the putamen, in particular, is the most susceptible area to demonstrate positive neuroimaging findings in DS.

Pathophysiological Basis of DS and Its Clinical and Neuroradiological Correlates and Controversies

The exact pathophysiological mechanisms remain elusive. We propose an “ominous octet” that includes (1) accumulation of gemistocytes (i.e., tumescent reactive astrocytes) due to ischemic events in turn sequentially leading to (2) petechial hemorrhage, (3) methemoglobin deposition, (4) mineral deposition, (5) cytotoxic edema, (6) myelinolysis, (7) gliosis, and (8) atrophy. Whether these intricately interrelated components of ominous octet come into play together or in isolation in every DS case is still enigmatic.

In a study to explain the possible mechanism behind the MRI changes in hemichorea-hemiballismus syndrome, Shan et al. [9] found a significant association with hyperglycemia (70% of patients). There is no definite answer to whether it is only the raised blood glucose or any particular substrate or some yet-to-know metabolic by-product that might be responsible for initiating movement disorders. On the contrary, even hypoglycemic episodes in diabetes mellitus may be associated with contralateral striatal involvement in neuroimaging [6]. One possibility is that the striatum, which is extremely sensitive to alteration of blood glucose levels, can be at risk of damage; however, it is unclear whether this vulnerability is more related to acute insults or chronic changes [10]. Whether acute or chronic hyperglycemia or rapid fluctuations of glycemic status are responsible for neuroradiological lesions is still unknown. Although the theory of dysfunctional γ-aminobutyric acid (GABA)-ergic projection neurons in the indirect loop of the basal ganglia circuit may address the clinical picture in DS patients, it is not satisfactory for the neuroradiological lesions [11].

Movement disorders associated with hyperglycemia without appreciable neuroradiological correlates support the hypothesis of a widespread neurotransmitter disruption in the basal ganglia circuit (dysfunctional GABA-ergic projection in basal ganglia). It remains elusive whether it involves direct or indirect pathways, but evidence suggests possible GABA-ergic dysfunction in the indirect pathways [11]. DS typically occurs in patients with poorly controlled long-standing type-2 diabetes mellitus [1, 5]. However, cases presaging acute hyperglycemic surge following viral infection in previously euglycemic individuals and type-3c diabetes mellitus have also been documented [1, 3, 12].

Not all patients with long-standing and acute hyperglycemic episodes show striatal changes on neuroimaging or show movement disorders. Therefore, genetic susceptibility (as evident from the fact that a more significant number of cases have been reported from Asian countries) [1, 5] may play a role in the involvement of striatum, particularly in patients with DS [13].

Neuroradiological Correlates and Controversies

Findings on CT and MRI of the brain are correlated; however, some evidence of mismatch exists between these two techniques. For example, Chua et al. [1] found the mismatch rate was approximately 17% (striatal changes were detected on MRI but no such findings on CT). Some variability in the location of striatal anomalies noted on CT and MRI was discussed in their review [1].

The time interval between the onset of damage at the ultrastructural level and the neuroradiologically evident structural lesion is unknown. Accumulation of gemistocytes due to ischemic events and neuronal dysfunction may partially explain the striatal hyperintensity on T1-WI but not hyperdensity on CT [1]. Again, theories supporting microhemorrhages in basal ganglia, the most plausible explanation of T1-WI hyperintense in the striatum, are not substantiated well on corresponding gradient-echo images [6]. The cause of restricted diffusion in a few cases of DS studied with diffusion-weighted imaging sequences remains elusive [11]. Noncontributory diffusion-weighted imaging, which is not uncommon, suggests different pathological insults in the striatum, although it needs further clarifications [6].

A study using MR spectroscopy for the diseased striatum revealed a decrease in the NAA/Cr ratio (1.35), standard Cho/Cr ratio (1.22), and a peak for myoinositol, while the spectrum on the contralateral side revealed a decrease in the NAA/Cr ratio (1.48), increase in Cho/Cr (1.32), but no peak for myoinositol [8]. The low NAA/Cr ratio in the diseased striatum suggests neuronal loss or damage [8]. Further, the low NAA/Cr ratio and high Cho/Cr ratio in the contralateral striatum suggest that it is functionally impaired, despite normal MRI appearance [8]. On the other hand, the peak of myoinositol suggests the possibility of functional impairment of the sorbitol pathway in the striatum and therefore a common pathogenetic mechanism for diabetic neuropathy and DS [8].

Some of the clinical-radiological discrepancies may be resolved with the help of SPECT study [14, 15]. However, apparently superior and sophisticated investigations like dopamine transporter (DAT) (to detect dopaminergic integrity) and positron emission tomography scan (to detect a failure in metabolism in different substrates of basal ganglia) may not always be devoid of drawbacks [16, 17]. The lesions involving the basal ganglia can lead to either a hypokinetic or hyperkinetic movement disorder depending on the involved pathway. Hence, a patient with a structural abnormality in the basal ganglia can have a hyperkinetic movement disorder despite an abnormal DAT scan [16].

MRI volumetric analysis by detecting atrophy reportedly has helped estimate the reoccurrence of movement disorders in DS with euglycemic status [18]. Multiparametric MRI with more dedicated specific sequence-based imaging and functional MRI, SPECT/positron emission tomography, and DAT studies on a larger scale with serial and sequential follow-ups at predetermined intervals may further address these unresolved facts in DS.

Evidenced-Based Basis of Clinical-Radiological Discordance

Negative neuroimaging findings, i.e., no obvious lesion identified on both CT and MRI of the brain, have been reported in symptomatic patients of DS. Chua et al. [1] found that nearly 7% of patients who presented with chorea did not show any striatal involvement in neuroimaging. Of interest is that 2% of patients may show radiological striatal lesions but no clinically manifested movement disorders (radiologically isolated DS) [1, 3, 19].

Incompatibility in correlating laterality of the lesion on neuroimaging and involved side of abnormal movements has been observed in cases of DS. Some patients with unilateral neuroradiological lesions manifest chorea in bilateral limbs [1], whereas some with bilateral striatal lesions show the unilateral manifestation of chorea [20]. Surprisingly, some show symptoms in the side of the body ipsilateral to the side of the neuroradiological lesion [21, 22]. No significant correlation has also been found between the active body region (arm/face/leg) and the location of striatal abnormalities [3]. These peculiar clinical-radiological conflicts have put forward significant challenges for researchers to decode the underlying pathogenesis of DS and questioned the conventional concept of neurological localization.

Outcome and Neuroimaging Follow-Up

Complete reversal of symptoms with the resolution of the imaging findings is the most prevalent outcome in patients with DS [1, 23]. Dramatic improvement of chorea could have been achieved by either insulin monotherapy or combination therapy of insulin and D2-blocker or, in some cases, even spontaneously [1, 5]. Generally, symptomatic improvement is achieved by correcting hyperglycemic status much earlier than neuroradiological reversal. In most cases, imaging findings on CT and MRI take around 3 and 8 months, respectively, to achieve complete resolution [1]. However, some cases demonstrate persisting striatal anomalies on neuroimaging follow-up, along with either persisting movement disorders or complete symptomatic recovery [1]. Chua et al. [1] found the striatal hyperintensity on T1-WI on follow-up MRI up to 3 months. No correlation of these persisting neuroimaging features has been found with location specificity within the striatum at the onset of disease or severity/duration of chorea or therapeutic course. It has also been noted that as high as 20% of cases may present with recurrent chorea, despite total resolution of the striatal lesions in earlier attacks [1]. It is unknown which patients are prone to develop chronic forms or may show recurrence. Even after normalization of blood glucose level, persistent neuroimaging features can be attributed to unrecovered or irreversible structural damage [9, 23]. The hyperglycemic attack in DS may manifest as an acute scenario, but the pathological changes may not be transient in the striatum region and, in some cases, may be chronic. There is not much study on DS that describes the course of signal intensity changes on MRI in the striatum at a regular serial interval [10]. It may be because most cases of DS are investigated in resource-poor Asian countries and thus unavailability of a large number of patients who agreed to attend regular follow-up visits [5]. It can be thoughtful if any neuroradiological staging protocol can be generated according to the time gap from onset to the resolution of clinically manifest chorea and during the post-recovery period.

Proposal of Classification of DS

The term “diabetic striatopathy” is ambiguous and controversial. We propose to divide the term into three subsets as follows:

1.Symptomatic DS: Striatal neuroimaging lesions associated with a clinically evident movement disorder and hyperglycemia. This subset can be divided into two subgroups: (a) concordant symptomatic striatopathy – lesion in neuroimaging contralateral to the side of the movement disorders; and (b) discordant symptomatic striatopathy – lesion in neuroimaging appeared to be on the same side of movement disorders or unilateral lesion in neuroimaging with bilateral movement abnormalities or bilateral striatal lesions with a unilateral manifestation of movement disorders.

2.Clinically isolated DS: Clinically evident movement disorders without striatal changes in neuroimaging, hyperglycemia, and after exclusion of other etiologies having the potential to do so.

3.Radiologically isolated DS: Striatal changes in brain imaging associated with hyperglycemia (after exclusion of all probable etiologies having the potential to cause similar changes) without any evidence of movement disorders clinically.

Pathological mechanisms behind clinical-radiological discordance in hyperglycemia-induced striatopathy need further exploration through well-designed studies [24, 25]. In this sense, improvement of bilateral motor clinical features (although asymmetric) in patients with Parkinson’s disease following unilateral functional neurosurgery/neuromodulation suggests that basal ganglia exert bilateral effects on motor functions [26]. Similar pathological mechanisms might be responsible for clinical-radiological discordances in DS. Alternatively, inhibition of excitatory signals from disinhibited ipsilateral basal ganglia structures to the opposite motor cortex via callosal connections may be a relevant explanation for such discordances [27]. Variable involvement and disruption of functional connectivity within the basal ganglia network in hyperglycemia-induced striatopathy may be responsible for clinical-radiological discordance [28].

We confirm that we have read the journal’s position on issues involved in ethical publication and affirm that this work is consistent with those guidelines.

We wish to confirm that there are no known conflicts of interest associated with this publication, and there has been no significant financial support for this work that could have influenced its outcome.

J. Benito-León is supported by the National Institutes of Health, Bethesda, MD, USA (NINDS #R01 NS39422), European Commission (Grant ICT-2011-287739, NeuroTREMOR), the Ministry of Economy and Competitiveness (Grant RTC-2015-3967-1, NetMD – platform for the tracking of movement disorder), and the Spanish Health Research Agency (Grant FIS PI12/01602 and Grant FIS PI16/00451).

Dr. Souvik Dubey () collaborated in (1) the conception, organization, and execution of the research project and (2) the writing of the manuscript. Dr. Payel Biswas () collaborated in (1) the conception, organization, and execution of the study and (2) the review and critique of the manuscript. Dr. Ritwik Ghosh () collaborated in (1) the conception, organization, and execution of the study and (2) the review and critique of the manuscript. Dr. Subhankar Chatterjee () collaborated in (1) the conception, organization, and execution of the research project and (2) the review and critique of the manuscript. Prof. (Dr.) Biman Kanti Ray () collaborated in (1) the conception, organization, and execution of the research project and (2) the review and critique of the manuscript. Dr. Julián Benito-León () collaborated in (1) the conception, organization, and execution of the research project and (2) the review and critique of the manuscript.

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