Cerebral Basal Ganglia Research Articles

Using Single-Photon Emission Computerized Tomography on Patients With Positive Quantitative Electroencephalogram to Evaluate Chronic Mild Traumatic Brain Injury With Persistent Symptoms.

BackgroundFollowing mild traumatic brain injury (mTBI), also known as concussion, many patients with chronic symptoms (>3 months post injury) receive conventional imaging such as computed tomography (CT) or magnetic resonance imaging (MRI). However, these modalities often do not show changes after mTBI. We studied the benefit of triaging patients with ongoing symptoms >3 months post injury by quantitative electroencephalography (qEEG) and then completing a brain single positron emission computed tomography (SPECT) to aid in diagnosis and early detection of brain changes.MethodsWe conducted a retrospective case review of 30 outpatients with mTBI. The patients were assessed by a neurologist, consented, and received a qEEG, and if the qEEG was positive, they consented and received a brain SPECT scan. The cases and diagnostic tools were collectively reviewed by a multidisciplinary group of physicians in biweekly team meetings including neurology, nuclear medicine, psychiatry, neuropsychiatry, general practice psychotherapy, neuro-ophthalmology, and chiropractic providers. The team noted the cause of injury, post injury symptoms, relevant past medical history, physical examination findings, and diagnoses, and commented on patients' SPECT scans. We then analyzed the SPECT scans quantitatively using the 3D-SSP software.ResultsAll the patients had cerebral perfusion abnormalities demonstrated by SPECT that were mostly undetectable by conventional imaging (CT/MRI). Perfusion changes were localized primarily in the cerebral cortex, basal ganglia, and cingulate cortex, and correlated with the patients' symptoms and examination findings. Qualitative and quantitative analyses yielded similar results. Most commonly, the patients experienced persistent headache, memory loss, concentration difficulties, depression, and cognitive impairment post mTBI. Because of their symptoms, most of the patients were unable to return to their previous employment and activity level.ConclusionOur findings outline the physical basis of neurological and psychiatric symptoms experienced by patients with mTBI. Increased detection of mTBI can lead to development of improved targeted treatments for mTBI and its various sequelae.

3.0 Tesla normative diffusivity in 3rd trimester fetal brain.

Apparent diffusion coefficient (ADC) values in the developing fetus provide valuable information on the diagnosis and prognosis of prenatal brain pathologies. Normative ADC data has been previously established in 1.5T MR scanners but lacking in 3.0T scanners. Our objective was to measure ADC values in various brain areas in a cohort of normal singleton fetuses scanned in a 3.0T MR scanner. DWI (diffusion-weighted imaging) was performed in 47 singleton fetuses with normal or questionably abnormal results on sonography followed by normal structural MR imaging. ADC values were measured in cerebral lobes (frontal, parietal, temporal lobes), basal ganglia, and pons. Regression analysis was used to examine gestational age-related changes in regional ADC. Median gestational age was 30.1weeks (range, 26-34weeks). There was a significant effect of region on ADC values, whereby ADC values were highest in cerebral lobes (parietal > frontal > temporal lobes), compared with basal ganglia. The lowest values were found in the pons. On regression analysis, there was a decrease in ADC values in basal ganglia and pons with increasing gestational age. ADC values in frontal, parietal, and temporal lobes were stable in our cohort. Regional brain ADC values in 3.0T scanners are comparable with previously reported values in 1.5T scanners, with similar changes over gestational age. Using 3.0T scanners is increasing worldwide. For fetal imaging, establishing normal ADC values is critical as DWI enables a sensitive and quantitative technique to evaluate normal and abnormal brain development.

Decompression Illness in Repetitive Breath-Hold Diving: Why Ischemic Lesions Involve the Brain?

Nitrogen (N2) accumulation in the blood and tissues can occur due to breath-hold (BH) diving. Post-dive venous gas emboli have been documented in commercial BH divers (Ama) after repetitive dives with short surface intervals. Hence, BH diving can theoretically cause decompression illness (DCI). “Taravana,” the diving syndrome described in Polynesian pearl divers by Cross in the 1960s, is likely DCI. It manifests mainly with cerebral involvements, especially stroke-like brain attacks with the spinal cord spared. Neuroradiological studies on Ama divers showed symptomatic and asymptomatic ischemic lesions in the cerebral cortex, subcortex, basal ganglia, brainstem, and cerebellum. These lesions localized in the external watershed areas and deep perforating arteries are compatible with cerebral arterial gas embolism. The underlying mechanisms remain to be elucidated. We consider that the most plausible mechanisms are arterialized venous gas bubbles passing through the lungs, bubbles mixed with thrombi occlude cerebral arteries and then expand from N2 influx from the occluded arteries and the brain. The first aid normobaric oxygen appears beneficial. DCI prevention strategy includes avoiding long-lasting repetitive dives for more than several hours, prolonging the surface intervals. This article provides an overview of clinical manifestations of DCI following repetitive BH dives and discusses possible mechanisms based on clinical and neuroimaging studies.

Idiopathic Moyamoya Disease Presenting as Isolated Hemichorea

AbstractThe study aimed to describe a case of a 7-year-old Caucasian girl who developed isolated chorea in her right upper and lower extremities progressively increasing over 2 years. This study is a case report and conducted at tertiary care center. A 7-year-old Caucasian girl who gradually developed worsening choreiform movements in her right upper and lower extremities over the course of 2 years until medical attention was sought. Literature review of children presenting with chorea as the only manifestation in moyamoya disease. A 7-year-old right-handed Caucasian girl presented with progressively worsening choreiform movements in her right upper and lower extremities affecting her fine motor skills and gait impairment There was no weakness, hyperreflexia, or spasticity on her neurological exam. Neuroimaging studies showed “ivy sign,” asymmetric prominence of vessels within the subarachnoid spaces overlying the left cerebral hemisphere with corresponding serpiginous T2 fluid-attenuated inversion recovery abnormality, but no parenchymal volume loss or diffusion restriction. Magnetic resonance angiography showed focal moderate-to-severe stenosis at the junction of the paraophthalmic and supraclinoid segments of the left internal carotid artery, with poststenotic dilatation. Angiography demonstrated focal stenosis involving the ophthalmic segment of the left internal carotid artery with 50% stenosis. There was compensation through a medium sized left posterior communicating artery as well as posterior cerebral artery to middle cerebral artery and anterior cerebral artery collateralization. Brain single-photon emission computerized tomography scan showed no evidence of perfusion defects in the cerebral hemispheres, basal ganglia, or thalami. She underwent successful revascularization procedure (left pial synangiosis) with resolution of her choreiform movements and normalization of her gait. Our case demonstrates that moyamoya disease should be suspected when evaluating a child with hemichorea and describes resolution of symptoms after revascularization surgery. Neuroimaging and vascular studies should be obtained in children with unilateral movement disorder.

Compressed Sensing Algorithm-Based Magnetic Resonance Imaging Guided for Prognosis of Early Neurological Deterioration after Intravenous Thrombolysis in Ischemic Stroke Patients

This work was aimed to study the risk factors and prognostic treatment for acute ischemic stroke (AIS) patients with early neurological deterioration (END) after intravenous thrombolytic therapy via compressed sensing algorithm-based magnetic resonance imaging (CS-MRI). 231 patients who were diagnosed with AIS were selected, and the final involved number of patients was 182. Patients with AIS were treated with intravenous thrombolysis with alteplase within 4.5 hours of onset. After treatment, patients with early neurological deterioration were defined as the deteriorating group and those without early neurological impairment were defined as the nondeteriorating group. In univariate analysis, hypertension, white blood cell count, and National Institutes of Health Stroke Scale (NIHSS) score were correlated with the occurrence of END. Under the CS-MRI theory, the two groups of patients were evaluated for middle cerebral artery basal ganglia infarction and internal watershed infarction. After univariate analysis, the P < 0.1 variables were taken as the independent variable, and the binary logistic regression model was adopted for multivariate regression analysis. It was disclosed that NIHSS score was not correlated with the occurrence of early neurological function deterioration, while homocysteine was. Hypertension, white blood cell count, homocysteine, and NIHSS score were risk factors for END. The image analysis revealed that the incidence of deteriorating basal ganglia infarction group was lower relative to the nondeteriorating group, and the incidence of watershed infarction was higher in the deteriorating group versus the nondeteriorating group. The image analysis suggested that predicting the occurrence of END through risk factors can actively provide endovascular treatment for patients with AIS.

PRRT2 Related Epilepsies: A Gene Review

AbstractPRRT2 encodes for proline-rich transmembrane protein 2 involved in synaptic vesicle fusion and presynaptic neurotransmitter release. Mutations in human PRRT2 have been related to paroxysmal kinesigenic dyskinesia (PKD), infantile convulsions with choreoathetosis, benign familial infantile epilepsies, and hemiplegic migraine. PRRT2 mutations cause neuronal hyperexcitability, which could be related to basal ganglia or cortical circuits dysfunction, leading to paroxysmal disorders. PRRT2 is expressed in the cerebral cortex, basal ganglia, and cerebellum. Approximately, 90% of pathogenic variants are inherited and 10% are de novo. Paroxysmal attacks in PKD are characterized by dystonia, choreoathetosis, and ballismus. In the benign familial infantile epilepsy (BFIE), seizures are usually focal with or without generalization, usually begin between 3 and 12 months of age and remit by 2 years of age. In 30% of cases of PRRT2-associated PKD, there is an association with BFIE, and this entity is referred to as PKD with infantile convulsions (PKD/IC). PRRT2 mutations are the cause of benign family childhood epilepsy and PKD/IC. On the other hand, PRRT2 mutations do not seem to correlate with other types of epilepsy. The increasing incidence of hemiplegic migraine in families with PRRT2-associated PKD or PKD/IC suggests a common disease pathway, and it is possible to assert that BFIE, paroxysmal kinesigenic dyskinesia, and PKD with IC belong to a continuous disease spectrum of PRRT2-associated diseases.

HYDRANCEPHALY : RARE ENTITY WITH INCIDENCE LESS THAN 1 IN 10000 LIVE BIRTHS

Hydranencephaly is a rare entity with incidence of 1 in 10000 live births and is characterized by near total absence of cerebral cortex and basal ganglia which are replaced by cerebrospinal fluid. Various aetiologies of hydranencephaly have been suggested which include: Infarction, leukomalacia, diffuse hypoxic-ischemic brain necrosis, intrauterine infections leading to necrotizing vasculitis. Ultrasonography, Computed Tomography and Magnetic Resonance Imaging can easily detect and diagnose hydranencephaly. We present a case of 2-month-old term infant diagnosed with hydranencephaly on computed tomography.

Neuroregenerative evidences demonstrated by diverse MRI analysis in cerebral palsy children who showed significant clinical improvement following repeated G-CSF injection

Background & Aim We tried to confirm the structural changes of magnetic resonance imaging (MRI) and their relation with clinical improvement in cerebral palsy (CP) children who treated with repeated granulocyte colony-stimulating factor (G-CSF) injection. Methods, Results & Conclusion We performed a phase II, randomized placebo controlled clinical trials to reveal clinical improvement after repeated G-CSF injection. Forty-four children with CP were enrolled, and their ages were 2-10 years old. G-CSF (5μg/kg) was administered for 5 days subcutaneously every 3 months during 18 months. We evaluated motor and cognitive functions along with MRI study. To compare the structural changes of MRI between treated and placebo groups, we analyzed the white matter integrity in region of interest as well as in functional networks. We also analyzed the subcortical volume and cortical thickness in MRI. The treated group showed significantly greater increases in cognitive function scores noted in picture memory subtest and expressive vocabulary test as well as increasing tendency in visual motor integrity test. Diverse neuroimaging analysis revealed decrease of mean diffusivity (MD) of region of superior longitudinal fasciculus and cingulum, and also decrease of MD of sensori-motor network and language network. Increase of cortical thickness of left inferior frontal gyrus was also noted. These changes suggested structural improvement in circuit of sensori-motor information and motor language area, and were compatible with the improvement of picture memory and expressive language in cognitive function tests. By the same method of analysis, the structural improvement in the area of cerebral cortex and basal ganglia were noted, which suggest the improvement of visual motor integration in cognitive function tests. The increase of subcortical volume of nucleus accumbens was also noted, suggesting improvement of socialization. In conclusion, we demonstrated the neuroregenerative evidences by diverse MRI analysis as well as the improvement of cognitive functions after repeated G-CSF injection in children with CP.

POSTERIOR FOSSA MENINGIOMA WITH CEREBELLAR MASS EFFECT PRESENTING AS DECLINE IN COGNITIVE FUNCTION AND IMPAIRED AFFECTIVE MODULATION: REVIEW OF THE CEREBELLAR COGNITIVE AFFECTIVE SYNDROME

POSTERIOR FOSSA MENINGIOMA WITH CEREBELLAR MASS EFFECT PRESENTING AS DECLINE IN COGNITIVE FUNCTION AND IMPAIRED AFFECTIVE MODULATION: REVIEW OF THE CEREBELLAR COGNITIVE AFFECTIVE SYNDROME

Attentional Reinforcement Learning in the Brain

Recently, attention mechanisms have significantly boosted the performance of natural language processing using deep learning. An attention mechanism can select the information to be used, such as by conducting a dictionary lookup; this information is then used, for example, to select the next utterance word in a sentence. In neuroscience, the basis of the function of sequentially selecting words is considered to be the cortico-basal ganglia-thalamocortical loop. Here, we first show that the attention mechanism used in deep learning corresponds to the mechanism in which the cerebral basal ganglia suppress thalamic relay cells in the brain. Next, we demonstrate that, in neuroscience, the output of the basal ganglia is associated with the action output in the actor of reinforcement learning. Based on these, we show that the aforementioned loop can be generalized as reinforcement learning that controls the transmission of the prediction signal so as to maximize the prediction reward. We call this attentional reinforcement learning (ARL). In ARL, the actor selects the information transmission route according to the attention, and the prediction signal changes according to the context detected by the information source of the route. Hence, ARL enables flexible action selection that depends on the situation, unlike traditional reinforcement learning, wherein the actor must directly select an action.

Effects of Brain Ischemic Preconditioning on Cognitive Decline and Motor Incoordination in 3-Nitropropionic Acid-Intoxicated Rats: Probable Mechanisms of Action

The paradigm of brain ischemic preconditioning (BIP) rendering protection from succeeding chemical insults has not been established in vivo. Systemic administration of 3-nitropropionic acid (3-NP) damages cerebral basal ganglia by inducing a mitochondrial dysfunction: this serves as a translational model for Huntington’s disease. We tested the potential of BIP against the neurotoxic effects of 3-NP and investigated the role of glycogen synthase kinase 3-beta (GSK-3β) and heat shock protein-72 (HSP72) signalling in the mentioned model. Male Wistar rats (n = 8; 180-200 g) were randomly assigned to seven groups, sham, BIP, 3NP, BIP+3NP, LiCl+BIP+3NP, Que (quercetin) +BIP+3NP, and LiCl+Que+BIP+3NP. Lithium chloride, 3-NP, and quercetin were administered in the doses of 40, 35, and 4 mg/kg i.p., respectively. Deficits in motor coordination and memory retention were assessed using the balance beam, accelerating rotarod, gait analysis, Morris water maze, and elevated plus maze. Brain biochemistry was assessed for the markers of lipid peroxidation and nitric oxide. The findings revealed noticeable differences in the measured indices in the examined animal groups vs. the sham group (P < 0.05 for motor coordination, memory retention, and brain biochemistry). A strong negative correlation between the rotarod performance of animals and their brain MDA levels was found. The findings reveal that BIP provides behavioral and biochemical recuperation against 3NP-induced neurodegeneration, and this is related to downregulation of GSK -3β and upregulation of HSP72.

Relationship between normalized distributional pattern and functional outcome in patients with acute cardiogenic cerebral embolism.

This study aimed to elucidate spatial characteristics for magnetic resonance imaging (MRI) of cardiogenic cerebral embolism, to determine imaging biomarkers predicting patient outcome and cerebral herniation in cardioembolic stroke. This retrospective study assessed 90 patients with cardiogenic cerebral embolism. All images from MRI were normalized using a voxel-based symptom lesion mapping technique. Patients were categorized into two subgroups based on the outcome and presence of cerebral herniation. Each subgroup was assessed individually. The distribution map of all analyzed patients revealed accumulated ischemic lesions in bilateral middle cerebral artery areas. Ischemic lesions for the poor outcome group accumulated at the corona radiata on the right side and throughout the entire left hemisphere. Receiver operating characteristic (ROC) analysis suggested that a normalized ischemic volume of 62.8 mL allowed optimal differentiation between good and poor outcomes (sensitivity, 0.923; specificity, 0.923; area under the curve (AUC), 0.91) for left-side-dominant infarction. The distribution map for the cerebral herniation group revealed large ischemic areas in the left hemisphere. The analysis of differential involvement map with random permutation analysis showed that left anterior circulation infarcts were associated with midline shift. Receiver operating characteristic analysis revealed that a normalized infarction volume of 192.9 mL was highly predictive of cerebral herniation (sensitivity, 0.929; specificity, 0.750; AUC, 0.895). The medial frontal and occipital lobes, caudate head and basal ganglia were significantly involved in those patients who developed cerebral herniation. Ischemic volume contributed to outcomes and cerebral herniation. Ischemic lesions of the anterior and posterior cerebral arteries and basal ganglia in addition to middle cerebral artery area were identified as differences on MRI images between with and without cerebral herniation patients.

PO-057 Motor Functional Connectivity Analysis of Brain Control Network on High Level Athletes with fMRI Research

Objective The nervous system is the control center that performs the function of the human body, including each nucleus of the cerebral cortex and basal ganglia, which can control the motion of the body through three pathways-direct pathway, indirect pathway and hyperdirect pathway. Long-term physical exercise can effectively improve the human respiratory and circulatory system function indicators and promote the development of nervous system.In order to discuss the mechanisms of the high level athletes' control of the brain function network and provide the experimental basis for the study of the motor control of the central nervous system, this research collects the activation images of the cortex and basal ganglia nuclei of the ordinary college students and the high level athletes and analyzes the function connection coefficient between the groups.&#x0D; Methods The subjects were 15 high level athletes and 15 ordinary college students. the changes of the brain structure and DTI fiber in the state of quiet and fatigue were collected by the functional magnetic resonance imaging (fMRI). Matlab software was used to compare images and data and to calculate the correlation coefficient between the related nuclear groups.&#x0D; Results (1) Compared with ordinary college students, the functional connectivity coefficient between the left thalamus and the left hippocampus is different in high level athletes (P&lt;0.05). (2) The high level athletes’ functional connectivity in the left premotor area-right premotor area, left premotor area-right striatum, right premotor area-left central buckle in supplementary motor area, right premotor area-right central buckle in supplementary motor area, right premotor area-right striatum and right premotor area-left cerebellum were changed significantly after exercise fatigue (P&lt;0.05).&#x0D; Conclusions The plasticity of brain function can be affected by long-term exercise training, which depends on sport training level. After exercise fatigue, the network connection system and nerve projection density change between cortical and subcortical nuclei, suggesting that exercise fatigue will change the functional connection between parts of the brain.（NSFC：31401018 SKXJX2014014).

Changes in cerebral CT perfusion after carotid endarterectomy

Objective To find the sensitive parameters for evaluating the cerebral CT perfusion changes in patients before and after carotid endarterectomy (CEA). Methods Between November 2015 and April 2017,the data of 27 patients who underwent CEA and conducted CT perfusion(CTP) examination before and after the operation were analyzed retrospectively.The different perfusion parameters of the cerebral hemisphere in different areas were analyzed before and after the operation.Absolute perfusion parameters include:cerebral blood volume (CBV), cerebral blood flow (CBF), mean transit time (MTT) and time to peak (TTP);relative perfusion parameters include: rCBV, rCBF, rMTT and rTTP;relative to brainstem perfusion parameters include:sCBV, sCBF, sMTT and sTTP.Paired sample t test (normal distribution of quantitative data) was used to analyze the parameters differences before and after the operation. Results The postoperative perfusion parameters of the operated side cerebral hemisphere compared with the preoperative:(1)The absolute perfusion parameters:the decreased of TTP in frontal lobe,anterior watershed region,middle cerebral artery territory and basal ganglia region[preoperative (22.4±3.0) s, (23.0±3.1) s, (23.2±2.2) s, (21.9±2.7) s,postoperative (20.1±2.4) s, (20.5±2.7) s, (20.7±2.8) s, (19.5±2.8) s] had statistical significance(t values were 2.437, 2.504, 2.882, 2.431, P<0.05).(2)The relative perfusion parameters:the decreased of rMTT in middle cerebral artery territory and basal ganglia region(preoperative 1.18±0.44, 1.06±0.22, postoperative 1.04±0.33, 0.97±0.16) and the decreased of rTTP in middle cerebral artery territory and basal ganglia region(preoperative 1.07±0.15, 1.04±0.05, postoperative 1.00±0.13, 0.97±0.06) had statistical significance(t values were 2.235, 2.244, 2.245, 2.268, P<0.05).(3)The relative to brainstem perfusion parameters:the decreased of sCBV in middle cerebral artery territory(preoperative 1.08±0.16, postoperative 0.98±0.15), the increased of sCBF in frontal lobe and middle cerebral artery territory(preoperative 1.07±0.19, 1.00±0.21,postoperative 1.17±0.21, 1.09±0.20),the decreased of sMTT in middle cerebral artery territory and basal ganglia region(preoperative 1.27±0.29, 0.94±0.11,postoperative 1.05±0.05, 0.86±0.10),the decreased sTTP in frontal lobe,anterior watershed region,middle cerebral artery territory and basal ganglia region(preoperative 1.05±0.05, 1.07±0.06, 1.10±0.08, 1.02±0.03, postoperative 0.97±0.05, 0.96±0.06, 0.98±0.07, 0.95±0.01) had statistical significance(t values were 2.882,-2.995,-2.737, 2.172, 2.425, 2.249, 2.263, 2.806, 3.267, P<0.05). Conclusion CTP is significant to evaluate the changes of cerebral perfusion in patients who underwent CEA. The relative to brainstem parameters are more valuable than relative parameters and absolute parameters in judging the perfusion changes after CEA. Key words: Endarterectomy, carotid; Tomography, X-ray computed; Perfusion imaging; Brain stem; Relative perfusion parameters

Abstract WMP13: The Prediction of the Hemorrhagic Transformation Locations After Reperfusion Therapy in Acute Stroke Patients: A Magnetic Resonance Perfusion Study Using Deep Learning

Objective: Hemorrhagic transformation (HT) is a major complication of reperfusion therapy in acute stroke. We aim to explore the feasibility of HT location prediction from baseline magnetic resonance perfusion (MRP) source images. Methods: Consecutive acute ischemic stroke patients who had HT after reperfusion therapy (IV tPA and/or endovascular thrombectomy) were reviewed from two stroke centers. Patients with MRP and diffusion-weighted imaging (DWI) before and 24h after treatment and follow-up susceptibility weighted imaging (SWI) were included. The HT was depicted on follow-up SWI semi-automatically. The DWI lesions and HT were classified into 12 cerebral vascular territories (Fig 1A). Then a total of 80,000 tissue-voxels were extracted from both HT region and non-HT region randomly with the ratio of 1:1. Each voxel included a set of values of MRP source image and baseline DWI. Convolutional neural networks (CNN) were trained with 3-fold cross-validation. Prediction maps were generated from the CNN for each patient. The prevalence of HT after infarction and the sensitivity and specificity of HT prediction in each vascular territory were calculated. Results: Seventy-seven HT patients were analyzed (40 male, age 73 ±14 years, median baseline NIHSS score 14 [IQR 8-19], median onset-to-treatment time 242 min [IQR 152-355], median modified Rankin score 3 [IQR 1-4], 28 with Parenchymal hematoma). HT occurred most frequently in the territory of middle cerebral artery superficial branches (67.5%) and basal ganglia (37.6%), and least frequently in brain stem or thalamus (3.9%). HT was not evenly distributed throughout the vascular territories (Fig 1A). The best model was a locally-connected CNN (area under curve of 0.88). The average sensitivity and specificity for HT location prediction in anterior circulation were 89% and 60% (Fig 1BC). Conclusion: The CNN trained from DWI and MRP source images could predict the HT locations in acute ischemic stroke patients.

Relationship between abnormal vagus nerve tension and basal ganglia cerebral infarction induced paroxysmal atrial fibrillation.

To investigate the relationship between basal ganglia cerebral infarction and paroxysmal atrial fibrillation (PAF) caused by abnormal vagus nerve tension. A total of 1483 cases of elder patients with cerebral infarction who received head CT or MRI examination during the period were enrolled, including 830 male and 613 female, with the average age as 78 years. These cases were divided into basal infarction ganglia group (n=1045) and non-basal ganglia infarction group (n=438) according to the anatomic site of cerebral infarction. The differences of the incidence of PAF, left atrial diameter and heart rate variability were compared between the two groups. In basal ganglia infarction group, the incidence rate of PAF was significantly higher than that of non-basal ganglia infarction group (P<0.05). The incidence trend of cerebral infarction in basal ganglia was age-related, in the >79 years basal ganglia cerebral infarction group, the incidence of PAF was significantly higher than that of non-basal ganglia infarction group (P<0.05). There was no significant difference in the left atrial diameter between the basal ganglia infarction group and non-basal ganglia infarction group. Basal ganglia cerebral infarction patients with high PAF had higher heart rate variability than non-basal ganglia infarction group. Elderly patients with basal ganglia infarction have high incidence of PAF. Sympathetic nerve damage in cerebral basal ganglia, increased vagal tension and cardiac vagal tension are the direct causes of PAF. The results indicates that the increased central vagal nerve tension mediated PAF probably is an indication of supplying sympathetic neurotransmitter or cardiac vagal denervation treatment.

The study of incidence, determinants and clinical correlates of vertebral spinal osteophytes

To investigate the relationship between basal ganglia cerebral infarction and paroxysmal atrial fibrillation (PAF) caused by abnormal vagus nerve tension.A total of 1 483 cases of elder patients with cerebral infarction who received head CT or MRI examination during the period were enrolled, including 830 male and 613 female, with the average age as 78 years. These cases were divided into basal infarction ganglia group (n = 1 045) and non-basal ganglia infarction group (n = 438) according to the anatomic site of cerebral infarction. The differences of the incidence of PAF, left atrial diameter and heart rate variability were compared between the two groups.In basal ganglia infarction group, the incidence rate of PAF was significantly higher than that of non-basal ganglia infarction group (P < 0.05). The incidence trend of cerebral infarction in basal ganglia was age-related, in the >79 years basal ganglia cerebral infarction group, the incidence of PAF was significantly higher than that of non-basal ganglia infarction group (P < 0.05). There was no significant difference in the left atrial diameter between the basal ganglia infarction group and non-basal ganglia infarction group. Basal ganglia cerebral infarction patients with high PAF had higher heart rate variability than non-basal ganglia infarction group.Elderly patients with basal ganglia infarction have high incidence of PAF. Sympathetic nerve damage in cerebral basal ganglia, increased vagal tension and cardiac vagal tension are the direct causes of PAF. The results indicates that the increased central vagal nerve tension mediated PAF probably is an indication of supplying sympathetic neurotransmitter or cardiac vagal denervation treatment.

A case of Fahr's syndrome with rare atypical presentation as hemiplegia

AbstractCalcification of basal ganglia or Fahr's disease is a rare disease characterized by bilateral and symmetrical intracranial deposition of calcium mainly in cerebral basal ganglia. Basal ganglia calcification secondary to endocrinological cause is known as Fahr's syndrome. Motor and neuropsychiatric symptoms are prominent features. We report a case presented with hemiplegia without any psychiatric symptoms. Radiological findings were suggestive of bilateral calcification of cerebellar hemispheres and basal ganglia. Parathyroid hormone levels were low with no significant findings in other investigations along with negative family history. Based on the radiological and biochemical findings the case was diagnosed as fahr's syndrome.

A Case of Masticatory Dystonia Following Cerebellar Haemorrhage

Dystonia is a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, and often repetitive, movements, postures, or both [1]. It has been attributed to basal ganglia abnormalities and to dysfunctional cortico-striato-thalamo-cortical circuitry [2–4]. Dystonia has a number of possible etiological causes. Focal dystonia is more common than generalized dystonia. In cranial and cervical focal dystonia, neurophysiological investigations have revealed abnormally excitable interneuronal pathways in the brainstem. For instance, several studies reported changes in the length of the recovery cycle of the eye blink reflex and the masseter inhibitory reflex [5–7]. Cortical dysfunctions have also been explored using transcranial magnetic stimulation [8, 9]. Acquired forms of dystonia have been associated with a wide variety of vascular, traumatic, infectious, toxic, and degenerative processes, which can affect either the central or peripheral nervous system [10–14]. The underlying mechanisms of acquired dystonia are not yet completely understood, although several different studies have implicated a neural network linking the cerebral cortex, basal ganglia, and cerebellum [2–4]. In such a network, dysfunctional activity at any level could lead to the onset of dystonia. While the role of the basal ganglia is well known and had been widely demonstrated with respect to the pathogenesis of acquired dystonia, the role of the cerebellum has not been well defined. Both animal studies [15–17] and clinical reports [3, 18–34] have explored the role of the cerebellum in the pathogenesis of dystonia. Overall, there is consensus regarding the idea that acquired dystonia is caused by lesions, leading to abnormal cerebellar output (Table 1). In this case report, we describe our diagnostic and therapeutic processes for a patient with masticatory dystonia resulting from cerebellar haemorrhage.

Idiopathic progressive chorea: misnomer or still reality? A case with neuropathological disconfirmation

Dear Sir,Most of the rarer causes of chorea have been clarified in thelast decades [1], so that the classic term of ‘‘idiopathicchorea’’ has been critically put into question.A 50-year-old Caucasian woman was referred formarked and progressive generalized chorea. The onset wasabout 1 year before and a depressive syndrome was alsopresent. Past medical and family histories were unre-markable. Slight dysarthria and adiadochokinesia werenoted. Ocular movements were normal. Deep tendonreflexes were diffusely enhanced and plantar response wasin extension bilaterally. Routine serology, ceruloplasmin,tumour markers, HIV serology, onconeural- and auto-antibodies were negative. The anti-streptolysin-O titre wasborderline and careful examination of blood smears failedto demonstrate acanthocytes. A magnetic resonance and a99mTc-ECD SPECT brain scans were not significant. Theneuropsychological assessment evidenced only minorimpairment in selective attention and slight dysexecutivenotes. Genetic testing for Huntigton’s disease (HD, 17/25triplets), DRPLA (150/150), SCA17 (36/37), SCA1 (21/30), SCA2 (23/23), SCA3 (20/22), SCA6 (11/12), SCA7(9/11), and FXTAS (23/23) were negative. Progranulin andPRNP mutations or C9orf72 expansions were absent. Anti-basal ganglia antibodies (ABGA) testing (courtesy ofDr. Giovannoni and Martino, UCL, UK) resulted in a weakpositive binding to pyruvate kinase M1 (60 kDa), while nobinding was shown for both gamma-neuron specific eno-lase, and aldolase C.Since neuroleptics were ineffective, a trial with high-dose IV steroids was attempted, with no immediateimprovement (HD Functional Capacities score: 2/13, stageIV; Folstein Chorea Scale score: 37/57). Three monthslater, only minor changes were noted (HDFCS: 3/13, stageIV; FCS: 27/57). The patient further deteriorated present-ing diffuse spasticity and dystonia. Due to worseningdysphagia the patient was referred for PEG positioning, butshe anyhow died of aspiration pneumonia about 4 yearssince the onset of chorea.The neuropathological study was carried out on forma-lin-fixed sections stained with hematoxylin-eosin, cresylviolet for Nissl substance, Heidenhain-Woelcke for myelin,thioflavine S for amyloid, and silver salts for neurofibrillarychanges (Bodian’s method). Immunohistochemistry wasperformed with antibodies to beta-amyloid (4G8), alpha-synuclein (4D6), ubiquitin (polyclonal), phosphorylated tau(AT8), prion protein (3F4), GFAP (polyclonal), CD3/43,leucocytes common antigen CD45, and MBP (polyclonal).Histopathological examination revealed mild neuronal lossin the cerebral cortex and basal ganglia. Reactive astrogl-iosis and microglia activation were marked in the thalamus,caudate, putamen and substantia nigra (SN) and morepronounced in the brainstem and cerebellum. Slight peri-vascular lymphocytic infiltration was present in the hemi-spheric and cerebellar white matter as well as in thestriatum, thalamus and brainstem. Extracellular deposits orintracellular inclusions were absent but esinophilic, ubiq-uitin-positive inclusions suggestive of Marinesco bodieswere found only in the SN. No clear retrospective corre-lation with imaging data was possible.