Hyperglycemia-induced hemichorea-hemiballismus syndrome - a systematic review.

Nonketotic hyperglycemia may occur as a cause of chorea in patients with chronic decompensated diabetes. Because it is rare and consequently poorly studied, diagnosis and treatment can be delayed. Therefore, our objective was to summarize clinical and radiological features, as well as treatments performed, from previously reported cases to facilitate adequate management in clinical practice. We searched MEDLINE/PubMed, EMBASE, Cochrane, CINAHL, Web of Science, Scopus, and LILACS databases for studies published before April 23, 2021. We included case reports and case series of adults (aged ≥ 18 years) that described hyperglycemic chorea with measurement ofglycated hemoglobin (HbA1c) and cranial magnetic resonance imaging (MRI). Studies were excluded if participants were pregnant women, aged < 18 years, and had no description of chorea and/or physical examination. We found 121 studies that met the inclusion criteria, for a total of 214 cases. The majority of the included studies were published in Asia (67.3%). Most patients were women(65.3%) aged > 65 years (67.3%). Almost all patients had decompensated diabetes upon arrival at the emergency department (97.2%). The most common MRI finding was abnormalities of the basal ganglia (89.2%). There was no difference in patient recovery between treatment with insulin alone and in combination with other medications. Although rare, hyperglycemic chorea is a reversible cause of this syndrome; therefore, hyperglycemia should always be considered in these cases.

Dnah9 mutant mice and organoid models recapitulate the clinical features of patients with PCD and provide an excellent platform for drug screening.

Primary cilia dyskinesia (PCD) is a rare genetic disease caused by ciliary structural or functional defects. It causes severe outcomes in patients, including recurrent upper and lower airway infections, progressive lung failure, and randomization of heterotaxy. To date, although 50 genes have been shown to be responsible for PCD, the etiology remains elusive. Meanwhile, owing to the lack of a model mimicking the pathogenesis that can be used as a drug screening platform, thereby slowing the development of related therapies. In the current study, we identified compound mutation of DNAH9 in a patient with PCD with the following clinical features: recurrent respiratory tract infections, low lung function, and ultrastructural defects of the outer dynein arms (ODAs). Bioinformatic analysis, structure simulation assay, and western blot analysis showed that the mutations affected the structure and expression of DNAH9 protein. Dnah9 knock-down (KD) mice recapitulated the patient phenotypes, including low lung function, mucin accumulation, and increased immune cell infiltration. Immunostaining, western blot, and co-immunoprecipitation analyses were performed to clarify that DNAH9 interacted with CCDC114/GAS8 and diminished their protein levels. Furthermore, we constructed an airway organoid of Dnah9 KD mice and discovered that it could mimic the key features of the PCD phenotypes. We then used organoid as a drug screening model to identify mitochondrial-targeting drugs that can partially elevate cilia beating in Dnah9 KD organoid. Collectively, our results demonstrated that Dnah9 KD mice and an organoid model can recapture the clinical features of patients with PCD and provide an excellent drug screening platform for human ciliopathies.

Influence of the site of injury on the spontaneous healing response in a rat model of total rupture of the anterior cruciate ligament.

AIM: The healing ability of the anterior cruciate ligament (ACL) injury is very poor; however, it has recently been shown to undergo self-healing with conservative treatments. In this study, we evaluated the influence of the site of injury on the healing process after complete transverse tear of ACL using a rat model. MATERIALS AND METHODS: A total of 58 skeletally mature Wistar rats were randomly assigned to various ACL injury groups: controlled abnormal movement-mid-portion (CAM-MP), controlled abnormal movement-femoral side (CAM-FS), ACL transection-mid-portion (ACLT-MP), or ACL transection-femoral side (ACLT-FS) injury groups. The ACL was completely transected in the mid-portion in the ACLT-MP and CAM-MP groups, and on the femoral side in the ACLT-FS and CAM-FS groups. Both CAM groups underwent extra-articular braking to control for abnormal tibial translation. The animals were allowed full cage activity until sacrifice postoperatively for histological and biomechanical assessment. RESULTS: Significant differences were found in the ratios of residual ligament lengths between the CAM-MP and CAM-FS groups, demonstrating the validity of each model. Spontaneous healing of the injured ACL was observed in the CAM-MP and CAM-FS groups but not in the ACLT-MP and ACLT-FS groups. The mechanical strength of the healing ACL did not differ between the CAM-MP and CAM-FS groups 8 weeks after injury; however, the former had better mechanical strength than the latter 12 weeks after the injury. CONCLUSION: ACL injuries in the mid-portion and on the femoral side may be treated with conservative therapy for spontaneous healing.

Hyperbilirubinemia and Asphyxia in Children With Dyskinetic Cerebral Palsy.

BACKGROUND: We aimed to study the clinical, etiologic, and radiological characteristics in children with dyskinetic cerebral palsy (DCP) and to compare the etiologic subtypes of hyperbilirubinemia and perinatal asphyxia. METHODS: This is a cross-sectional, observational study that enrolled consecutive children with DCP, aged one to 14 years. RESULTS: Sixty-five children with DCP were evaluated. Most children were boys (77%, n = 50), and term gestation (80%, n = 52). Presenting concerns were global developmental delay (97%, n = 63) and involuntary movements (60%, n = 39). Hyperbilirubinemia (66%, n = 43) and perinatal asphyxia (29%, n = 19) were the most important causes. The majority (83%, n = 54) of children were severely disabled (level V and IV). The hyperbilirubinemia group had significant motor delay (63% vs 37%, P = 0.03) and upward gaze palsy (69.7% vs 31.5%, P = 0.005) when compared with the perinatal asphyxia group. Hyperbilirubinemia significantly involved pallidi (86% vs 10% P = 0.0001) and subthalamic nucleus (26% vs none, P = 0.01), whereas asphyxia significantly involved the putamen (58% vs none, P = 0.0001), thalamus (63% vs none, P = 0.0001), and periventricular white matter (79% vs 19%, P = 0.0001). CONCLUSIONS: DCP is the dominant type of cerebral palsy seen in term-born babies with severe dystonia, developmental delay, and motor impairment. Hyperbilirubinemia is the major cause of DCP in the study. Hyperbilirubinemia is associated with motor delay, upward gaze palsy, prominent dystonia, and involvement of globus pallidi and subthalamic nuclei.

ß­Lapachone ameliorates L­DOPA­induced dyskinesia in a 6­OHDA­induced mouse model of Parkinson's disease.

The dopamine precursor 3,4­dihydroxyphenyl­ l­alanine (L­DOPA) is the most widely used symptomatic treatment for Parkinson's disease (PD); however, its prolonged use is associated with L­DOPA­induced dyskinesia in more than half of patients after 10 years of treatment. The present study investigated whether co­treatment with ß­Lapachone, a natural compound, and L­DOPA has protective effects in a 6­hydroxydopamine (6­OHDA)­induced mouse model of PD. Unilateral 6­OHDA­lesioned mice were treated with vehicle or ß­Lapachone (10 mg/kg/day) and L­DOPA for 11 days. Abnormal involuntary movements (AIMs) were scored on days 5 and 10. ß­Lapachone (10 mg/kg) co­treatment with L­DOPA decreased the AIMs score on both days 5 and 10. ß­Lapachone was demonstrated to have a beneficial effect on the axial and limb AIMs scores on day 10. There was no significant suppression in dopamine D1 receptor­related and ERK1/2 signaling in the DA­denervated striatum by ß­Lapachone­cotreatment with L­DOPA. Notably, ß­Lapachone­cotreatment with L­DOPA increased phosphorylation at the Ser9 site of glycogen synthase kinase 3ß (GSK­3ß), indicating suppression of GSK­3ß activity in both the unlesioned and 6­OHDA­lesioned striata. In addition, astrocyte activation was markedly suppressed by ß­Lapachone­cotreatment with L­DOPA in the striatum and substantia nigra of the unilateral 6­OHDA model. These findings suggest that ß­Lapachone cotreatment with L­DOPA therapy may have therapeutic potential for the suppression or management of the development of L­DOPA­induced dyskinesia in patients with PD.

Neurological Soft Signs Predict Auditory Verbal Hallucinations in Patients With Schizophrenia.

Neurological soft signs (NSS) are well documented in individuals with schizophrenia (SZ), yet so far, the relationship between NSS and specific symptom expression is unclear. We studied 76 SZ patients using magnetic resonance imaging (MRI) to determine associations between NSS, positive symptoms, gray matter volume (GMV), and neural activity at rest. SZ patients were hypothesis-driven stratified according to the presence or absence of auditory verbal hallucinations (AVH; n = 34 without vs 42 with AVH) according to the Brief Psychiatric Rating Scale. Structural MRI data were analyzed using voxel-based morphometry, whereas intrinsic neural activity was investigated using regional homogeneity (ReHo) measures. Using ANCOVA, AVH patients showed significantly higher NSS in motor and integrative functions (IF) compared with non-hallucinating (nAVH) patients. Partial correlation revealed that NSS IF were positively associated with AVH symptom severity in AVH patients. Such associations were not confirmed for delusions. In region-of-interest ANCOVAs comprising the left middle and superior temporal gyri, right paracentral lobule, and right inferior parietal lobule (IPL) structure and function, significant differences between AVH and nAVH subgroups were not detected. In a binary logistic regression model, IF scores and right IPL ReHo were significant predictors of AVH. These data suggest significant interrelationships between sensorimotor integration abilities, brain structure and function, and AVH symptom expression.

Complete loss of KCNA1 activity causes neonatal epileptic encephalopathy and dyskinesia.

BACKGROUND: Since 1994, over 50 families affected by the episodic ataxia type 1 disease spectrum have been described with mutations in KCNA1, encoding the voltage-gated K+ channel subunit Kv1.1. All of these mutations are either transmitted in an autosomal-dominant mode or found as de novo events. METHODS: A patient presenting with a severe combination of dyskinesia and neonatal epileptic encephalopathy was sequenced by whole-exome sequencing (WES). A candidate variant was tested using cellular assays and patch-clamp recordings. RESULTS: WES revealed a homozygous variant (p.Val368Leu) in KCNA1, involving a conserved residue in the pore domain, close to the selectivity signature sequence for K+ ions (TVGYG). Functional analysis showed that mutant protein alone failed to produce functional channels in homozygous state, while coexpression with wild-type produced no effects on K+ currents, similar to wild-type protein alone. Treatment with oxcarbazepine, a sodium channel blocker, proved effective in controlling seizures. CONCLUSION: This newly identified variant is the first to be reported to act in a recessive mode of inheritance in KCNA1. These findings serve as a cautionary tale for the diagnosis of channelopathies, in which an unreported phenotypic presentation or mode of inheritance for the variant of interest can hinder the identification of causative variants and adequate treatment choice.

Effects of Integrin ß1 on behavior and neurovascular regeneration in rats with cerebral ischemia-reperfusion injury.

OBJECTIVE: The aim of this study is to investigate the effect of Integrin ß1 on neurological behavior and neurovascular regeneration in rats with a cerebral ischemia-reperfusion injury. MATERIALS AND METHODS: Rat middle cerebral artery occlusion (MCAO) was performed with a modified suture embolization method. Neurological function score of each rat was recorded. Cerebral infarct volume was calculated by Image J after TTC stain. Subsequently, behavioral tests were performed to evaluate neuronal damage, including griping strength test, corner test, cylinder test and sucrose preference test. The expression levels of VEGF, HIF-1α, Claudin5, and ZO-1 in rat brain tissues were detected by Western blot and quantitative Reverse Transcriptase-Polymerase Chain Reaction (qRT-PCR), respectively. RESULTS: Neurological function score of the rat was remarkably decreased after cerebral ischemia-reperfusion. Anti-Integrin ß1 administration aggravated neurological deficit and increased cerebral infarct volume of I/R rats. Symptoms of hemidysesthesia, dyskinesia, and affective disorder of rats were worse after anti-Integrin ß1 administration in I/R rats. Anti-Integrin ß1 administration downregulated VEGF and HIF-1α in rat brain tissues (p<0.05). However, no significant differences in Claudin5 and ZO-1 expressions were found before and after Integrin ß1 treatment. CONCLUSIONS: The inhibition of Integrin ß1 pathway during cerebral ischemia-reperfusion aggravates the behavior and neurovascular regeneration of I/R rats. In the process of cerebral ischemia-reperfusion, Integrin ß1 plays a key role in the repair and protection of neurovascular units by promoting angiogenesis.

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.

Methods to Investigate the Role of ß-Arrestin Signaling in Parkinson's Disease.

ß-Arrestin function has largely been investigated in cell culture-based systems. Here we describe methods to investigate ß-arrestin2 signaling in vivo by developing novel mouse models and viral methods to overexpress ß-arrestin2 in the mouse brain. The methods and concepts described here are in the context of Parkinson's disease (PD) and developing automated in vivo drug screening platforms.

ALDH1A1 regulates postsynaptic µ-opioid receptor expression in dorsal striatal projection neurons and mitigates dyskinesia through transsynaptic retinoic acid signaling.

Aldehyde dehydrogenase 1A1 (ALDH1A1), a retinoic acid (RA) synthase, is selectively expressed by the nigrostriatal dopaminergic (nDA) neurons that preferentially degenerate in Parkinson's disease (PD). ALDH1A1-positive axons mainly project to the dorsal striatum. However, whether ALDH1A1 and its products regulate the activity of postsynaptic striatal neurons is unclear. Here we show that µ-type opioid receptor (MOR1) levels were severely decreased in the dorsal striatum of postnatal and adult Aldh1a1 knockout mice, whereas dietary supplement of RA restores its expression. Furthermore, RA treatment also upregulates striatal MOR1 levels and signaling and alleviates L-DOPA-induced dyskinetic movements in pituitary homeobox 3 (Pitx3)-deficient mice that lack of ALDH1A1-expressing nDA neurons. Therefore, our findings demonstrate that ALDH1A1-synthesized RA is required for postsynaptic MOR1 expression in the postnatal and adult dorsal striatum, supporting potential therapeutic benefits of RA supplementation in moderating L-DOPA-induced dyskinesia.

Diametric neural ensemble dynamics in parkinsonian and dyskinetic states.

Loss of dopamine in Parkinson's disease is hypothesized to impede movement by inducing hypo- and hyperactivity in striatal spiny projection neurons (SPNs) of the direct (dSPNs) and indirect (iSPNs) pathways in the basal ganglia, respectively. The opposite imbalance might underlie hyperkinetic abnormalities, such as dyskinesia caused by treatment of Parkinson's disease with the dopamine precursor L-DOPA. Here we monitored thousands of SPNs in behaving mice, before and after dopamine depletion and during L-DOPA-induced dyskinesia. Normally, intermingled clusters of dSPNs and iSPNs coactivated before movement. Dopamine depletion unbalanced SPN activity rates and disrupted the movement-encoding iSPN clusters. Matching their clinical efficacy, L-DOPA or agonism of the D2 dopamine receptor reversed these abnormalities more effectively than agonism of the D1 dopamine receptor. The opposite pathophysiology arose in L-DOPA-induced dyskinesia, during which iSPNs showed hypoactivity and dSPNs showed unclustered hyperactivity. Therefore, both the spatiotemporal profiles and rates of SPN activity appear crucial to striatal function, and next-generation treatments for basal ganglia disorders should target both facets of striatal activity.

Identification of an Immortalized Human Airway Epithelial Cell Line with Dyskinetic Cilia.

Primary ciliary dyskinesia is an inherited, currently incurable condition. In the respiratory system, primary ciliary dyskinesia causes impaired functioning of the mucociliary escalator, leading to nasal congestion, cough, and recurrent otitis media, and commonly progresses to cause more serious and permanent damage, including hearing deficits, chronic sinusitis, and bronchiectasis. New treatment options for the condition are thus necessary. In characterizing an immortalized human bronchial epithelial cell line (BCi-NS1.1) grown at an air-liquid interface to permit differentiation, we have identified that these cells have dyskinetic motile cilia. The cells had a normal male karyotype, and phenotypic markers of epithelial cell differentiation emerged, as previously shown. Ciliary beat frequency (CBF) as assessed by high-speed videomicroscopy was lower than normal (4.4 Hz). Although changes in CBF induced by known modulators were as expected, the cilia displayed a dyskinetic, circular beat pattern characteristic of central microtubular agenesis with outer doublet transposition. This ultrastructural defect was confirmed by electron microscopy. We propose that the BCi-NS1.1 cell line is a useful model system for examination of modulators of CBF and more specifically could be used to screen for novel drugs with the ability to enhance CBF and perhaps repair a dyskinetic ciliary beat pattern.

Presynaptic dopamine depletion determines the timing of levodopa-induced dyskinesia onset in Parkinson's disease.

PURPOSE: Reduced presynaptic dopaminergic activity plays an important role in the development of levodopa-induced dyskinesia (LID) in Parkinson's disease (PD). In this study, we investigated whether dopaminergic function in the nigrostriatal system is associated with the timing of LID onset. METHODS: From among 412 drug-naive PD patients who underwent a dopamine transporter (DAT) PET scan during their baseline evaluation, we enrolled 65 patients who developed LID during a follow-up period of >2 years. Based on the time from PD onset, LID was classified as early, intermediate or late onset. We then compared DAT availability in the striatal subregions of the patients in the three groups. RESULTS: The demographic characteristics did not differ among the three patient groups except for earlier intervention of levodopa therapy in the early LID onset group (p = 0.001). After adjusting for age at PD onset, gender, timing of levodopa therapy from PD onset, and the severity of PD motor symptoms, DAT activity in the posterior putamen was found to be significantly lower in the early LID onset group than in the late LID onset group (p = 0.017). Multivariate linear regression analysis showed that low DAT activity in the posterior putamen was significantly associated with the early appearance of LID in the early LID onset group (ß = 16.039, p = 0.033). CONCLUSION: This study demonstrated that low DAT activity in the posterior putamen at baseline is a major risk factor for the early onset of LID in patients with PD, suggesting that the degree of presynaptic dopaminergic denervation plays an important role in determining the timing of LID onset.

Movement Pattern of Scapular Dyskinesis in Symptomatic Overhead Athletes.

This study investigated the characteristics of arm elevation via principal component analysis in symptomatic overhead athletes with scapular dyskinesis. One hundred-thirty-four overhead athletes with scapular dyskinesis [24: inferior angle prominence (pattern I); 46: medial border prominence (pattern II), 64: pattern I + II] were evaluated by three-dimensional electromagnetic motion and electromyography to record the scapular kinematics (upward rotation/posterior tipping/exterior rotation) and muscle activation (upper trapezius: UT; middle trapezius: MT; lower trapezius: LT; serratus anterior: SA) during lowering phase of arm elevation. The results showed: (1) for pattern I and II, the first 3 principal component (PCs) explained 41.4% and 42.6% of total variance of movement; (2) the first PCs were correlated with MT, LT activity (r = 0.41~0.61) and upward rotation, posterior tipping (r = -0.59~-0.33) in pattern I, and UT, MT, SA (r = 0.30~0.70) activity in pattern II; (3) contour plots of muscle activity demonstrated that muscle activities varied with dyskinesis patterns. In summary, for the pattern I, the major characteristics are coactivation of MT and LT and corresponding scapular posterior tipping and upward rotation. For the pattern II, the major characteristics are coactivation of UT, MT and SA without corresponding scapular external rotation.

Current Nondopaminergic Therapeutic Options for Motor Symptoms of Parkinson's Disease.

OBJECTIVE: The aim of this study was to summarize recent studies on nondopaminergic options for the treatment of motor symptoms in Parkinson's disease (PD). DATA SOURCES: Papers in English published in PubMed, Cochrane, and Ovid Nursing databases between January 1988 and November 2016 were searched using the following keywords: PD, nondopaminergic therapy, adenosine, glutamatergic, adrenergic, serotoninergic, histaminic, and iron chelator. We also reviewed the ongoing clinical trials in the website of clinicaltrials.gov. STUDY SELECTION: Articles related to the nondopaminergic treatment of motor symptoms in PD were selected for this review. RESULTS: PD is conventionally treated with dopamine replacement strategies, which are effective in the early stages of PD. Long-term use of levodopa could result in motor complications. Recent studies revealed that nondopaminergic systems such as adenosine, glutamatergic, adrenergic, serotoninergic, histaminic, and iron chelator pathways could include potential therapeutic targets for motor symptoms, including motor fluctuations, levodopa-induced dyskinesia, and gait disorders. Some nondopaminergic drugs, such as istradefylline and amantadine, are currently used clinically, while most such drugs are in preclinical testing stages. Transitioning of these agents into clinically beneficial strategies requires reliable evaluation since several agents have failed to show consistent results despite positive findings at the preclinical level. CONCLUSIONS: Targeting nondopaminergic transmission could improve some motor symptoms in PD, especially the discomfort of dyskinesia. Although nondopaminergic treatments show great potential in PD treatment as an adjunct therapy to levodopa, further investigation is required to ensure their success.

Direct Intracranial Injection of AAVrh8 Encoding Monkey ß-N-Acetylhexosaminidase Causes Neurotoxicity in the Primate Brain.

GM2 gangliosidoses, including Tay-Sachs disease and Sandhoff disease, are lysosomal storage disorders caused by deficiencies in ß-N-acetylhexosaminidase (Hex). Patients are afflicted primarily with progressive central nervous system (CNS) dysfunction. Studies in mice, cats, and sheep have indicated safety and widespread distribution of Hex in the CNS after intracranial vector infusion of AAVrh8 vectors encoding species-specific Hex α- or ß-subunits at a 1:1 ratio. Here, a safety study was conducted in cynomolgus macaques (cm), modeling previous animal studies, with bilateral infusion in the thalamus as well as in left lateral ventricle of AAVrh8 vectors encoding cm Hex α- and ß-subunits. Three doses (3.2 × 1012 vg [n = 3]; 3.2 × 1011 vg [n = 2]; or 1.1 × 1011 vg [n = 2]) were tested, with controls infused with vehicle (n = 1) or transgene empty AAVrh8 vector at the highest dose (n = 2). Most monkeys receiving AAVrh8-cmHexα/ß developed dyskinesias, ataxia, and loss of dexterity, with higher dose animals eventually becoming apathetic. Time to onset of symptoms was dose dependent, with the highest-dose cohort producing symptoms within a month of infusion. One monkey in the lowest-dose cohort was behaviorally asymptomatic but had magnetic resonance imaging abnormalities in the thalami. Histopathology was similar in all monkeys injected with AAVrh8-cmHexα/ß, showing severe white and gray matter necrosis along the injection track, reactive vasculature, and the presence of neurons with granular eosinophilic material. Lesions were minimal to absent in both control cohorts. Despite cellular loss, a dramatic increase in Hex activity was measured in the thalamus, and none of the animals presented with antibody titers against Hex. The high overexpression of Hex protein is likely to blame for this negative outcome, and this study demonstrates the variations in safety profiles of AAVrh8-Hexα/ß intracranial injection among different species, despite encoding for self-proteins.

T2*-based MR imaging of hyperglycemia-induced hemichorea-hemiballism.

INTRODUCTION: Hyperglycemia can induce hemichorea-hemiballism, especially in elderly type II diabetics. CT and MRI findings include hyperdensity and T1-shortening in the contralateral lentiform nucleus, respectively. This study explores the associated imaging findings on T2*-based sequences. METHODS: Six patients with clinically documented hyperglycemia-induced hemichorea-hemiballism who had undergone MR imaging with a T2*-based sequence (T2* gradient echo or susceptibility-weighted imaging) were included in this retrospective case series. RESULTS: All six patients demonstrated T1-shortening contralateral to their hemichorea-hemiballism. T2*-based sequences demonstrated unilateral hypointense signal within the striatum in four patients. One patient had mild bilateral striatal hyperintensities, while another did not show significant signal changes. CONCLUSION: It is important for the radiologist to be aware of the signal changes that can be seen on T2*-based sequences in hyperglycemia-induced hemochorea-hemiballism.

Ultrasound-guided botulinum toxin A injection in the treatment of belly dancer's dyskinesia.

BACKGROUND: Belly dancer's dyskinesia is an extremely rare condition. It manifests as semicontinuous, slow, writhing, sinuous abdominal wall movements that are bothersome to the patient. Management of this condition is extremely difficult and challenging. METHODS: We describe four patients with belly dancer's dyskinesia who were treated with Botulinum Toxin A (BTX) injections under ultrasound guidance. RESULTS: All patients underwent the same BTX injection procedure using an aseptic technique under ultrasound guidance. The patients responded well to the BTX injections after an unsatisfactory course of medical treatment. The patients reported complete abolishment of abnormal abdominal movements with no side effects. CONCLUSIONS: We report a cohort of patients with belly dancer dyskinesia treated successfully with BTX injections. Ultrasound guidance for injections increases the accuracy and reduces the risk of the complications. BTX injection under ultrasound guidance is a safe and effective treatment modality that should be employed as a first-line in the management of patients with belly dancer's dyskinesia.