Spectrum Of Neurological Disorders Research Articles

Advances in Graphene Field Effect Transistors (FETs) for Amine Neurotransmitter Sensing

Amine neurotransmitters (NTs) are crucial in the central nervous system, and dysregulation in their levels is implicated in a spectrum of neurological disorders. Thus, a precise and timely assessment of their concentrations is critical for early diagnosis and treatment efficacy monitoring. Graphene-based field effect transistors (GFETs) have become a ground-breaking instrument in the detection of these NTs because of their exceptional electrical characteristics and adaptability. This paper summarises the significant advancements in GFET biosensors in amine NT detection and highlights developments in the selectivity, sensitivity, and limit of detection (LOD) attained by selecting various graphene materials and functionalisation approaches.

Gas6/Axl signaling promotes hematoma resolution and motivates protective microglial responses after intracerebral hemorrhage in mice

BackgroundIntracerebral hemorrhage (ICH) stands out as the most fatal subtype of stroke, currently devoid of effective therapy. Recent research underscores the significance of Axl and its ligand growth arrest-specific 6 (Gas6) in normal brain function and a spectrum of neurological disorders, including ICH. This study is designed to delve into the role of Gas6/Axl signaling in facilitating hematoma clearance and neuroinflammation resolution following ICH. MethodsAdult male C57BL/6 mice were randomly assigned to sham and ICH groups. ICH was induced by intrastriatal injection of autologous arterial blood. Recombinant mouse Gas6 (rmGas6) was administered intracerebroventricularly 30 min after ICH. Virus-induced knockdown of Axl or R428 (a selective inhibitor of Axl) treatment was administrated before ICH induction to investigate the protective mechanisms. Molecular changes were assessed using western blot, enzyme-linked immunosorbent assay and immunohistochemistry. Coronal brain slices, brain water content and neurobehavioral tests were employed to evaluate histological and neurofunctional outcomes, respectively. Primary glia cultures and erythrophagocytosis assays were applied for mechanistic studies. ResultsThe expression of Axl increased at 12 h after ICH, peaking on day 3. Gas6 expression did not remarkably changed until day 3 post-ICH. Early administration of rmGas6 following ICH significantly reduced hematoma volume, mitigated brain edema, and restored neurological function. Both Axl-knockdown and Axl inhibitor treatment abolished the neuroprotection of exogenous Gas6 in ICH. In vitro studies demonstrated that microglia exhibited higher capacity for phagocytosing eryptotic erythrocytes compared to normal erythrocytes, a process reversed by blocking the externalized phosphatidylserine on eryptotic erythrocytes. The erythrophagocytosis by microglia was Axl-mediated and Gas6-dependent. Augmentation of Gas6/Axl signaling attenuated neuroinflammation and drove microglia towards pro-resolving phenotype. ConclusionsThis study demonstrated the beneficial effects of recombinant Gas6 on hematoma resolution, alleviation of neuroinflammation, and neurofunctional recovery in an animal model of ICH. These effects were primarily mediated by the phagocytotic role of Axl expressed on microglia.

The Biallelic Inheritance of Two Novel SCN1A Variants Results in Developmental and Epileptic Encephalopathy Responsive to Levetiracetam.

Loss-, gain-of-function and mixed variants in SCN1A (Nav1.1 voltage-gated sodium channel) have been associated with a spectrum of neurologic disorders with different severity and drug-responsiveness. Most SCN1A variants are heterozygous changes occurring de novo or dominantly inherited; recessive inheritance has been reported in a few cases. Here, we report a family in which the biallelic inheritance of two novel SCN1A variants, N935Y and H1393Q, occurs in two siblings presenting with drug-responsive developmental and epileptic encephalopathy and born to heterozygous asymptomatic parents. To assess the genotype-phenotype correlation and support the treatment choice, HEK 293 cells were transfected with different combinations of the SCN1A WT and mutant cDNAs, and the resulting sodium currents were recorded through whole-cell patch-clamp. Functional studies showed that the N935Y and H1393Q channels and their combinations with the WT (WT + N935Y and WT + H1393Q) had current densities and biophysical properties comparable with those of their respective control conditions. This explains the asymptomatic condition of the probands' parents. The co-expression of the N935Y + H1393Q channels, mimicking the recessive inheritance of the two variants in siblings, showed ~20% reduced current amplitude compared with WT and with parental channels. This mild loss of Nav1.1 function may contribute in part to the disease pathogenesis, although other mechanisms may be involved.

Membrane depolarization mediates both the inhibition of neural activity and cell-type-differences in response to high-frequency stimulation

Neuromodulation using high frequency (>1 kHz) electric stimulation (HFS) enables preferential activation or inhibition of individual neural types, offering the possibility of more effective treatments across a broad spectrum of neurological diseases. To improve effectiveness, it is important to better understand the mechanisms governing activation and inhibition with HFS so that selectivity can be optimized. In this study, we measure the membrane potential (Vm) and spiking responses of ON and OFF α-sustained retinal ganglion cells (RGCs) to a wide range of stimulus frequencies (100–2500 Hz) and amplitudes (10–100 µA). Our findings indicate that HFS induces shifts in Vm, with both the strength and polarity of the shifts dependent on the stimulus conditions. Spiking responses in each cell directly correlate with the shifts in Vm, where strong depolarization leads to spiking suppression. Comparisons between the two cell types reveal that ON cells are more depolarized by a given amplitude of HFS than OFF cells—this sensitivity difference enables the selective targeting. Computational modeling indicates that ion-channel dynamics largely account for the shifts in Vm, suggesting that a better understanding of the differences in ion-channel properties across cell types may improve the selectivity and ultimately, enhance HFS-based neurostimulation strategies.

Harlequin mice exhibit cognitive impairment, severe loss of Purkinje cells and a compromised bioenergetic status due to the absence of Apoptosis Inducing Factor

The functional integrity of the central nervous system relies on complex mechanisms in which the mitochondria are crucial actors because of their involvement in a multitude of bioenergetics and biosynthetic pathways. Mitochondrial diseases are among the most prevalent groups of inherited neurological disorders, affecting up to 1 in 5000 adults and despite considerable efforts around the world there is still limited curative treatments.Harlequin mice correspond to a relevant model of recessive X-linked mitochondrial disease due to a proviral insertion in the first intron of the Apoptosis-inducing factor gene, resulting in an almost complete depletion of the corresponding protein. These mice exhibit progressive degeneration of the retina, optic nerve, cerebellum, and cortical regions leading to irremediable blindness and ataxia, reminiscent of what is observed in patients suffering from mitochondrial diseases.We evaluated the progression of cerebellar degeneration in Harlequin mice, especially for Purkinje cells and its relationship with bioenergetics failure and behavioral damage.For the first time to our knowledge, we demonstrated that Harlequin mice display cognitive and emotional impairments at early stage of the disease with further deteriorations as ataxia aggravates. These functions, corresponding to higher-order cognitive processing, have been assigned to a complex network of reciprocal connections between the cerebellum and many cortical areas which could be dysfunctional in these mice.Consequently, Harlequin mice become a suitable experimental model to test innovative therapeutics, via the targeting of mitochondria which can become available to a large spectrum of neurological diseases.

ADCY5-related dyskinesia - case series with literature review.

ADCY5-related dyskinesia is a rare neurological disease caused by mutations in the gene encoding the adenylyl cyclase 5 (ADCY5) isoform, a protein that plays an important role in intracellular transmission. Variants in ADCY5 are associated with a spectrum of neurological disease encompassing dyskinesia, chorea, and dystonia. State of the-art. ADCY5 mutations result in clinically heterogeneous manifestations which comprise a range of core and less to highly variable symptoms. Due to the heterogeneous nature and difficulty in diagnosis of the disorder, available treatments are highly limited. ADCY5-related dyskinesia was reported in 52 individuals in the literature over a five-year period (January 2017 to January 2022). We have listed all the symptoms and their frequency. The most common symptom reported in these patients was dystonia. Over 50% of patients developed dyskinesia and chorea. We report two cases of familial occurrence of symptomatic ADCY5-related dyskinesia. A 45-year-old patient presented with involuntary movements which had been occurring since childhood. The proband's neurological examination revealed dysarthria, involuntary myoclonic twitches, and choreic movements. The patient's 9-year-old son had developed involuntary movements, mainly chorea and dystonia. This paper aims to summarise the recent literature on ADCY5-related neurological disorders and to present a new case of a Polish family with ADCY5 mutation. Genetic diagnostics are important in the context of possible future targeted treatments.

De novo GRIN variants in M3 helix associated with neurological disorders control channel gating of NMDA receptor

N-methyl-d-aspartate receptors (NMDARs) are members of the glutamate receptor family and participate in excitatory postsynaptic transmission throughout the central nervous system. Genetic variants in GRIN genes encoding NMDAR subunits are associated with a spectrum of neurological disorders. The M3 transmembrane helices of the NMDAR couple directly to the agonist-binding domains and form a helical bundle crossing in the closed receptors that occludes the pore. The M3 functions as a transduction element whose conformational change couples ligand binding to opening of an ion conducting pore. In this study, we report the functional consequences of 48 de novo missense variants in GRIN1, GRIN2A, and GRIN2B that alter residues in the M3 transmembrane helix. These de novo variants were identified in children with neurological and neuropsychiatric disorders including epilepsy, developmental delay, intellectual disability, hypotonia and attention deficit hyperactivity disorder. All 48 variants in M3 for which comprehensive testing was completed produce a gain-of-function (28/48) compared to loss-of-function (9/48); 11 variants had an indeterminant phenotype. This supports the idea that a key structural feature of the M3 gate exists to stabilize the closed state so that agonist binding can drive channel opening. Given that most M3 variants enhance channel gating, we assessed the potency of FDA-approved NMDAR channel blockers on these variant receptors. These data provide new insight into the structure–function relationship of the NMDAR gate, and suggest that variants within the M3 transmembrane helix produce a gain-of-function.

Utilising biosensor-based approaches for identifying neurotropic viruses.

Neurotropic viruses, with their ability to invade the central nervous system, present a significant public health challenge, causing a spectrum of neurological diseases. Clinical manifestations of neurotropic viral infections vary widely, from mild to life-threatening conditions, such as HSV-induced encephalitis or poliovirus-induced poliomyelitis. Traditional diagnostic methods, including polymerase chain reaction, serological assays, and imaging techniques, though valuable, have limitations. To address these challenges, biosensor-based methods have emerged as a promising approach. These methods offer advantages such as rapid results, high sensitivity, specificity, and potential for point-of-care applications. By targeting specific biomarkers or genetic material, biosensors utilise technologies like surface plasmon resonance and microarrays, providing a direct and efficient means of diagnosing neurotropic infections. This review explores the evolving landscape of biosensor-based methods, highlighting their potential to enhance the diagnostic toolkit for neurotropic viruses.

Are TrkB receptor agonists the right tool to fulfill the promises for a therapeutic value of the brain-derived neurotrophic factor?

Brain-derived neurotrophic factor signaling via its receptor tropomyosin receptor kinase B regulates several crucial physiological processes. It has been shown to act in the brain, promoting neuronal survival, growth, and plasticity as well as in the rest of the body where it is involved in regulating for instance aspects of the metabolism. Due to its crucial and very pleiotropic activity, reduction of brain-derived neurotrophic factor levels and alterations in the brain-derived neurotrophic factor/tropomyosin receptor kinase B signaling have been found to be associated with a wide spectrum of neurological diseases. However, because of its poor bioavailability and pharmacological properties, brain-derived neurotrophic factor itself has a very low therapeutic value. Moreover, the concomitant binding of exogenous brain-derived neurotrophic factor to the p75 neurotrophin receptor has the potential to elicit several unwanted and deleterious side effects. Therefore, developing tools and approaches to specifically promote tropomyosin receptor kinase B signaling has become an important goal of translational research. Among the newly developed tools are different categories of tropomyosin receptor kinase B receptor agonist molecules. In this review, we give a comprehensive description of the different tropomyosin receptor kinase B receptor agonist drugs developed so far and of the results of their application in animal models of several neurological diseases. Moreover, we discuss the main benefits of tropomyosin receptor kinase B receptor agonists, concentrating especially on the new tropomyosin receptor kinase B agonist antibodies. The benefits observed both in vitro and in vivo upon application of tropomyosin receptor kinase B receptor agonist drugs seem to predominantly depend on their general neuroprotective activity and their ability to promote neuronal plasticity. Moreover, tropomyosin receptor kinase B agonist antibodies have been shown to specifically bind the tropomyosin receptor kinase B receptor and not p75 neurotrophin receptor. Therefore, while, based on the current knowledge, the tropomyosin receptor kinase B receptor agonists do not seem to have the potential to reverse the disease pathology per se, promoting brain-derived neurotrophic factor/tropomyosin receptor kinase B signaling still has a very high therapeutic relevance.

Emerging Promise of Phytochemicals in Ameliorating Neurological Disorders.

The field of medicine and synthetic drug development have advanced rapidly over the past few decades. However, research on alternative medicine such as phytochemicals cannot be ignored. The main reason for prominent curiosity about phytochemicals stems from the belief that usage of natural compounds is safer and has lesser detrimental side effects. The aim of the present review was to discuss in detail with several phytochemicals that have been studied or are being studied in the context of various neurological disorders including depression, Alzheimer's disease, Huntington's disease and even neuroinflammatory disorders such as encephalitis. The potential role of phytochemicals in the treatment or management of symptoms associated with neurological disorders have been included in this article. All data included in this paper has been pooled from various databases including Google Scholar, PubMed, Science Direct, Springer and Wiley Online Library. Phytochemicals have been widely studied for their therapeutic properties associated with neurological disorders. Using various experimental techniques for both in vivo and in vitro experiments, studies have shown that phytochemicals do have antioxidant, anti-inflammatory and neuroprotective activities which play major roles in the treatment of neurological diseases. Even though there has been compelling evidence of the therapeutic role of phytochemicals, further research is still required to evaluate the safety and efficacy of these medicines. Using previously published papers as foundation for additional research such as preclinical studies and clinical trials, phytochemicals can become a safer alternative to synthetic drugs for treating a spectrum of neurological diseases.

Spectrum of Diseases Affecting the Nervous System Associated with JC - Virus: A Review

The JC polyomavirus (JCPyV) belongs to the family Polyomaviridae, genus Betapolyomavirus. These are small, non-enveloped, double-stranded DNA viruses. Approximately 60-80% of the population is carriers of JC polyomavirus. Various ways of spread are being studied. These viruses are associated with a large spectrum of neurological diseases, including progressive multifocal leukoencephalopathy, JC-associated meningitis and encephalitis, JCV granule cell neuronopathy and numerous central nervous system malignancies. In the majority of individuals, the virus remains latent in the kidney tissue. However, in certain subgroups, it leads to the development of severe and frequently disabling or fatal diseases. These subgroups are usually immunosuppressed, which causes the virus to undergo lytic rearrangement. Understanding these diseases and the mechanisms by which they occur is paramount for making accurate diagnoses. Studying these diseases is necessary to develop effective treatments and limit their harmful effects.

Utility of next-generation sequencing in the diagnosis of neurological disorders

ABSTRACT Background: The spectrum of neurological diseases encompasses a large number of disorders, including neuromuscular disorder (NMDs), ataxias, and muscular dystrophies. A detailed clinical examination, followed by electromyography and muscle biopsy, is a traditional diagnostic approach. However, it is never helpful in the identification of the subgroups of either neuropathies or muscular dystrophies apart from being a painful procedure. Aim: The present study was to assess the diagnostic yield of next-generation sequencing (NGS) in the diagnosis of neurological disorders. Materials and Methods: It was a cross-sectional study where consecutive neurological patients for whom NGS was done were included. These variants were classified as pathogenic/likely pathogenic, variants of uncertain significance (VUS), likely benign and benign. Results: Among the 45 cases included, 31 variants were identified in 30 genes, and in 15 patients, no variants were detected. Among 31 variants, 14 were previously reported for the causal of neurological disorder, including NMD, whereas 16 were novel variants (14 missense, 1 frameshift, and 1 splice donor). A definite molecular diagnosis was achieved in 21 cases that were either pathogenic/likely pathogenic, whereas 9 came to be VUS; however, the clinical manifestations correlated well. The phenotype-based sequencing showed a high diagnostic yield of 66% in the present study. Conclusion: NGS improves diagnostic efficiency with quicker and earlier diagnosis. In addition, it is a reliable and noninvasive technique that is effective in the detection of single nucleotide polymorphisms and small deletions.

Enterovirus characterized from cerebrospinal fluid in a cohort from the Eastern United States.

Enteroviruses (EVs) are predominant causes of a spectrum of neurological diseases. To better understand the origins of the outbreaks of disease associated with EV, it is essential to develop an efficient surveillance system that identifies the circulating EVs and correlate their genomic evolution with the disease presentations. The clinical presentations of patients with positive EV from cerebrospinal fluid (CSF) between 2014 and 2022, diagnosed at the Johns Hopkins Medical Microbiology Laboratory, were compared from year to year. EV typing and whole genome sequencing were performed and correlated to the spectrum of disease. A total of 95 CSF specimens were positive for EV between 2014 and 2022. The percentage positivity ranged from the lowest of 1.1% in 2020 to the highest of 3.2% in 2015. The median ages declined from 22 years in 2014 to less than one year starting in 2016 to 34 in 2022. Typing using VP1 sequencing revealed that E30 and E6 were associated with meningitis in adults but coxsackieviruses (CVs-B3 and B5) were detected from pediatric patients with fever. Whole genome sequencing revealed multiple recombination events. In 2020, a recombinant CV-A9 was detected in a CSF sample associated with unusual presentation of sepsis, profound acute bilateral sensory neural hearing loss, and myofasciitis. EV genomic surveillance is needed for a better understanding of the genetic determinants of neurovirulence. Whole genome sequencing can reveal recombination events missed by traditional molecular surveillance methods.

PDZ interaction of the GABA transporter GAT1 with the syntenin-1 in Neuro-2a cells

The GABA transporter GAT1 regulates brain inhibitory neurotransmission and it is considered a potential therapeutic target for the treatment of wide spectrum of neurological diseases including epilepsy, stroke and autism. Syntenin-1 binds to syntaxin 1A, which is known to regulate the plasma membrane insertion of several neurotransmitter transporters. Previously, a direct interaction of syntenin-1 with the glycine transporter GlyT2 was reported. Here, we show that the GABA transporter GAT1 also directly interacts with syntenin-1, involving both unidentified protein interaction interface and the GAT1 C-terminal PDZ binding motif interacting mainly with syntenin-1 PDZ domain 1. The PDZ interaction was eliminated by the mutation of GAT1 isoleucine 599 and tyrosine 598 located in PDZ positions 0 and -1, respectively. This indicates an unconventional PDZ interaction and possible regulation of the transporter PDZ motif via tyrosine phosphorylation. Whole syntenin-1 protein fused to GST protein and immobilised on glutathione resin coprecipitated intact GAT1 transporter from an extract of GAT1 transfected neuroblastoma N2a cells. This coprecipitation was inhibited by tyrosine phosphatases inhibitor pervanadate. The fluorescence tagged GAT1 and syntenin-1 colocalized upon coexpression in N2a cells. The above results show that syntenin-1 might be, in addition to GlyT2, directly involved in the trafficking of GAT1 transporter.

Seasonal Variation in Neurologic Hospitalizations in the United States.

Certain neurologic diseases have been noted to vary by season, and this is important for understanding disease mechanisms and risk factors, but seasonality has not been systematically examined across the spectrum of neurologic disease, and methodologic guidance is also lacking. Using nationally representative data from the National Inpatient Sample, a stratified 20% sample of all non-federal acute care hospitalizations in the United States, we calculated the monthly rate of hospitalization for 14 neurologic diseases from 2016 to 2018. For each disease, we assessed seasonality of hospitalization using chi-squared, Edward, and Walter-Elwood tests and seasonal time series regression models. Statistical tests were adjusted for multiple hypothesis testing using Bonferroni correction. Meningitis, encephalitis, ischemic stroke, intracerebral hemorrhage, Guillain-Barre syndrome, and multiple sclerosis had statistically significant seasonality according to multiple methods of testing. Subarachnoid hemorrhage, status epilepticus, myasthenia gravis, and epilepsy had significant seasonality according to Edwards and Walter-Elwood tests but not chi-square tests. Seasonal time series regression illustrated seasonal variation in all 14 diseases of interest, but statistical testing for seasonality within these models using the Kruskal-Wallis test only achieved statistical significance for meningitis. Seasonal variation is present across the spectrum of acute neurologic disease, including some conditions for which seasonality has not previously been described, and can be examined using multiple different methods. ANN NEUROL 2023;93:743-751.

Natural History of SURF1 Deficiency: A Retrospective Chart Review

BackgroundThis retrospective chart review evaluated the clinical characteristics of SURF1-related neurological disease spectrum to better characterize the phenotypes. MethodsPatient demographics, magnetic resonance imaging abnormalities, neurological events, motor abnormalities, and gastrointestinal and respiratory assistance were evaluated in 27 patients with genetically diagnosed SURF1 deficiency. ResultsThe mean (S.D.) age of symptom onset collected from 13 patients was 19.7 (11.8) months. Mean (S.D.) age of diagnosis collected from 24 patients was 44.0 (45.1) months. The most common symptoms were gross motor delay (14 of 14), fine motor delay (10 of 11), verbal delay (9 of 10), and intellectual and learning disability (14 of 19). Neurological symptoms included ataxia (14 of 15), other abnormal movements (8 of 9), hypotonia (9 of 11), and dystonia (6 of 9). Three of nine reporting patients (33.3%) had a history of seizure, and 84.6% (11 of 13) had a history of regression/loss of acquired skills. Extraneurological clinical features included pulmonary complications (10 of 11) and feeding difficulties (13 of 13); cardiac complications were noted in three patients. Brainstem is frequently involved with the medulla and midbrain being the most common sites. As of July 2021, three patients were deceased. ConclusionsThe most common clinical symptoms were motor delay, verbal delay, intellectual and learning disability, dysphagia, feeding difficulties, and reflux. Neurological presentations include ataxia, hypotonia, visual/ocular abnormalities, dystonia, and imaging abnormalities include basal ganglia and brainstem lesions. Although heterogeneous, SURF1 deficiency should be considered with these clinical and imaging presentations and may support earlier identification.

A KCNC1-related neurological disorder due to gain of Kv3.1 function.

To further clarify genotype:phenotype correlations associated with variants in KCNC1 encoding the voltage-gated potassium (K+) channel subunit Kv3.1 and which are an emerging cause of a spectrum of neurological disease including intellectual disability, isolated myoclonus, progressive myoclonus epilepsy, and developmental and epileptic encephalopathy. We describe the clinical and genetic characteristics of a series of three patients with de novo heterozygous missense variants in KCNC1 associated with nonspecific developmental delay/intellectual disability and central hypotonia without epilepsy or ataxia. All three variants lead to amino acids alterations with mild predicted differences in physicochemical properties yet are localized to the S6 pore region of the Kv3.1 protein between the selectivity filter and PXP motif important for K+ channel gating. We performed whole-cell voltage clamp electrophysiological recording of wild-type versus variants in a heterologous mammalian expression system. We demonstrate a prominent leftward (hyperpolarized) shift in the voltage dependence of activation and slowed deactivation of all variants in the clinically defined series. Electrophysiological recordings are consistent with a gain of K+ channel function that is predicted to exert a loss of function on the excitability of Kv3-expressing high frequency- firing neurons based on the unique electrophysiological properties of Kv3 channels. These results define a clinical-genetic syndrome within the spectrum of KCNC1-related neurological disorders.

Spectrum of Common Pediatric Neurological Disorders: A Cross-Sectional Study From Three Tertiary Care Centres Across Pakistan

BackgroundThere is dearth of information on the spectrum of neurological disorders among children less than 18 years of age. The aim of this study is to identify the commonly presenting neurological disorders among children aged ≤ 18 years in Pakistan. MethodsWe conducted a cross-sectional study at three tertiary care hospitals in Pakistan. ResultsA total of 17,176 children were included in our study; 61.8% were boys and 38.2% females. The most commonly presenting neurological disorder was epilepsy (36%), followed by behavior disorders (16%) and cerebral palsy (10.5%). There was significant difference between children less than 5 years and greater than 5 years age groups, with less than 5 years age group showing higher prevalence for behavioral disorders (P < 0.001), cerebral palsy (P < 0.001), infections (P = 0.014), sequalae (P < 0.001), and developmental disorders (P < 0.001). Gender-wise distribution showed epilepsy to be the most common neurological disorder among both genders, with a significant difference being reported between gender and epilepsy (P = 0.009), headache disorders (P < 0.001), neuroinflammatory disorders (P = 0.025), neurocutaneous syndromes (P < 0.001), behavioral diseases (P < 0.001), cerebral palsy (P = 0.009), and movement disorders (P < 0.001). ConclusionsThe result of this analysis helps to assess the commonly presenting neurological disorders in children. This study will help health care workers in resource-poor settings within Pakistan to be mindful of the common neurological disorders while diagnosing a child with neurological symptoms in an outpatient setting. Health care providers need to be trained to identify and treat these common conditions; however, there is still a dire need for more trained neurologists across the country.

Parental perceptions of dental health in children with neurological disorders

Introduction: Neurological disorders present in different age groups. In children, the spectrum of neurological diseases is multifactorial and varies between motor delay, speech delay, cognitive delay, and global developmental delay. Dental caries constitutes a public health problem that impacts approximately 80% of children nationwide. Aims: This study aims to evaluate the magnitude of dental problems in children with neurological disorders. Materials and Methods: An epidemiological investigation using a cross-sectional design was conducted. A total number of 2451 electronic surveys were sent to parents of children attending the pediatric neurology clinic. Children who attended the clinic from January 2017 to January 1, 2021, were included. Six hundred and seventy-five parents (28%) answered the survey. Statistical Analysis Used: For statistical analysis, IBM SPSS Statistics for Windows (Version 21.0; IBM Corp., Armonk, NY, USA) software was used. Categorical variables were presented using numbers, associated frequencies, and percentages (%). Categorical variables were correlated using the Chi-square test. Results and Discussion: A total number of 2451 surveys were distributed. The response rate was 28%. A total of 675 patients were labeled eligible. Patients' gender characteristics were as follows: 389 (58%) were male while 286 (42%) were female. Patients were distributed into two age groups, a group aged &lt;7 years old and 7–14 years old. Conclusions: Neurological disorders proved to be a burden on patients with dental caries and their families. Socioeconomic status was an important aspect in the families' ability to manage dental caries. Patients with complicated seizures and require multiple drugs were more prone to worse states of oral hygiene. Multidisciplinary care that combines dentists and medical physicians is required.

Spectrum of Neurological Disorders in Neurology Outpatients Clinic in Tertiary Care Hospital: A Cross Sectional Study

Background: Neurological disorders are one of the most noticeable causes of morbidity and mortality that have a negative impact on patient’s lifestyle. A significant rate of these diseases exists in developing populations. However, there is lack and shortage of literature on neurological illnesses in Pakistan. This study was therefore carried out to determine the pattern of neurological diseases in this setting which can also provide a benchmark for planning and care for neurological illnesses at tertiary care level. Methodology: This is a Descriptive cross-sectional review conducted at the neurology outpatient clinic of the Lahore General Hospital, Lahore over the duration of 9 months between April, 2021 and December, 2021. Data was gathered through a predesigned questionnaire from the patients which included data regarding gender, age, marital status, occupation, residential status and affected disease. Results: Among all patients (140) who visited the neurology clinic over this duration, the most frequent neurological disorder was migraine (40%), followed by stroke (25%) and seizures (20%). The major age group that visited the neurology clinics was between 51 and 60 years (30%) and among them, most were males (60%). Conclusion: Stroke, migraine, and Parkinson's disease were the most common neurological disorders among participants of present study. Neurological diseases outnumber other diseases in Pakistan, affecting all age groups and genders. Headache, migraine, stroke, and seizure were found to be more common than AD and other dementias in Western countries and as significant reasons of morbidity. Keywords: Neurological disorders, neurology clinic, outpatients