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Background The clinical diagnosis of multiple system atrophy (MSA) is challenged by overlapping features with Parkinson's disease (PD) and late-onset ataxias. Additional biomarkers are needed to confirm MSA and to advance the understanding of pathophysiology. Positron emission tomography (PET) imaging of the translocator protein (TSPO), expressed by glia cells, has shown elevations in MSA. Objective In this multicenter PET study, we assess the performance of TSPO imaging as a diagnostic marker for MSA. Methods We analyzed [11 C]PBR28 binding to TSPO using imaging data of 66 patients with MSA and 24 patients with PD. Group comparisons were based on regional analysis of parametric images. The diagnostic readout included visual reading of PET images against clinical diagnosis and machine learning analyses. Sensitivity, specificity, and receiver operating curves were used to discriminate MSA from PD and cerebellar from parkinsonian variant MSA. Results We observed a conspicuous pattern of elevated regional [11 C]PBR28 binding to TSPO in MSA as compared with PD, with "hotspots" in the lentiform nucleus and cerebellar white matter. Visual reading discriminated MSA from PD with 100% specificity and 83% sensitivity. The machine learning approach improved sensitivity to 96%. We identified MSA subtype-specific TSPO binding patterns. Conclusions We found a pattern of significantly increased regional glial TSPO binding in patients with MSA. Intriguingly, our data are in line with severe neuroinflammation in MSA. Glia imaging may have potential to support clinical MSA diagnosis and patient stratification in clinical trials on novel drug therapies for an α-synucleinopathy that remains strikingly incurable. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

OBJECTIVEReports on basal ganglia cavernous malformations (BGCMs) are rare. Here, the authors report on their experience in resecting these malformations to offer insight into this infrequent disease subtype.METHODSThe authors retrospectively reviewed a prospectively managed departmental database of all deep-seated cerebral cavernous malformations (CCMs) treated at Stanford between 1987 and 2019 and included for further analysis those with a radiographic diagnosis of BGCM. Moreover, a systematic literature review was undertaken using the PubMed and Web of Science databases.RESULTSThe departmental database search yielded 331 patients with deep-seated CCMs, 44 of whom had a BGCM (13.3%). Headache was the most common presenting sign (53.5%), followed by seizure (32.6%) and hemiparesis (27.9%). Lesion location involved the caudate nucleus in 21.4% of cases compared to 78.6% of cases within the lentiform nucleus. Caudate BGCMs were larger on presentation and were more likely to present to the ependymal surface (p < 0.001) with intraventricular hemorrhage and hydrocephalus (p = 0.005 and 0.007, respectively). Dizziness and diplopia were also more common with lesions involving the caudate. Because of their anatomical location, caudate BGCMs were preferentially treated via an interhemispheric approach and were less likely to be associated with worsening perioperative deficits than lentiform BGCMs (p = 0.006 and 0.045, respectively). Ten patients (25.6%) were clinically worse in the immediate postoperative period, 4 (10.2%) of whom continued to suffer permanent morbidity at the last follow-up. A long-term good outcome (modified Rankin Scale [mRS] score 0–1) was attained in 74.4% of cases compared to the 69.2% of patients who had presented with an mRS score 0–1. Relative to their presenting mRS score, 89.8% of patients had an improved or unchanged status at the last follow-up. The median postoperative follow-up was 11 months (range 1–252 months). Patient outcomes after resection did not differ among surgical approaches; however, patients presenting with hemiparesis and lesions involving the globus pallidus or posterior limb of the internal capsule were more likely to suffer neurological deficits during the immediate perioperative period. Patients who had undergone awake surgeries were more likely to suffer neurological decline at the early as well as the late follow-up. When adjusting for awake craniotomy as a potential confounder of lesion location, a BGCM involving the posterior limb was predictive of developing early postoperative deficits, but this finding did not persist at the long-term follow-up.CONCLUSIONSSurgery is a safe and effective treatment modality for managing BGCMs, with an estimated long-term permanent morbidity rate of around 10%.

Introduction: Wilson’s disease (WD) is an autosomal recessive disorder involving cellular copper transport. A defect in biliary excretion leads to accumulation of copper in the liver, causing progressive liver injury and cirrhosis. Approximately 1 in 40,000 people have Wilson’s Disease. It affects both men and women equally. Symptoms appear between ages 5 and 35. Case Presentation: This is a case of 17 years old girl came with complained of dysphagia, irritability, breathlessness, weakness in both upper and lower limb at left side for 6 months. She had difficulty in going up and coming down a staircase and in getting up from the squatting position. She could walk with support for the first 6 months of his illness but later, had required crutches. After her admission diagnostic evaluation was done, and in the findings was chest x-ray was done which was normal. ECG showing normal sinus rate and rhythm. Ophthalmology call was done and slit lamp examination was noted which was showing KF ring was present bilaterally. MRI brain suggested symmetrical altered signal intensity lesion in bilateral thalami and lentiform nucleus, midbrain and pons appearing hyper intense on T2/FLAIR sequences in bilateral gangliocapsular region (mainly in putamen) and thalami as well as midbrain and dorsal aspect of pons as described above. A possibility of Wilson’s Disease can be considered, blood test show that Hb was decrease that is -9.7gm%, S.G.O.T was 34.0U/L, S.G.P.T was 32.0U/L, was normal at the time of discharge early ambulation, nutrition, psychological support was given. Therapeutic interventions and outcome: In the present case received syndopa 110/4, BD, orally. Tablet Zinc, OD, orally. Tablet Pan D, OD, orally., inj. Dexamethasone 2 mg I.V, T.D.S., Syrup Sumax, 10ml, BD. Now the patient condition is stable. Conclusion: This presented case of Wilson’s Disease is a rare disease condition. It is an autosomal recessive disease.In this case study, author mainly focus on expert medical management and excellent nursing care which leads to fast recovery of patient. After conversation with patient her response was positive and after nursing management and treatment she was discharged with satisfaction of recovery.

BACKGROUND The literature on white matter anatomy underlying the human orbitofrontal cortex (OFC) is scarce in spite of its relevance for glioma surgery. OBJECTIVE To describe the anatomy of the OFC and of the underlying white matter fiber anatomy, with a particular focus on the surgical structures relevant for a safe and efficient orbitofrontal glioma resection. Based on anatomical and radiological data, the secondary objective was to describe the growth pattern of OFC gliomas. METHODS The study was performed on 10 brain specimens prepared according to Klingler's protocol and dissected using the fiber microdissection technique modified according to U.T., under the microscope at high magnification. RESULTS A detailed stratigraphy of the OFC was performed, from the cortex up to the frontal horn of the lateral ventricle. The interposed neural structures are described together with relevant neighboring topographic areas and nuclei. Combining anatomical and radiological data, it appears that the anatomical boundaries delimiting and guiding the macroscopical growth of OFC gliomas are as follows: the corpus callosum superiorly, the external capsule laterally, the basal forebrain and lentiform nucleus posteriorly, and the gyrus rectus medially. Thus, OFC gliomas seem to grow ventriculopetally, avoiding the laterally located neocortex. CONCLUSION The findings in our study supplement available anatomical knowledge of the OFC, providing reliable landmarks for a precise topographical diagnosis of OFC lesions and for perioperative orientation. The relationships between deep anatomic structures and glioma formations described in this study are relevant for surgery in this highly interconnected area.

Summary Background Acute extrapyramidal movement disorders in dialysis patients are rare, inconsistently defined and have uncertain aetiology and prognosis. Aim Define diagnostic criteria, prognosis and risk factors Design and Methods Retrospective case series review of 20 patients (14 female, mean age 62 years) receiving dialysis for a median of 15 (interquartile range 4–35) months who presented with acute parkinsonism (AP = 11) or chorea/athetosis (CA = 9). Results All patients had type 2 diabetes (HbA1c 6.8 ± 1.0) and had received metformin. Lactic acidosis was present in 2 patients at presentation and serum lactate was elevated in 7/15 patients tested. No patient had abnormal copper or thyroid metabolism and 5/8 patients tested returned marginal abnormalities in heavy metal screening. Magnetic resonance imaging (MRI) revealed characteristic bilateral symmetric T2 hyperintensity of the basal ganglia (BG), predominantly putamen and globus pallidus (the lentiform nucleus) and more extensive involvement of the external and internal capsules in patients with AP presentation. Post-mortem demonstrated cytotoxic necrosis of the BG. Therapy included thiamine, intensive dialysis and cessation of metformin. Two patients died acutely, nine recovered and nine had residual symptoms. Median survival did not differ by presentation: AP 24 [95% confidence interval (CI) 21–27] and CA 33 (95% CI 32–35) months, P = 0.21. Conclusions There are two distinct clinical extrapyramidal movement disorders associated with specific diagnostic MRI imaging that support the diagnosis of the extrapyramidal syndromes of chronic kidney disease and dialysis. The associations with diabetes, metformin and metabolic acidosis suggest a common pathogenic mechanism but require additional study. Early recognition and treatment may improve outcomes.

Background Tourette syndrome (TS) is a neurodevelopmental disorder defined by the continual presence of primary motor and vocal tics. Grey matter abnormalities have been identified in numerous studies of TS, but conflicting results have been reported. This study was an unbiased statistical meta-analysis of published neuroimaging studies of TS structures. Methods A voxel quantitative meta-analysis technique called activation likelihood estimation (ALE) was used. The meta-analysis included six neuroimaging studies involving 247 TS patients and 236 healthy controls. A statistical threshold of p Results We found that grey matter volumes were significantly increased in the bilateral thalamus, right hypothalamus, right precentral gyrus, left postcentral gyrus, left inferior parietal lobule, right lentiform nucleus, and left insula of TS patients compared to those of healthy controls. In contrast, grey matter volumes were significantly decreased in the bilateral postcentral gyrus, bilateral anterior cingulate, bilateral insula, left posterior cingulate and left postcentral gyrus of TS patients compared to those of healthy controls. Conclusions Our present meta-analysis primarily revealed significant increases in grey matter volumes in the thalamus and lentiform nucleus, and decreased grey matter volumes in the anterior cingulate gyrus, of TS patients compared to those in healthy controls. Most of these identified regions are associated with cortico-striato-thalamo-cortical circuits. Further studies with larger sample sizes are needed to confirm these changes in grey matter volumes in TS patients.

Iron plays an important role in many neurobiological processes, especially in the basal ganglia, the brain structures with the highest concentration. Composed of the pallidum and putamen, the lentiform nucleus plays a key role in the basal ganglia circuitry. With MRI advances, iron-based sequences such as R2* and quantitative susceptibility mapping (QSM) are now available for detecting and quantifying iron in different brain structures. Since their validation using classic iron detection techniques (histology or physical techniques), these sequences have attracted growing clinical attention, especially in the field of extrapyramidal syndromes that particularly affect the basal nuclei. Accurate mapping of iron in these nuclei and their connections is needed to gain a better understanding of this specific anatomy, before considering its involvement in the physiopathological processes. We performed R2* and QSM along with Perls histology, to gain new insights into the distribution of iron in the lentiform nucleus and its surrounding structures, based on four specimens obtained from voluntary donors. We found that iron is preferentially distributed in the anterior part of the globus pallidus externus and the posterior part of the putamen. The lateral wall of the putamen is iron-poor, compared with the lateral medullary lamina and intraputaminal fibers. The relevance of perivascular iron concentration, along with pallido- and putaminofugal iron-rich fibers, is discussed.

The most common approaches in the treatment of epilepsy, the trans-sylvian selective amygdalohippocampectomy (SAH) and the anterior temporal lobe resection (ATLR) reach the medial temporal lobe through different surgical routes. Our aim was to delineate the white matter (WM) fiber tracts at risk in relation to trans-sylvian SAH and ATLR by defining each fascicle en route to medial temporal lobe during each approach. ATLR and trans-sylvian SAH were performedand related WM tracts en route to medial temporal region were presented in relation to the relevant approaches and surrounding neurovascular structures. The WM tracts most likely to be disrupted during trans-sylvian SAH along the roof of the temporal horn were the UF - and less commonly IFOF - at the layer of the external capsule, anterior commissure, anterior bend of optic radiations, and sublenticular internal capsule. Amygdaloid projections to the claustrum, putamen and globus pallidus, the tail of caudate and the peduncle of the lentiform nucleus were also in close proximity to the resection cavity. Fiber tracts most likely to be impaired during ATLR included the UF, ILF, IFOF, anterior commissure, optic radiations, and, less likely, the vertical ventral segment of the arcuate fascicle. Both ATLR and trans-sylvian SAH carry the risk of injury to WM pathways, which may result in unpredictable functional loss. A detailed 3-D knowledge of the related connectional anatomy will help subside neurocognitive, neuroophtalmologic, neurolinguistic complications of epilepsy surgery, providing an opportunity to tailor the surgery according to patient's unique connectional and functional anatomy.

Objective. To explore altered regional neuronal activity in patients with nonarteritic anterior ischemic optic neuropathy (NAION) and its correlation with clinical performances using the regional homogeneity (ReHo) method, which is based on resting-state functional magnetic resonance imaging (fMRI). Method. Thirty-one patients with NAION (20 males, 11 females) and 31 age- and sex-matched normal controls (NCs) (20 males, 11 females) were enrolled in the study. All patients underwent ophthalmic examination, including eyesight, intraocular pressure measurement, optimal coherence tomography (OCT), visual field analysis, and fMRI scans. After ReHo was calculated, we investigated group differences in results between the patients and NCs. We analyzed the relationship between ReHo values for different brain regions in patients with NAION and intraocular pressure, visual field analysis, and OCT. A receiver operating characteristic (ROC) curve was used to assess the diagnostic ability of the ReHo method. Results. Compared with NCs, patients with NAION exhibited higher ReHo values in the left middle frontal gyrus, left middle cingulate gyrus, left superior temporal gyrus, and left inferior parietal lobule. Additionally, they exhibited lower ReHo values in the right lingual gyrus, left putamen/lentiform nucleus, and left superior parietal lobule. ReHo values in the left superior parietal lobule were negatively correlated with right retinal nerve fiber layer values (r=−0.462, P=0.01). The area under the ROC curve for each brain region indicated that the ReHo method is a credible means of diagnosing patient with NAION. Conclusion. NAION was primarily associated with dysfunction in the default mode network, which may reflect its underlying neural mechanisms.

Background The caudate nucleus is a C-shaped structure that is located in the center of the brain and is divided into 3 parts: the head, body, and tail. Methods We detail the anatomic connections, relationships with other basal ganglia structures, and clinical implications of injury to the caudate nucleus. Results Anatomically, the most inferior transcapsular gray matter is the lentiform peduncle, which is the connection between the lentiform nucleus and caudate nucleus as well as the amygdala. The border between the tail and body of the caudate nucleus is the posterior insular point. The tail of the caudate nucleus is extraependymal in some parts and intraependymal in some parts of the roof of the temporal horn of the lateral ventricle. The tail of the caudate nucleus crosses the inferior limiting sulcus (temporal stem), and section of the tail during approaches to lesions involving the temporal stem may cause motor apraxia. The mean distance from the temporal limen point, which is the junction of the limen insula and inferior limiting sulcus, to the tail of the caudate nucleus in the temporal stem is 15.87 ± 3.10 mm. Conclusions Understanding of the functional anatomy and connections of the distinct parts of the caudate nucleus is essential for deciding the extent of resection of lesions involving the caudate nucleus and the types of deficits that may be found postoperatively.

Recent evidence of gadolinium deposition in the brain has raised safety concerns. Iron oxide nanoparticles are re-emerging as promising alternative MR contrast agents, because the iron core can be metabolized. However, long-term follow up studies of the brain after intravenous iron oxide administration have not been reported thus far. In this study, we investigated, if intravenously administered ferumoxytol nanoparticles are deposited in porcine brains. Methods: In an animal care and use committee-approved prospective case-control study, ten Gottingen minipigs received either intravenous ferumoxytol injections at a dose of 5 mg Fe/kg (n=4) or remained untreated (n=6). Nine to twelve months later, pigs were sacrificed and the brains of all pigs underwent ex vivo MRI at 7T with T2 and T2*-weighted sequences. MRI scans were evaluated by measuring R2* values (R2*=1000/T2*) of the bilateral caudate nucleus, lentiform nucleus, thalamus, dentate nucleus, and choroid plexus. Pig brains were sectioned and stained with Prussian blue and evaluated for iron deposition using a semiquantitative scoring system. Data of ferumoxytol exposed and unexposed groups were compared with an unpaired t-test and a Mann-Whitney U test. Results: T2 and T2* signal of the different brain regions was not visually different between ferumoxytol exposed and unexposed controls. There were no significant differences in R2* values of the different brain regions in the ferumoxytol exposed group compared to controls (p>0.05). Prussian blue stains of the same brain regions, scored according to a semiquantitative score, were not significantly different either between the ferumoxytol exposed group and unexposed controls (p>0.05). Conclusions: Our study shows that intravenous ferumoxytol doses of 5-10 mg Fe/kg do not lead to iron deposition in the brain of pigs. We suggest iron oxide nanoparticles as a promising alternative for gadolinium-enhanced MRI.

BackgroundPrevious studies have found that elevated copper levels induce oxidation, which correlates with the occurrence of major depressive disorder (MDD). However, the mechanism of abnormal cerebral metabolism of MDD patients remains ambiguous. The main function of the enzyme ATPase copper-transporting alpha (ATP7A) is to transport copper across the membrane to retain copper homeostasis, which is closely associated with the onset of mental disorders and cognitive impairment. However, less is known regarding the association of ATP7A expression in MDD patients.MethodsA total of 31 MDD patients and 21 healthy controls were recruited in the present study. Proton magnetic resonance spectroscopy was used to assess the concentration levels of N-acetylaspartate, choline (Cho), and creatine (Cr) in brain regions of interest, including prefrontal white matter (PWM), anterior cingulate cortex (ACC), thalamus, lentiform nucleus, and cerebellum. The mRNA expression levels of ATP7A were measured using polymerase chain reaction (SYBR Green method). The correlations between mRNA expression levels of ATP7A and/or ceruloplasmin levels and neuronal biochemical metabolite ratio in the brain regions of interest were evaluated.ResultsThe decline in the mRNA expression levels of ATP7A and the increase in ceruloplasmin levels exhibited a significant correlation in MDD patients. In addition, negative correlations were noted between the decline in mRNA expression levels of ATP7A and the increased Cho/Cr ratios of the left PWM, right PWM, and right ACC in MDD patients. A positive correlation between elevated ceruloplasmin levels and increased Cho/Cr ratio of the left PWM was noted in MDD patients.ConclusionsThe findings suggested that the decline in the mRNA expression levels of ATP7A and the elevated ceruloplasmin levels induced oxidation that led to the disturbance of neuronal metabolism in the brain, which played important roles in the pathophysiology of MDD. The decline in the mRNA expression levels of ATP7A and the elevated ceruloplasmin levels affected neuronal membrane metabolic impairment in the left PWM, right PWM, and right ACC of MDD patients.

Transcranial sonography (TCS) can reveal pathology in brain structures including insula. This study compared insula echogenicity among 22 patients with Wilson's disease (WD), 21 patients with early-onset Parkinson's disease (EO-PD) and 24 healthy patients. Echogenicity of predefined brain structures (insula, lentiform nucleus, caudate nucleus, substantia nigra and raphe nuclei) was evaluated using digitized analysis of TCS fusion imaging with magnetic resonance. Cortical, subcortical and cerebellar atrophy and ventricle diameters were determined from magnetic resonance images. The mean echogenicity index of insula did not differ between males and females (p = 0.92), but the echogenicity of insula was higher in patients with WD than in patients with EO-PD and healthy patients (p0.05). The substantia nigra echogenicity was higher in patients with EO-PD, and lentiform nucleus echogenicity was higher in patients with WD (p0.05). The echogenicity of insula correlated with lentiform nucleus echogenicity (r = 0.75) but not with age (r = -0.14), disease duration (r = -0.36), symptom severity (r = 0.28), cortical (r = 0.11) nor subcortical (r = 0.05) atrophy.

BackgroundStudies of Internet gaming disorder (IGD) suggest an imbalanced relationship between cognitive control and reward processing in people with IGD. However, it remains unclear how these two systems interact with each other, and whether they could serve as neurobiological markers for IGD.MethodsFifty IGD subjects and matched individuals with recreational game use (RGU) were selected and compared when they were performing a cue-craving task. Regions of interests [anterior cingulate cortex (ACC), lentiform nucleus] were selected based on the comparison between brain responses to gaming-related cues and neutral cues. Directional connectivities among these brain regions were determined using Bayesian estimation. We additionally examined the posterior cingulate cortex (PCC) in a separate analysis based on data implicating the PCC in craving in addiction.ResultsDuring fixed-connectivity analyses, IGD subjects showed blunted ACC-to-lentiform and lentiform-to-ACC connectivity relative to RGU subjects, especially in the left hemisphere. When facing gaming cues, IGD subjects trended toward lower left-hemispheric modulatory effects in ACC-to-lentiform connectivity than RGU subjects. Self-reported cue-related craving prior to scanning correlated inversely with left-hemispheric modulatory effects in ACC-to-lentiform connectivity.ConclusionsThe results suggesting that prefrontal-to-lentiform connectivity is impaired in IGD provides a possible neurobiological mechanism for difficulties in controlling gaming-cue-elicited cravings. Reduced connectivity ACC-lentiform connectivity may be a useful neurobiological marker for IGD.

Minimal hepatic encephalopathy (MHE) is characterized by diffuse abnormalities in cerebral structure, such as reduced cortical thickness and altered brain parenchymal volume. This study tested the potential of gray matter (GM) volumetry to differentiate between cirrhotic patients with and without MHE using a support vector machine (SVM) learning method. High-resolution, T1-weighted magnetic resonance images were acquired from 24 cirrhotic patients with MHE and 29 cirrhotic patients without MHE (NHE). Voxel-based morphometry was conducted to evaluate the GM volume (GMV) for each subject. An SVM classifier was employed to explore the ability of the GMV measurement to diagnose MHE, and the leave-one-out cross-validation method was used to assess classification accuracy. The SVM algorithm based on GM volumetry achieved a classification accuracy of 83.02%, with a sensitivity of 83.33% and a specificity of 82.76%. The majority of the most discriminative GMVs were located in the bilateral frontal lobe, bilateral lentiform nucleus, bilateral thalamus, bilateral sensorimotor areas, bilateral visual regions, bilateral temporal lobe, bilateral cerebellum, left inferior parietal lobe, and right precuneus/posterior cingulate gyrus. Our results suggest that SVM analysis based on GM volumetry has the potential to help diagnose MHE in cirrhotic patients.

Poststroke complex regional pain syndrome (CRPS) is characterized by swelling, pain, and changes in the skin that appear on the affected wrist and hand. In this retrospective study, we analyzed the relationship between poststroke CRPS and the location of stroke lesion. From all patients admitted to our hospital from 2009 to 2019, we recruited 80 patients affected by their first unilateral stroke who met the inclusion/exclusion criteria. Thirty-eight patients diagnosed with CRPS after stroke were assigned to the experimental group according to the "Budapest criteria" adopted by the International Association for the Study of Pain, and 42 patients without CRPS were included as controls. Regions of interest were manually drawn on T1-weighted magnetic resonance images, and data were normalized to a standard brain template. In the poststroke CRPS group, the relationship between the location of brain lesion and pain severity was analyzed using Freedman-Lane multivariable regression adjusting for Medication Quantification Scale rating, which was the only parameter to show a statistically significant correlation with pain intensity. A threshold of P < 0.01 was considered statistically significant for all voxel-based lesion symptom mapping tests, corrected for multiple comparisons with 5000 permutations. Analyses using voxel-wise subtraction and Liebermeister statistics indicated that the corticospinal tract (CST) was associated with the development of poststroke CRPS. Statistically significant correlations were found between pain intensity and the CST and the adjacent lentiform nucleus. Our results suggest that the CST may be a relevant neural structure for development of poststroke CRPS and the intensity of pain caused by the syndrome.

Chorea‑hemiballismus is the most common movement disorder, and it commonly results from vascular lesions in the subthalamic nucleus. Rarely, it can result from lacunar infarcts. Here is illustrated a 95‑year‑old male with sudden‑onset left-sided chorea‑hemiballismus of 2 weeks, without any other neurological deficit, who was not a diabetic patient and had no form of acidosis or electrolyte abnormality. Computerized tomogram, serial 32 slides pre‑ and post‑contrast images showed small non-enhancing, hypodense foci within the right frontal subcortical region adjacent to the frontal horn of the right lateral ventricle as well as within the lentiform nucleus. There were no mass effects seen. A diagnosis of hemiballismus from subcortical lacunar infarct was made. The hemiballismus was controlled after 2 weeks of haloperidol and clonazepam therapy, among others, with a substantial reduction in the abnormal movements. Hemiballismus attributable to subcortical lacunar infarcts though rare was presented. Keywords: Hemiballismus, lacunar infarcts, lentiform nucleus, Nigeria, subcortical infarcts, subthalamic nucleus

Introduction: Cognitive decline is the core schizophrenia symptom, which is now well accepted. Holding a role in various aspects of cognition, lentiform nucleus (putamen and globus pallidus) dysfunction contributes to the psychopathology of this disease. However, the effects of lentiform nucleus function on cognitive impairments in schizophrenia are yet to be investigated.Objectives: We aim to detect the fractional amplitude of low-frequency fluctuation (fALFF) alterations in patients with schizophrenia, and examine how their behavior correlates in relation to the cognitive impairments of the patients.Methods: All participants underwent magnetic resonance imaging (MRI) and cognitive assessment (digit span and digit symbol coding tests). Screening of brain regions with significant changes in fALFF values was based on analysis of the whole brain. The data were analyzed between Jun 2020 and Mar 2021. There were no interventions beyond the routine therapy determined by their clinicians on the basis of standard clinical practice.Results: There were 136 patients (75 men and 61 women, 24.1 ± 7.4 years old) and 146 healthy controls (82 men and 64 women, 24.2 ± 5.2 years old) involved in the experiments seriatim. Patients with schizophrenia exhibited decreased raw scores in cognitive tests (p < 0.001) and increased fALFF in the bilateral lentiform nuclei (left: 67 voxels; x = −24, y = −6, z = 3; peak t-value = 6.90; right: 16 voxels; x = 18, y = 0, z = 3; peak t-value = 6.36). The fALFF values in the bilateral lentiform nuclei were positively correlated with digit span-backward test scores (left: r = 0.193, p = 0.027; right: r = 0.190, p = 0.030), and the right lentiform nucleus was positively correlated with digit symbol coding scores (r = 0.209, p = 0.016).Conclusion: This study demonstrates that cognitive impairments in schizophrenia are associated with lentiform nucleus function as revealed by MRI, involving working memory and processing speed.

Acute to subacute onset chorea is commonly due to stroke, metabolic, post-infectious, and autoimmune disorders. Chorea in diabetes (DM) patient is mostly due to hyperglycemia, and few cases were reported due to hypoglycemia. The mechanism at the cellular level is still evolving. The MRI changes in diabetic chorea patients are variably reported. It is important to discuss our patient with hypoglycemic hemichorea because of unique features like low BMI, recently diagnosed DM on sulphonylurea with a history of hypoglycemic episodes, and acute left hemichorea that was controlled with neuroleptics, and her MRI brain showed reversible lentiform nucleus T1 hyperintensity without diffusion restriction and blooming on SWI.

Parkinson disease (PD) is a heterogeneous neurodegenerative disorder. Dopamine transporter imaging using 123I-2β-carbomethoxy-3β-(4-iodophenyl)-N-(3-fluoropropyl)-nortropane (FP-CIT) and noradrenergic cardiac imaging using 123I-meta-iodobenzylguanidine (MIBG) have been used in combination or separately to study PD patients. Published results regarding uptake of the 2 tracers in each motor subtype are fairly abundant and mostly in agreement. However, data on the intrasubject association between dopaminergic and noradrenergic systems in PD patients are relatively scant and vary. We aimed to assess the intrasubject relationship between striatal dopamine transporter density using a PET tracer and cardiac sympathetic innervation in tremor-dominant subtype (TD) and akinetic-rigid subtype (AR) of PD. This study has a cross-sectional design. Thirty-one patients with early PD (17 TD/14 AR) who underwent both 123I-MIBG cardiac scintigraphy and 18F-FP-CIT PET/CT were retrospectively selected. We assessed the relationship between heart-to-mediastinum ratio (H/M) of 123I-MIBG and specific (striatal)-to-nonspecific (cerebellar) dopamine transporter binding ratio (S/N) measured from 4 separate regions-of-interest (bilateral caudate nuclei and lentiform nuclei) of 18F-FP-CIT in each motor subtype. S/N of all 4 striatal regions were significantly lower in the AR subgroup than in the TD subgroup. H/M was not significantly different. There was a significant intrasubject correlation between H/M and S/N of the lentiform nucleus in AR-PD but no correlation between H/M and any of 4 S/N in TD-PD. Our data suggest a coupled degeneration of nigrostriatal dopaminergic and myocardial sympathetic denervation in AR subtype, but not in TD subtype, of early PD patients. These different results between the 2 motor subtypes likely reflects the heterogeneous pathophysiology of PD.

Background: Schistosomiasis is a helminthic infestation of public health importance. Central nervous system involvement is a severe but under reported complication. Case report: This was a case of neuroschistosomiasis in an eight year old male who lived in a rural community in Enugu, South East Nigeria. Patient had presented with terminal haematuria, headache and neurological complications. Urine microscopy showed many ova of schistosoma haematobium while ultrasound showed urinary bladder base changes that appeared irregular with hyper echoic mucosa and focal mucosal thickening on the right side. Computed tomography of the brain revealed a hyper dense oval area surrounded by an irregular hypo dense area in the left parietal region overlying the left thalamus and lentiform nucleus. Patient showed good clinical response to praziquantel and corticosteroid. Conclusion: Neuroschistosomiasis is a rare complication of schistosomiasis. A high index of suspicion should be entertained in endemic areas as early treatment with praziquantel and steroids has good outcome.

Over the past few decades, it has been recognized that traumatic brain injury (TBI) may result in various movement disorders. However, moderate or mild TBI only rarely causes persistent post-traumatic movement disorders. In the present report, we describe a case of secondary tremor due to a mild head injury with a transitory loss of consciousness. A 26-year-old man developed an isolated rest tremor of the hands and legs without other neurologic signs. The interval between the head trauma and the onset of the symptoms was 4 months. Neuroimaging studies reveled gliosis in the lentiform nucleus. Haloperidol administration resulted in tremor reduction. A rest tremor, similar to essential tremor, can be a rare complication of head trauma. Haloperidol may be an effective and safe treatment modality for post-traumatic tremor. Further studies are needed to clarify the optimal drug for the treatment of post-traumatic tremor.

Neuropsychiatric disease has polygenic determinants but is often precipitated by environmental pressures, including adverse perinatal events. However, the way in which genetic vulnerability and early-life adversity interact remains obscure. We hypothesised that the extreme environmental stress of prematurity would promote neuroanatomic abnormality in individuals genetically vulnerable to psychiatric disorders. In 194 unrelated infants (104 males, 90 females), born before 33 weeks of gestation (mean gestational age 29.7 weeks), we combined Magnetic Resonance Imaging with a polygenic risk score (PRS) for five psychiatric pathologies to test the prediction that: deep grey matter abnormalities frequently seen in preterm infants are associated with increased polygenic risk for psychiatric illness. The variance explained by the PRS in the relative volumes of four deep grey matter structures (caudate nucleus, thalamus, subthalamic nucleus and lentiform nucleus) was estimated using linear regression both for the full, mixed ancestral, cohort and a subsample of European infants. Psychiatric PRS was negatively associated with lentiform volume in the full cohort (β = −0.24, p = 8 × 10−4) and a European subsample (β = −0.24, p = 8 × 10−3). Genetic variants associated with neuropsychiatric disease increase vulnerability to abnormal lentiform development after perinatal stress and are associated with neuroanatomic changes in the perinatal period.

The brainstem has been a focus of sudden infant death syndrome (SIDS) research with amassing evidence of increased neuronal apoptosis. The present study extends the scope of brain regions examined and determines associations with known SIDS risk factors. Immunohistochemical expression of cell death markers, active caspase-3 and TUNEL, was studied in 37 defined brain regions in infants (aged 1–12 months) who died suddenly and unexpectedly (SUDI). A semi-quantitative mean score of marker expression was derived for each region and scores compared between three SUDI subgroups: explained SUDI (eSUDI; n = 7), SIDS I (n = 8) and SIDS II (n = 13). In eSUDI, active caspase-3 scores were highest in several nuclei of the rostral medulla, and lowest in the hypothalamus and cerebellar grey matter (GM). TUNEL was highest in regions of the hippocampus and basal ganglia, and lowest in the thalamus and cerebellar GM. TUNEL scores were higher in SIDS II compared to eSUDI in the amygdala (p = 0.03) and 5/9 nuclei in the rostral medulla (p = 0.04 − 0.01), and higher in SIDS II compared to SIDS I in the amygdala (p

A 73-year-old woman with hyperammonemic encephalopathy presented with recurrent, transient episodes of diminished memory and confusion that lasted for 2–3 days. Except for ammonia levels of 208.7 μ mol/L (normal range 10.71–32.13 µmol/L), the laboratory tests, including all liver tests, were normal. Neuropsychological assessment showed cognitive decline (4/30 on Mini-Mental State Examination and 1/30 on Montreal Cognitive Assessment). EEG showed triphasic waves, which disappeared along with clinical remission. MRI showed bilateral symmetrical lesions in cortex, cingulate, lentiform nucleus, and insular (figure 1).1 Abdominal CT angiography found congenital portosystemic shunts connecting the superior mesenteric vein and the inferior vena cava, without liver cirrhosis signs (figure 2).2