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Background: The challenges being faced during the lockdown period may worsen motor or non-motor symptoms in Parkinson's disease (PD). Objective: This study was undertaken to investigate the impact of lockdown on the disease activity, caregiver perceptions and the quality of life of patients with PD. Materials and Methods: This cross-sectional study was conducted from June till September 2020. Sixty-four patients with PD and caregivers were interviewed telephonically after obtaining consent. The responses were recorded by means of a structured questionnaire. Non-motor symptoms scale (NMSS) and the Parkinson Disease Questinnaire-8 (PDQ-8) were applied. PDQ-8 severity index (PDQ-8 SI) scores were expressed as percentage of the raw PDQ-8 score of the total score. Data were analsyed by using SPSS version 20.0. Results: Of 64 patients, 39 (60.9%) were men and 25 (39.1%) were women. The overall median age of the patients was 65 (55.25–69.75) years. The median duration was 48 (30–84) months. Twenty-six (40.6%) patients reported symptomatic worsening during the lockdown period. Slowness in activities of daily living and walking worsened in 15 (57.7%) and 14 (53.8%) patients, respectively, while tremors increased in 12 (46.2%) patients. Mood and sleep disturbances were the most common non-motor symptoms to worsen. Increase in non-motor symptoms and the NMSS total score were independent predictors of PDQ-8 scores. Increase in non-motor symptoms during the lockdown was an independent predictor of the highest quartile of PDQ-8 SI scores. Conclusions: Motor and non-motor symptoms have worsened in patients with PD during the lockdown. The increase in non-motor symptoms was independently associated with poorer quality of life among patients with PD during the lockdown.

Subacute combined degeneration of the spinal cord is a typical clinical syndrome due to vitamin B12 deficiency, characterised by the involvement of the posterior column and corticospinal tracts. Occasionally, it may present with atypical features such as a sensory level and Lhermitte's sign, both traditionally considered to be a feature of compressive myelopathy. Spinal magnetic resonance imaging strongly augments the diagnosis by exhibiting changes in the posterior column in the form of a ‘dot’. We describe such a patient who responded to therapy.

Drug-resistant tuberculosis is an increasing healthcare challenge. Drug regimen building demands the use of different therapeutic groups, many of which harbor neurotoxicity as a side-effect, whether central or peripheral. Peripheral neuropathy is a major concern as it tends to be severe and usually irreversible. Anti-tubercular drugs that may contribute to peripheral neuropathy include INH, ethambutol, linezolid, cycloserine and para-amino salicylic acid. This potential adverse effect must be balanced against the intrinsically grave prognosis that drug resistant tuberculosis harbors. We present such a clinically challenging case of a 25 years-old female with extremely drug resistant tuberculosis whose treatment necessitated the use of several neurotoxic anti-tubercular drugs, leading to severe sensory peripheral neuropathy who did not improve despite the withdrawal of culprit drugs. She developed positive and negative sensory symptoms in both lower limbs. Nerve conduction studies were suggestive of sensory neuropathy affecting both lower limbs. Alternate causes of peripheral neuropathy including HIV, vasculitis, B12 deficiency and diabetes were ruled out. Despite drug withdrawal, the patient did not improve significantly. This case emphasizes the irreversibility of anti-tubercular therapy-induced peripheral neuropathy, demanding more rigorous clinical screening for the same while managing such patients.

Glutaric aciduria type 1 is an autosomal recessive disorder caused by mutations in GCDH gene on chromosome 19 leading to the deficiency of glutaryl-CoA dehydrogenase which causes an abnormal metabolism of lysine, hydroxylysine and tryptophan with resultant accumulation of glutaric acid and 3-hydroxy glutaric acid. Usual presentations include macrocephaly with recurrent dystonic episodes, along with developmental regression. The diagnosis is based on characteristic magnetic resonance imaging finding of widening of sylvian fissures and urinary tandem mass spectroscopic analysis of excess glutarylcarnitine and hydroxyglutaric acid. Management includes lysine-free diet and carnitine supplementation.

Background: The complex relationship between migraine and epilepsy has frequently been described to represent a clinical and electrographic “borderland.” These two conditions share clinical expressions such as paroxysmal and chronic nature, as well as semiology, particularly visual phenomenon. Objective: We aimed to review the current literature on the overlapping phenomena of migraine and epilepsy. Materials and Methods: We searched the PubMed for relevant literature and conducted a narrative review on migraine and epilepsy. Results: Migraine and epilepsy share a complex and pathophysiologically intriguing relationship. The International Classification of Headache Disorders, 3rd edition (ICHD-3) makes diagnostic provisions for migraine aura–triggered seizures (Subchapter 1.4.4) and headache attributed to epileptic seizure (Subchapter 7.6), the latter being further categorized as 7.6.1 Ictal epileptic headache, and 7.6.2 post-ictal headache. Neurological conditions such as certain channelopathies and epilepsy syndromes exhibit both conditions within their phenotypic spectrum, suggesting shared genetic and molecular underpinnings. Diagnostic confusion may arise, particularly between occipital epilepsy and the visual aura of migraine. Antiseizure medications may be effective for the treatment of migraines that occur in concert with epilepsy. Conclusions: Migraine and epilepsy share several clinical features and have intertwined genetic and molecular underpinnings, which may contribute to common pathogenesis. Electroencephalography may be useful as a diagnostic tool in selected cases.

Autoimmune encephalitis (AE) is being increasingly recognized as a cause of new-onset movement disorders. Movement disorders in AE are diverse and range from hyperkinetic conditions such as oromandibular dyskinesias, tremors and chorea to hypokinetic ones such as bradykinesia and parkinsonism. Stereotypies have been described in association with anti-NMDAR encephalitis. Similarly, sleep dysfunction is an underrecognized feature in many AE subtypes, prominently anti-IgLON5 although the correlation of phenotype of sleep dysfunction with a particular antibody subtype in AE is unclear. Despite the recognition of both these features as part of an overreaching spectrum in any patient with AE, seldom are they the sole presenting manifestations. Additionally, the challenge is further compounded in a patient who has seronegative AE since neither sleep disturbances nor stereotypies have been well characterized with this condition yet, and the diagnosis is conditional to exhausting a list of ancillary supportive features. In this brief communication, we describe the case of a young man who presented with hypersomnolence and an unusual focal nose-pinching stereotypy of subacute onset who lacked the presence of other typical clinical characteristics such as cognitive/memory impairment and seizures and had negative autoimmune antibodies but responded to immune therapy dramatically. We propose that the presence of de novo hypersomnolence and stereotypy should inform a potential diagnosis of AE.

Spinal tuberculosis is the most common form of extrapulmonary tuberculosis. It is of great importance to neurologists because of the potentially devastating complication of paraplegia, which may set in during active disease or the healed phase. Due to the deep-seated nature of the disease, definitive diagnosis is often challenging. There is no clear consensus on the appropriate duration of therapy for spinal tuberculosis, with various guidelines recommending treatment from as short as 6 months to up to 18 months. In this article, we present a critical appraisal of the evidence on the same. In our opinion, the duration of antitubercular therapy needs to be individualized and the decision to terminate therapy should be multifactorial (clinical, radiological, pathological/microbiological where possible) rather than being enmeshed within any particular guideline.

It is estimated that there are around 50 million people living with epilepsy (PWE) globally. Around one-sixth of this population resides in India. Around 10–12 million people with epilepsy reside in India. A significant proportion of PWE do not receive appropriate treatment, leading to a large treatment gap (TG). Poor awareness of antiepileptic drugs (AEDs), cultural practices, social stigma surrounding epilepsy, lack of accessibility to healthcare, and a severe shortage of medical professionals trained in the management of epilepsy are major contributors to the TG. Infectious diseases, particularly neurocysticercosis, form a major bulk of underlying cause for epilepsy. Certain geographical regions exhibit typical patterns of epilepsy. In this article, we attempt to provide a broad overview of the incidence, prevalence, etiology, types, mortality, and treatment of epilepsy derived from the data from Indian studies. India provides particular challenges in the management of patients with epilepsy, not only in terms of the wide spectrum of epileptic conditions but also in the demand for medical practice based on economic constraints.

Langerhans cell histiocytosis (LCH) is a rare disorder in adults which usually manifests with involvement of multiple organ systems, including the central nervous system. We describe an unusual case of biopsy-proven LCH presenting with frontotemporal-dominant cognitive impairment with hypothalamic involvement, along with multisystem disease. We propose that the dementia was probably an immune-mediated process triggered by LCH which responded dramatically to high-dose steroids.

Neurological complications related to anti-rabies vaccine are uncommon. The involvement of the optic nerve is extremely rare. It has been occasionally reported after Semple’s vaccine administration due to the presence of highly antigenic sheep brain tissue in the vaccine. To our knowledge, this is the first case report of optic neuritis after chick embryo-derived anti-rabies vaccine.

Subacute sclerosing panencephalitis (SSPE) is a slowly progressive degenerative disorder caused by measles virus. It is characterised by typical clinical and electrophysiological features in the form of slow myoclonic jerks, with progressive cognitive impairment, visual symptoms, and periodic complexes on EEG, with raised titres of anti-measles antibodies in CSF and serum. Atypical presentations of SSPE have been reported including brainstem involvement, ADEM-like presentation, acute encephalitis, and cerebellar ataxia. Presentation with predominant extrapyramidal features is uncommon. We describe a case of SSPE presenting with extensive rigidity with highly elevated CPK values, mimicking neuroleptic malignant syndrome (NMS) which was most probably due to central dopaminergic blockade induced by the disease process. To our knowledge, this is the first case of SSPE presenting with a NMS-like syndrome.

Neurosyphilis has become an uncommon diagnosis in the current era. Neurological manifestations of syphilis usually lie within the spectrum of meningovascular syphilis, tabes dorsalis or general paresis of the insane. Although sensory ataxia may occur as part of spinal cord involvement, cerebellar ataxia has been rarely described as a manifestation of neurosyphilis. In this report, we describe a rare case neurosyphilis presenting in the form of a pure pancerebellar syndrome of subacute progression.