Gender Inequity in Neurological Health Care in India: Socio-Cultural Influences, Clinical Challenges, and Potential Pathways to Equity

The issue of gender-based inequity in health care, particularly in neuromedicine, is indeed a matter of serious concern in India.From birth, girls often face discrimination, which can manifest in malnutrition, unequal access to education, and inadequatehealth care, all of which impact their neurological health. Neurological conditions such as epilepsy, stroke, psychosomaticdisorders, and demyelinating disorders reveal stark disparities in diagnosis, treatment, and care based on gender. Keyfactors contributing to this gender-based inequity in neuromedicine are socio-cultural barriers (deep-rooted societal normsand cultural practices in India often prioritize the health of male family members over females. These norms can result inwomen delaying seeking medical attention or being denied care altogether. This contributes to late diagnoses and pooroutcomes for women with neurological conditions; myths misconceptions and misbeliefs (neurological disorders, particularlyepilepsy and psychosomatic disorders, carry significant stigma, especially for women). Misconceptions around conditionslike epilepsy can lead to social isolation, exclusion from marriage prospects, and neglect in care. Additionally, women’shealth issues are often dismissed as psychological or “hormonal”, leading to misdiagnoses; access to health care (womenoften face structural barriers, such as lack of autonomy in decision-making, lower financial independence, and restrictedmobility), which limit their access to neuromedical care. Health care resources in rural and underserved areas are limited,and gender biases in treatment mean that women are less likely to receive timely and adequate interventions for neurologicalconditions; malnutrition (poor nutrition among women), starting from childhood, is a significant contributor to neurologicalhealth problems. Malnutrition during pregnancy, which affects fetal development, can result in a higher prevalence ofdevelopmental neurological disorders in children, with gender-based neglect often continuing into adulthood. Potentialsolutions include awareness campaigns, policy changes, health care provider training, and community empowerment. Bydelving into these areas, we can begin to understand the complexities of gender inequity in neuromedicine and work towardmore equitable health care solutions

Wernicke’s encephalopathy precipitated by neuromyelitis optica spectrum disorder and Graves’ disease: A tale of clinical and radiological dilemmas

Background Neuromyelitis optica spectrum disorder (NMOSD), an autoimmune astrocytopathy, may share common clinico-radiological features with Wernicke's encephalopathy (WE). A variant of NMOSD, known as area postrema syndrome (APS), that presents with intractable hiccups and associated vomiting, might lead to the depletion of nutrients if not detected and treated early. Autoimmune thyroid disorders (i.e., Graves’ disease) may be associated with NMOSD. Rarely, thyrotoxicosis can give rise to thiamine depletion and WE. Case presentation Here, we present a case of untreated hyperthyroidism in an Indian female who presented with thyrotoxicosis and later developed WE, possibly also contributed by NMOSD (APS)-induced recurrent vomiting. The patient recovered with antithyroid drugs, parenteral thiamine, and immunomodulatory therapy. The possible pathogenic mechanisms have been discussed. Conclusion Our case establishes the importance of considering NMOSD variants in metabolic encephalopathy, especially if neuroimaging is suggestive and in the backdrop of another autoimmune disorder

Acute onset movement disorders in diabetes mellitus: A clinical series of 59 patients

Background and purpose: No previous study has assessed the frequency and clinical– radiological characteristics of patients with diabetes mellitus (DM) and acute onset non-choreic and nonballistic movements. We conducted a prospective study to investigate the spectrum of acute onset movement disorders in DM.Methods: We recruited all the patients with acute onset movement disorders and hyper-glycemia who attended the wards of three hospitals in West Bengal, India from August 2014 to July 2021.Results: Among the 59 patients (mean age = 55.4± 14.3 years, 52.5% men) who were included, 41 (69.5%) had choreic or ballistic movements, and 18 (30.5%) had nonchoreic and nonballistic movements. Ballism was the most common movement disorder (n= 18, 30.5%), followed by pure chorea (n= 15, 25.4%), choreoathetosis (n= 8, 13.6%), tremor (n= 5, 8.5%), hemifacial spasm (n= 3, 5.1%), parkinsonism (n= 3, 5.1%), myoclonus (n= 3, 5.1%), dystonia (n= 2, 3.4%), and restless leg syndrome (n= 2, 3.4%). The mean duration of DM was 9.8 ± 11.4 years (89.8% of the patients had type 2 DM). Nonketotic hypergly-cemia was frequently (76.3%) detected. The majority (55.9%) had no magnetic resonance imaging (MRI) changes; the remaining showed striatal hyperintensity. Eight patients with MRI changes exhibited discordance with sidedness of movements. Most of the patients (76.3%) recovered completely.Conclusions: This is the largest clinical series depicting the clinical–radiological spectrum of acute onset movement disorders in DM. Of note was that almost one third of patients had nonchoreic and nonballistic movements. Our findings highlight the importance of a capillary blood glucose measurement in patients with acute or subacute onset movement disorders, irrespective of their past glycemic status

Phrenic nerve conduction study in the early stage of guillain–barre syndrome as a predictor of respiratory failure

Background: Guillain-Barré syndrome (GBS) has unpredictable clinical course with severe complication of respiratory failure. Objective: To identify clinical profiles and electrophysiological study particularly non-invasive Phrenic nerve conduction study in patients of early GBS to predict respiratory failure. Methods: 64 adult (age≥18yrs) patients of early GBS (onset ≤ 14 days) during the study period from January 2014 to October 2015 were evaluated by clinical profiles of age, gender, antecedent infection, time to peak disability, single breath counts, cranial nerve involvement, autonomic dysfunction and non-invasive Phrenic nerve conduction study. Patients with predisposition factors of polyneuropathy like diabetes mellitus, hypothyroidism, vitamin deficiency, renal failure were excluded. Results: Among 64 patients abnormal phrenic nerve conduction study was seen in 65.62% cases (42/64) and 45.23% (19/42) of them developed respiratory failure. Phrenic nerve sum latency, amplitude, duration and area were abnormal in those who developed respiratory failure and they had sum of phrenic nerve latency >28 msec, sum of CMAP amplitude 50 msec and sum of area 0.05). Rapid disease progression to peak disability, more severe disease, shorter single breath counts and cranial nerve involvement were seen more often in patients with respiratory failure. Conclusion: Abnormal Phrenic nerve conduction study in the early Guillain-Barré syndrome might be of great value independently in predicting impending respiratory failure

Magnetic Resonance Imaging and Multidetector Computed Tomography Evaluation of Craniovertebral Junction Abnormalities

BACKGROUND The craniovertebral junction is a complex articulation between occiput, atlas, axis and supporting ligaments enclosing the soft tissue structures of cervicomedullary junction which includes medulla, spinal cord and lower cranial nerves. The incidence of different types of CVJ anomalies varies with demographic environment &amp; ill-defined genetic factors. CVJ anomalies are more frequently found in Indian subcontinent than anywhere else in the world. Even in India, these anomalies are more frequently documented from Bihar, Uttar Pradesh, Rajasthan and Gujarat. The reason for this geographical clustering is more speculative. The CVJ anomalies can be either due to bony or soft tissue anomalies. They are common in all age groups and almost equal in both sex groups. The anomalies can be due to congenital or acquired causes. There has been a renewed interest in the normal anatomy &amp; pathological lesions of CVJ anomalies with dynamic xrays, computed tomography (CT) and magnetic resonance imaging (MRI). The clinical features are often delayed up to 2 nd or 3rd decade, since they are subtle and often missed. Various congenital anomalies and acquired disease processes can affect the craniovertebral junction. They often cause diagnostic dilemmas. Only few studies have been conducted in this regard. This study is an attempt to define importance of precise diagnosis for pre-treatment evaluation and systematic classification of CVJ abnormalities with MRI and multi-detector computed tomography (MDCT). METHODS We conducted this cross-sectional descriptive study with 55 patients, who had been referred to us for CT / MRI from Department of Neurology. 3 Tesla MRI (GE Healthcare) and 16 slice MDCT (Philips) were used in this study. RESULTS In our study, congenital anomalies were the most common type of CVJ abnormality followed by degenerative changes and trauma. MRI proved to be better at detecting soft tissue abnormalities and assessing spinal cord compression, although CT was very much accurate at demonstrating bony lesions with short scan times and ability to reconstruct in three orthogonal planes. CONCLUSIONS CT and MRI cannot be compared in imaging the craniovertebral junction and should be complementary to each other. KEYWORDS Craniovertebral Junction, MRI, MDCT</jats:p

Sjögren-Larsson syndrome: a rare disease of the skin and central nervous system

Sjögren-Larsson syndrome is a recessively inherited disease caused by a deficiency of fatty aldehyde dehydrogenase with presenting features of congenital ichthyosis, spastic diplegia or tetraplegia, and mental retardation. The basic pathogenic mechanism is deficiency of fatty aldehyde dehydrogenase, which may lead to an accumulation of long-chain fatty alcohols hampering cell membrane integrity, which further disrupts the barrier function of skin and white matter of the brain. MRI of the brain shows diffuse symmetrical white matter hyperintensities on T2-weighted sequences. Although there is no definitive cure for Sjögren-Larsson syndrome, most patients survive until adulthood and management involves therapies directed towards controlling specific problems. We present a case of Sjögren-Larsson syndrome with classical clinical and MRI features, including a few distinctly atypical characteristics in various attributes

Higher order visual dysfunction and myoclonic-atonic seizure: an atypical presentation of CLN6 neuronal ceroid lipofuscinosis

Neuronal ceroid lipofuscinosis is a rare childhood neurodegenerative disease, classified under the spectrum of progressive myoclonic epilepsy (PME). Cognitive decline, seizures including myoclonus, vision loss and ataxia are the commonly described manifestations of this illness. While visual failure in this disease is largely attributed to retinal, macular degeneration and optic atrophy, with this index case, we report an atypical presentation in the form of higher order visual dysfunction. The pattern of cognitive regression has further been explored here with higher order visual dysfunction and language regression being the predominant manifestations, stemming from an involvement of bilateral occipitoparietal/occipitotemporal networks. Yet another unique feature of this case also lies in the occurrence of myoclonic-atonic seizure, a semiology rarely reported before in PME.</jats:p