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Erdoğan Hacı Ali, Yayla Vildan, Sözer Nejla, Aydın Filiz Yıldız, Acır Ibrahim, Vural Meltem
Journal of Neuroscience and Neurological Disorders, Volume 6, pp 016-019;

Introduction: Fatigue is a common non-motor symptom of Idiopathic Parkinson’s Disease (IPD). The aim is to research the relationship between fatigue of IPD patients and the clinical findings, of mood disorders. Material and methods: A total of 39 patients with IPD were included in the study. The relationship between fatigue severity and demographic characteristics and the treatment was evaluated in IPD. The severity of fatigue was evaluated by Fatigue Severity Scale (FSS). Motor impairment was scored by the modified Hoehn and Yahr scale. The patients were assessed for the presence of depression and anxiety with the Hospital Anxiety and Depression Scale (HADS). Results: The mean age of the patients was 70.62 ± 8.35 years. 23 were men and 16 were women. The mean disease duration was 6.18 ± 3.35 years. The patients were assigned into two groups according to the presence of fatigue measured by FSS with less than 5 (Group I) and 5 or more (Group II). There were no statistically significant differences between the two groups with respect to mean age, mean age of onset, and mean disease duration of the patients (p > 0.05). There were no significant differences between the two groups for HADS depression, anxiety values, and terms of antiparkinsonian therapies (p > 0.05). The severity of fatigue was correlated with the HADS anxiety levels (p < 0.05). Discussion: Fatigue is an important non-motor symptom that is underestimated in clinical follow-up. We didn’t find any correlation between fatigue and age, duration of disease onset, or drug use. There was no significant correlation between the fatigue score and depression, and pain. However, the fatigue scores were higher in patients with high anxiety scores and females.
Hatim Ghita, Chekrine Tarik, Houjami Majdouline, Boughafour Mouna, Bouchbika Zineb, Benchakroun Nadia, Jouhadi Hassan, Tawfiq Nezha, Benider Abdelatif, Sahraoui Souha
Journal of Neuroscience and Neurological Disorders, Volume 6, pp 001-004;

Background and objectives: Brainstem gliomas are tumors of the central nervous system which have varying presentations and clinical courses. This study aims to analyze the frequency, clinical and therapeutic aspects of brainstem glioma. Methods: We retrospectively analyzed the data from the record of the patients treated for brainstem glioma under the age of 20 between January 2007 and July 2020 in the Radiation Oncology department of the Ibn Rochd UHC. Results: There were fifteen patients (10 males and 5 females). The mean age of onset was 12 years (range 8 - 14 years). The duration of symptoms varied from 1 month to 2 years. Nine of the patients had intracranial hypertension due to hydrocephalus, six had cranial nerve deficits at presentation, and five patients had cerebellar signs. The lesion was pontine in 12 cases. None of the patients had a tumoral resection, nine had a ventriculo-peritoneal shunt insertion for the hydrocephalus and three had a Stereotactic biopsy that revealed one astrocytoma grade 1, one low grade glioma and one glioblastoma. The radiotherapy was indicated in all the cases but only nine patients had a 3D radiotherapy with a total dose of 54 Gy. Three patients received chemotherapy. Six patients are still alive, two are lost to follow up and seven patients are dead with a mean survival period of 8 months. Conclusion: Brainstem glioma is a devastating disease with a bad prognosis. The clinical presentation is variable and the management is multidisciplinary. Our study illustrates the importance of treatment by radiation.
, Balestrieri Antonio, Dalila Fuschillo, Nasi Maria Teresa, Tosatto Luigino
Journal of Neuroscience and Neurological Disorders, Volume 6, pp 011-015;

Intrasellar meningioma (IM) is a rare occurrence that is difficult to distinguish preoperatively from the most common non-functioning pituitary adenoma. Here we describe a case of psammomatous IM occurring in a 68-year-old woman, presented with visual defects. On magnetic resonance imaging (MRI) she was found to have an intrasellar mass with suprasellar extension that was approached with transsphenoidal surgery. Subtle radiological hints, namely dural tail sign, intralesional calcifications and a marked and homogenous early enhancement of IM on MRI after gadolinium administration, may aid clinicians in achieving an accurate pre-operative diagnosis and choosing the proper surgical approach. The clinical and neuroradiological features of IM described in the literature has been reviewed.
, Montazeri Zeinab, Rafati Mehravar
Journal of Neuroscience and Neurological Disorders, Volume 6, pp 005-010;

Air pollution exposure is among the most prevalent reasons for environmentally-induced oxidative stress and inflammation, both of which are implicated in the central nervous system (CNS) diseases. The CNS has emerged as an important target for adverse health effects of exposure to air pollutants, where it can cause neurological and neurodevelopmental disorders. Air pollution includes various components of gases, particulate matter (PM), ultrafine particulate (UFPs), metals, and organic compounds. An important source of PM and UFPM in the ambient air is associated with air pollution-related trafficking, and primarily diesel exhaust particles (DEPs). Controlled animal studies and epidemiological studies show that exposure to air pollution, and in particular urban air pollution or DEPs, may lead to neurotoxicity. In specific, exposure to air pollutants as an important factor may be in neurodevelopmental disorders (eg Autism) and neurological disorders (eg.., Alzheimer’s Disease (AD)). The most noticeable effects of exposure to air pollutants in animals and humans are oxidative stress and neurodegeneration. Studies in rats exposed to DEPs showed microglial activity, increased lipid peroxidation, and neuronal accumulation in various areas of the brain, especially the olfactory bulb (OB) and the hippocampus (HI). Disorders of adult neurogenesis were also found. In most cases, the effects of DEP are more pronounced in male mice, probably due to lower antioxidant capacity due to less expression of paraoxonase 2.
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 072-082;

Huntington’s disease (HD) is an incurable neurodegenerative disease that causes involuntary movements, emotional lability, and cognitive dysfunction. HD symptoms usually develop between ages 30 and 50, but can appear as early as 2 or as late as 80 years. Currently no neuroprotective and neurorestorative interventions are available. Early multimodal intervention in HD is only possible if the genetic diagnosis is made early. Early intervention in HD is only possible if genetic diagnosis is made at the disease onset or when mild symptoms manifest. Growing evidence and understanding of HD pathomechanism has led researchers to new therapeutic targets. Here, in this article we will talk about the multimodal treatment strategies and recent advances made in this field which can be used to target the HD pathogenesis at its most proximal level.
, Marabathina Nageswara Rao, Mareddy Rama Krishnareddy, Yeddanapudi Sivaramanjaneyulu
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 029-033;

Aim: To assess the efficacy of decompressive craniectomy in patients with large basal ganglia (BG) bleed. To establish predictive criteria of mortality after surgery in patients with BG bleed. Materials: This prospective study includes all patients of large spontaneous BG bleed operated by decompressive craniectomy without hematoma evacuation from October 2012 to September 2015. Data was collected on patient age, gender, distribution of bleed, affected hemisphere dominancy, preexisting medical conditions, admission Glasgow Coma Score (GCS), midline shift on CT or MRI Brain, hematoma volume and anisocoria, duration (hours) between the onset of stroke and operation, post-operative complications, and the duration of hospital stay. This data was correlated with one month mortality of the patients. Results: Total number of patients were 27. Mean age was 51 years and mean GCS was 7.55(range 5-11). The mean volume of the bleed was 68.51 ml. Mortality was noted in 17 out of 27 patients (63%) in 30 days. Thirteen of the 16 patients with intraventricular extension of BG bleed had mortality. The factors that showed statistically significant correlation with one month mortality were age, GCS at admission, volume of the bleed and the intraventricular extension. Conclusion: Large BG bleed was associated with high mortality and morbidity. Age of 50 years or more and GCS ≤ 8 at presentation were poor prognostic factors for decompressive craniectomy in patients with BG bleed. Patients with large BG bleed of volume > 60 ml and intraventricular extension had poor prognosis.
, Ciardi Celina, Lopez Matias, Scrivano Esteban V, Lundquist Javier, Esteban V Scrivano, Perez Nicolas, Lylyk Pedro
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 055-060;

Iurato Giuseppe
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 094-095;

This very brief communication is aimed to highlight some recent contact points between neurosciences and dynamical system theory, passing through paleoneurology, with some remarks suggesting further possible interdisciplinary developments.
Dave Sonya, Zhou An
Journal of Neuroscience and Neurological Disorders, Volume 5;

Repressive regulation of potassium channel genes by Polycomb group (PcG) proteins contributes to PcG protein-mediated neuroprotection against neuronal ischemic injury, as seen in an ischemic stroke. Here we asked the question whether Trithorax group (TrxG) proteins, the antagonistic partners of PcG proteins (i.e, epigenetic activators targeting the same genes) may also regulate potassium channels. Results of patch-clamp studies on cultured neuronal cells showed that inhibition of TrxG protein MLL-1 led to an increase in potassium channel activity, an unexpected effect for a presumed gene activator. In contrast, decreased sodium currents were observed with MLL-1 inhibition. Increased or decreased levels of potassium channel protein Kv2.1 or sodium channel protein Nav1.2, respectively, were seen with MLL-1 inhibition, as determined by immunocytochemistry. These results, for the first time, demonstrate an involvement of TrxG protein MLL-1 in regulating neuronal ion channels, potentially repressing potassium channel genes.
Pérez-López Carlos, Flores Alexis J Palpán, Azriel Sharona, Rodríguez-Domínguez Víctor, Frutos Remedios, Álvarez-Escolá Cristina, Isla Alberto
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 087-088;

Juntas-Morales Raul, De La Cruz Elisa, Esselin Florence, Pageot Nicolas, Taieb Guillaume, Camu William
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 069-071;

Objectives: To describe a patient with facial-onset sensory-motor neuronopathy (FOSMN) that later developed Huntington’s disease (HD). Case report: A 62-year-old woman complained of progressive dysphagia 8 years before referral. At initial evaluation, there was excessive salivation, dysphagia, and sensory-motor trigeminal impairment. Denervation was noted on the upper limbs and the tongue. Blink reflexes were abolished. Genetic study of amyotrophic lateral sclerosis (ALS)-related genes was normal. She was diagnosed with FOSMN syndrome. Her clinical state progressively worsened with corneal anesthesia, severe denutrition, right arm and axial weakness. Seven years after referral, she was unable walk and developed generalized chorea. Abnormal huntingtin gene repeat expansion confirmed the diagnosis of HD. She died 16 years after onset of dysphagia. Conclusion: Cases with both HD and ALS have already been reported but not FOSMN and HD, to our knowledge. Some FOSMN cases have been linked to ALS-related gene mutations and HD phenocopies have been associated with C9ORF72 repeat expansions. Recently, huntingtin repeat expansions were described in the ALS population. Although a chance association cannot be excluded, data from the literature are in favor of a pathogenic relationship between FOSMN and HD in this particular case. We suggest that huntingtin gene be more systematically studied in patients with FOSMN.
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 061-068;

Parkinson’s disease (PD) is thought to be the most common neurodegenerative disease with movement disorder. The key motor symptoms are rigidity, tremor, akinesis/hypokinesia/bradykinesia, and postural instability. However, in our day-to-day clinical practice we tend to see several other symptoms which may be motor or non-motor. Non-motor symptoms (NMS) are quite common and debilitating. The pathological hallmarks of PD are loss of dopaminergic neurons in the substantia nigra pars compacta (SNPc) and accumulation of unfolded or misfolded alpha-synuclein. Diagnosis of PD is difficult in the pre-motor stage. Late diagnosis renders a substantial loss of dopaminergic neurons in SNPc and spread of disease in other parts of the brain. This may manifest as either full blown symptoms requiring multiple medications or may even lead to life threatening condition due to lack of early diagnostic tools and techniques. Biomarkers are required to diagnose PD at a very early stage when prevention is possible. Hence, we see a lot of interest among researchers involved in finding a biomarker specific to the disease. Biomarkers may be clinical, image based, genetic, and biochemical. Cerebrospinal fluid (CSF) and serum markers which may correlate with disease pathophysiology are of great significance. One such molecule which recently gained a lot of attention is neuron-specific enolase (NSE). The main aim of this paper is to highlight the role of NSE in predicting neurodegeneration and neuroinflammation ultimately reflecting damage of brain cells in PD.
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 034-047;

Medical benefits of cannabis and related compounds is widely known. Discovery of psychotropic plant cannabinoid Δ9-tetrahydrocannabinol have urged researchers to study more about the cannabinoid system and related therapeutics in the field of neurology and medicine. Where activation of cannabinoid receptor type 1 (CB1R) yielded in unwanted and serious side effects, discovery of cannabinoid receptor type 2 (CB2R) and its ligands gave a new hope. Till now there is limited success in this field because of complex expanded endocannabinoid system comprising of receptors, ligands and enzymes. In this review we will update about the role of endocannabinoidome relevant to neurological disorders.
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 048-054;

Mitochondrial and lysosomal dysfunction accounts for a large group of inherited metabolic disorders most of which are due to a dysfunctional mitochondrial respiratory chain (MRC) leading to deficient energy production and defects in phagocytosis in endosomal-lysosomal pathway respectively. MRC function depends on the coordinated expression of both nuclear (nDNA) and mitochondrial (mtDNA) genomes. Thus, mitochondrial diseases can be caused by genetic defects in either the mitochondrial or the nuclear genome, or in the cross-talk between the two. The mitochondrial DNA depletion syndromes (MDSs) are a clinically heterogeneous group of disorders with an autosomal recessive pattern of inheritance that have onset in infancy or early childhood and are characterized by a reduced number of copies of mtDNA in affected tissues and organs. In this review article, we summarized the spectrum of mtDNA depletion disorders along with minor learning of lysosomal storage diseases. This current article offers a perspective on the role of genetics in medical practice and how this role may evolve over the next several years.
Chiriboga Nicolas, Muñoz-Pareja Jennifer,
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 022-025;

Background: A misguided auto-reactive injury is responsible for several types of central nervous system (CNS) conditions in pediatrics. We propose that, in some of these conditions, the adaptive immune system has a common cellular immune pathogenesis, driven predominantly by T cells, despite variability on the phenotypical clinical presentation. Methods: We have characterized the CD4+/CD8+ adaptive immune response (AIR) on pediatric patients presenting with clinical symptoms compatible with Neuroimmune Disorders (NID). Flow cytometry with deep immunophenotyping of T cells was performed on peripheral blood obtained during the acute clinical phase and compared to an age-matched cohort group (Co). Results: We found that pediatric patients with confirmed NID, exhibit a pattern of dysregulation of CD4+ lineages associated with autoimmune processes. Discussion: The autoimmune associated CD4+ dysregulation was associated with patients with NID, as compared to healthy controls and patients with non-autoimmune diagnoses. If we can improve our capacity for early accurate diagnosis and meaningful disease monitoring of pathogenic T cell subsets, we can both expedite disease detection and may serve as a guide to the administration of effective immunotherapeutic agents.
Do Amaral Leandro Custódio
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 016-021;

Delayed cerebral ischemia (DCI) is one of the main complications of spontaneous subarachnoid haemorrhage and one of its causes is the cortical spreading depolarizations (CSDs). Cortical spreading depolarizations are waves of neuronal and glial depolarizations in which there is loss of neuronal ionic homeostasis with potassium efflux and sodium and calcium influx. In damaged brain areas and brain areas at risk, such as those adjacent to subarachnoid haemorrhage (SAH), CSDs induce microvascular vasoconstriction and, therefore, hypoperfusion and spread of ischemia. Several studies have been devoted to minimize secondary injuries that occur hours to days after an acute insult. Ketamine, a drug until recently contraindicated in the neurosurgical population for potentially causing intracranial hypertension, has re-emerged as a potential neuroprotective agent due to its pharmacodynamic effects at the cellular level. These effects include anti-inflammatory mechanisms, and those of microthrombosis and cell apoptosis controls, and of modulation of brain excitotoxicity and CSDs. A literature review was performed at PubMed covering the period from 2002 to 2019. Retrospective studies confirmed the effects of ketamine on the control of CSDs and, consequently, of DCI in patients with SAH, but did not show improvement in clinical outcome. The influence of ketamine on the occurrence/development of DCI needs to be further confirmed in prospective randomized studies.
Erdoğan Hacı Ali, Acır İbrahim, Yayla Vildan
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 026-028;

Background and Objective: Thrombolytic and mechanical thrombectomy therapies are proven treatment methods in patients with acute stroke. Aim is to share our experience in acute stroke therapy with colleagues. Material and methods: In this study we evaluated the patients who underwent MT or MT + IV-tPA between 2018-2019 retrospectively. Demographic features, comorbid diseases of patients, symptom onset-to-gate and symptom gate-to-puncture durations, mRS (Modified Rankin Score) and NIHSS (National Institutes of Health Stroke Scale) score, treatment method and degree of recanalization were listed. Results: MT was applied to 29 patients, MT + bolus IV-tPA was applied to 12 patients and MT + full dose IV-tPA was applied to 7 patients. The mean age was 66 ± 15 years, arrival mRS was 2 ± 2, arrival NIHSS score was 14 ± 5, onset-to-gate duration was 185 minutes and gate-to-puncture duration was 118 minutes. Conclusion: The rate of recanalization, functional independence and mortality were similar to the HERMES study. It was observed a higher rate of intracranial hemorrhage in patients who received bolus or full dose IV-Tpa compared to patients who underwent MT. These results have led us to question the necessity of giving bolus or full dose IV-tPA before MT. Onset-to-gate and gate-to-puncture durations were found longer than the recommended durations. Rapid and effective management of AIS patients will provide good clinical results.
, Ugur Umran, Anstadt Mark P, Pedoto Michael J
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 006-015;

Systemic arterial air embolism (SAAE) is a rare but serious complication of CT-guided hook wire localization of pulmonary nodule usually with catastrophic and poor outcome. Hook wire needle localization is done pre-operatively by placing wire around or into the pulmonary nodule to provide the thoracic surgeon accurate location guidance of the target nodule for Video-Assisted Thoracoscopic Surgery (VATS) wedge resection with safety margins. Physicians should be aware of this possible complication during the procedure in order to rescue the patient promptly as it requires rapid diagnosis and management. We describe a 55-year-old male who underwent a CT-guided hook wire needle localization of left upper lobe lung cancer and left lower lobe pulmonary nodule prior to planned VATS wedge resection who developed altered mental status and bilateral lower extremities paralysis after wire placement was completed. His CT head demonstrated small air embolism in the left occipital area, confirming the diagnosis of cerebral air embolism and follow up CT and MRI of the head revealed multiple areas of brain infarction. In addition, he was diagnosed with anterior spinal cord syndrome (ACS), most likely due to anterior spinal artery ischemia from micro air embolism on the basis of clinical findings but with negative ischemic changes on MRI of the spinal cord. His mental status recovered but he remained paraplegic and transferred to inpatient rehabilitation service.
Erkabu Samson, Taddese Zerihun, Bearega Biniam, Daniel Eyuel, Birhanu Mekonen
Journal of Neuroscience and Neurological Disorders, Volume 5, pp 001-003;

A mass arising from the pituitary gland commonly damages cells of the anterior pituitary gland and affects the secretion of gonadotropins and growth hormone. However, central hypothyroidism and secondary adrenal insufficiency from such damage is a rare phenomenon. Acute urinary retention as the main symptom of central hypothyroidism is also an unusual initial presentation. We report a male patient who comes with frequent urinary retention and hyponatremia at our hospital.
Er Cuspineda-Bravo, M García- Menéndez, F Castro-Batista, Sm Barquín-García, D Cadelo-Casado, Aj Rodríguez, Km Sharkey
Journal of Neuroscience and Neurological Disorders, Volume 4, pp 088-098;

, Uygun Turgut
Journal of Neuroscience and Neurological Disorders, Volume 4, pp 084-087;

Atrial septal defect (ASD) is common among adult congenital heart diseases but rarely causes paradoxical cerebral embolism. By sharing the ASD diagnosed after the first ischemic stroke attack at the age of 49 and a case of paradoxical cerebral embolism developing accordingly, we aimed to draw attention to the necessity of detailed cardiac examination in patients with cryptogenic stroke.
, Cremonini Anna Maria, Gessaroli Manlio
Journal of Neuroscience and Neurological Disorders, Volume 4, pp 079-083;

We report a case of 30-year-old immunocompetent man, with a previous history of cranial-facial trauma, who presented with progressive left exophthalmos due to an intracranial left frontal-ethmoidal-orbital mass. Histology of the resected tumor revealed a classical Hodgkin’s Lymphoma (HL). Epstein-Barr virus encoded RNA/EBER was detected in typical Hodgkin and Reed-Sternberg cells. After postoperative radiotherapy and chemotherapy administration, the patient remains free of systemic disease or recurrence on 4 years of follow-up. Intracranial involvement by HL has rarely been described, mostly as a late localization or as a recurrence of a disseminated disease, in a setting of immunosuppression. Primary HL of the central nervous system occurring as an isolated disease is even more uncommon, with only 16 reported cases documented to date. The prognosis of these rare cases appears comforting with appropriate treatment. Tumor resection and, in appropriate cases, treatment with radiation and/or chemotherapy seem to warrant a durable response. For this reason a systemic disease should be excluded in all cases intracranial HL by a comprehensive work-up. To the best of our knowledge, this case represents the first report that documents the association of intracranial HL and local trauma with subsequent intracranial infection.
Journal of Neuroscience and Neurological Disorders, Volume 4, pp 053-062;

Blood vessels that supply and feed the central nervous system (CNS) possess unique and exclusive properties, named as blood–brain barrier (BBB). It is responsible for tight regulation of the movement of ions, molecules, and cells between the blood and the brain thereby maintaining controlled chemical composition of the neuronal milieu required for appropriate functioning. It also protects the neural tissue from toxic plasma components, blood cells and pathogens from entering the brain. In this review the importance of BBB and its disruption causing brain pathology and progression to different neurological diseases like Alzheimer’s disease (AD), Parkinson’s disease (PD), Amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD) etc. will be discussed.
, Goto Satoshi
Journal of Neuroscience and Neurological Disorders, Volume 4, pp 075-078;

Many patients with chronic cerebrovascular diseases complain “dizziness”, which is a distortion of static gravitational orientation, or an erroneous perception of motion of the sufferer or of the environment. In the vestibular cortical system, the parieto-insular vestibular cortex (PIVC) serves as the core region having the strong interconnections with other vestibular cortical areas and the vestibular brainstem nuclei. By forming the reciprocal inhibitory interactions with the visual cortex (VISC), it also plays a pivotal role in a multisensory mechanism for self-motion perception. In a line of our studies on post-stroke patients, we found that there was a significant decrease in the cerebral blood flow in both the VISC and PIVC in the patients who suffered from dizziness. In this article, we provide a new concept that due to dysfunction of the visual-vestibular interaction loop, low cerebral blood perfusion in the PIVC and VISC might elicit post-stroke dizziness.
Bugeme Marcellin, Sow Adjratou Djeynabou, , Millogo Athanase, Luboya Oscar Numbi, Touré Kamadore
Journal of Neuroscience and Neurological Disorders, Volume 4, pp 063-068;

Introduction: Neurocysticercosis (NCC) is a common helminthic infection of the nervous system that occurs when humans become intermediate hosts in the life cycle of the pig tapeworm (Taenia solium) after ingesting its eggs. The objective of this study was to analyze socio-demographic, clinical and paraclinical features of patients with NCC in Lubumbashi, DRC. Methods: This is a cross-sectional study conducted over a period of 2 years within the Neuropsychiatric Center of Lubumbashi. Socio-demographic, clinical, paraclinical and therapeutic features were studied. Results: A total of 18 patients with NCC were listed. Epilepsy was found in 72.2% (13/18) of the cases. The mean age of the patients was 30.2 ± 13.5 years; males accounted for 61.2% of the cases. 84.6% were consumers of pork. Generalized epilepsy was found in 84.6% of the cases and hypereosinophilia in 38% of the cases. On the neuroimaging, the parietal location of lesions represented 92.3%; calcifications were the type of lesion in 53.8% of the cases and 69.2% of the cases presented lesions in the 4th evolutionary stage. Electroencephalogram was normal in 84.4% of the cases. Phenobarbital was the antiepileptic drug used in 69.3%; albendazole and prednisone were used in 53.9% of the cases. Conclusion: This study shows that NCC is one of the causes of epilepsy in Lubumbashi. Generalized tonic-clonic seizures are the most common form of presentation and calcified parenchymal lesions are the most common radiological feature of NCC. So, any patient with acute onset of afebrile seizure should be screened for NCC provided other common causes been ruled out.
, Christie Catherine, Snee Isabel A, Iqbal Hamail
Journal of Neuroscience and Neurological Disorders, Volume 4, pp 069-074;

Objective: Atlantoaxial subluxation (AAS) occurs when there is misalignment of the atlantoaxial joint. Several etiologies confer increased risk of AAS in children, including neck trauma, inflammation, infection, or inherent ligamentous laxity of the cervical spine. Methods: A single-center, retrospective case review was performed. Thirty-four patients with an ICD-10 diagnosis of S13.1 were identified. Demographics and clinical data were reviewed for etiology, imaging techniques, treatment, and clinical outcome. Results: Out of thirty-four patients, twenty-two suffered cervical spine trauma, seven presented with Grisel’s Syndrome, four presented with ligamentous laxity, and one had an unrecognizable etiology. Most diagnoses of cervical spine subluxation and/or instability were detected on computerized tomography (CT), while radiography and magnetic resonance imaging (MRI) were largely performed for follow-up monitoring. Six patients underwent cervical spine fusion, five had halo traction, twelve wore a hard and/or soft collar without having surgery or halo traction, and eight were referred to physical therapy without other interventions. Conclusion: Pediatric patients with atlantoaxial subluxation may benefit from limited 3D CT scans of the upper cervical spine for accurate diagnosis. Conservative treatment with hard cervical collar and immobilization after reduction may be attempted, but halo traction and halo vest immobilization may be necessary. If non-operative treatment fails, cervical spine internal reduction and fixation may be necessary to maintain normal C1-C2 alignment.
Bugeme Marcellin, , Diop-Sène Marième Soda, Massi Daniel Gams, Seck Lala Bouna
Journal of Neuroscience and Neurological Disorders, Volume 3, pp 049-52;

Zhong Li Xue, Adebisi Muslimat Kehinde, Liuyi Liuyi, Salim Mzee Said Abdulraman, Mahmud Abdul Nazif, Kanton Aaron Gia, Mustapha Abdullateef Taiye
Journal of Neuroscience and Neurological Disorders, Volume 4, pp 024-028;

Rebecca Renata Lapenda Do Monte, Karina De Andrade Vidal Costa, As Nunes Jr, Amália Cinthia Meneses Rêgo,
Journal of Neuroscience and Neurological Disorders, Volume 3, pp 145-147;

Yazdani So, Saeed Oraee-Yazdani, Maryam Golmohammadi, MohammadHosein Akhlaghpasand, Maryam Oraee-Yazdani
Journal of Neuroscience and Neurological Disorders, Volume 2, pp 098-100;

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