Delay in the diagnosis of dementia in urban India: Role of dementia subtype and age at onset.

BACKGROUND: Early diagnosis of dementia is crucial for timely intervention. However, frequently, there is a substantial delay in diagnosis. Therefore, it is essential to recognise and address the barriers to early diagnosis. These have not been systematically studied in India. We at a specialist memory clinic in India investigated the time from symptom onset to diagnosis of dementia and factors contributing to the delay. METHODS: In this cross-sectional study, consecutive patients with dementia (n = 855) seen at a private hospital underwent a standard clinical assessment and investigations. The primary outcome variable was time from symptom onset to diagnosis (TTD). The association of age, education, gender, dementia subtype, and age of onset on TTD were examined using a univariate analysis of covariance. RESULTS: The median TTD was 24 months; 43% were diagnosed after 24 months. There was a significant association between TTD and age at onset (young onset-median 36 months vs. late onset-24 months) and dementia subtype. Patients with vascular dementia were diagnosed significantly earlier as compared to patients with Alzheimer's disease (AD) and frontotemporal dementia (FTD) [median 18, 24, and 30 months, respectively]. There was no effect of gender or education on the TTD. CONCLUSION: About 40% of patients with dementia were diagnosed more than 2 years after symptom onset, particularly young onset dementias and FTD. Our study findings highlight the gaps in diagnosing patients with dementia in urban India and have significant implications for developing and implementing multifaceted interventions to improve the early diagnosis of dementia.

Clarithromycin-induced Seizures and Status Epilepticus.

Clarithromycin is a commonly used antibiotic. Neuropsychiatric adverse effects are recognized, but the occurrence of seizures and status epilepticus (SE) has been rarely reported. We report the case of an elderly patient who developed generalized tonic-clonic seizures (GTCS) followed by nonconvulsive status epilepticus (NCSE), 2 days after starting clarithromycin. Other causes of seizures were excluded by magnetic resonance imaging (MRI) of the brain, CSF analysis, and routine laboratory studies, thus establishing the causal role of clarithromycin. Clarithromycin was stopped and parenteral antiepileptic drugs started, which controlled the status. In the elderly, symptoms like delirium, drowsiness, confusion, or seizures can occur due to an underlying systemic disease, brain pathology, or adverse effects of medications, all of which must be correctly differentiated. This case illustrates the occurrence of seizures and SE due to clarithromycin. Awareness about this possibility will help physicians recognize and treat such situations promptly. How to cite this article: Seetharam R, Iyer RB, Nooraine J, Ramachandran J. Clarithromycin-induced Seizures and Status Epilepticus. Indian J Crit Care Med 2021;25(8):945-947.

Mild malformation of cortical development with oligodendroglial hyperplasia and epilepsy (MOGHE): a widespread disease with an apparently focal epilepsy.

Mild malformation of cortical development with oligodendroglial hyperplasia and epilepsy (MOGHE) is a recently recognized, highly epileptogenic, distinct histopathological entity in drug-resistant epilepsy that primarily involves the frontal lobes. Surgical outcomes in MOGHE are variable. Although the diagnosis is based on histopathology, high-resolution MRI helps to differentiate MOGHE preoperatively from other forms of cortical malformations (i.e., mMCD II and FCD IIa). We discuss the clinical, electrographic, radiological and histopathological characteristics of MOGHE in two patients who underwent evaluation for drug-resistant epilepsy followed by electrocorticography-based resection. Both patients presented with childhood-onset refractory frontal lobe epilepsy with a high seizure burden. Interictal epileptiform discharges were widespread. PET abnormalities were disproportionate to the MRI findings. Cognitive impairment, persistent epileptiform discharges on post-resection electrocorticography and sub-optimal surgical outcomes suggest that MOGHE is a widespread pathology in focal epilepsy.

Apomorphine: The Initial Indian Experience in Relation to Response Tests and Pumps.

BACKGROUND: Apomorphine is an option for continuous dopaminergic therapy in Parkinson's disease (PD). However, its effects in varied populations are limited due to its availability. OBJECTIVE: To assess the efficacy and outcomes of apomorphine in Indian patients. MATERIALS AND METHODS: Retrospective analysis of PD patients who underwent apomorphine response test (ART), along with the subset, who went on to apomorphine pumps. RESULTS: Twenty-nine confirmed PD patients underwent ART and all PD patients showed good clinical response. 19 subjects developed adverse events which included: nausea (n-15, 51.7%), vomiting (n-10, 34.4%), sleepiness (n-08; 27.5%), yawning (n-07, 24.1%), postural hypotension (n-03, 10.3%), dizziness (n-03, 10.3%), and profuse sweating (n-01, 3.4%). Apomorphine pumps were initiated in six subjects, with significant clinical improvement. Adverse events on pump included subcutaneous nodules, nausea, hypersexuality. Two among them subsequently discontinued the pump primarily due to financial constraints. CONCLUSIONS: Apomorphine adds up to the armamentarium for treatment of PD patients in India with good clinical responses.

Dual/double pathology in neurocysticercosis causing drug resistant epilepsy - Chance association or causal?

INTRODUCTION: Neurocysticercosis (NCC) as cause of drug resistant epilepsy (DRE) is commonly reported from India. We reviewed the neuropathological findings in patients undergoing resective surgery for DRE due to NCC, to determine the pathomechanism of epileptogenesis. METHODS: Clinical, demographic and neuropathological findings of histologically confirmed cases of NCC causing DRE between 2005-2019 were reviewed. NeuN, GFAP, phosphorylated neurofilament, vimentin, CD34 for glial/ neuronal alterations, and Masson trichrome, Luxol Fast blue for evidence of fibrosis/ demyelination was used to determine cause of epileptogenesis. RESULTS: There were 12 cases of NCC associated with dual/ double pathology, which constituted 3.02 % (12/398) of all the operated DRE. [Age range: 17-37y, Male:Female = 1.4:1]. Seizure duration ranged from 3-32y, with seizure onset between 4-27y. On MRI, lesions were of variable signal intensity on T1 and isointense on T2 with blooming on GRE/ SWI, and CT revealed calcification. Majority (11/12) had associated hippocampal sclerosis (HS) type 1 (dual pathology), localised to the same side as cysticercal cyst, suggesting it may be involved in the pathogenesis of HS. Ten had single cysticercal lesion involving ipsilateral hippocampus in 6, parahippocampal gyrus in 2, amygdala and temporal lobe in 1 case each. One had multiple NCC located in bilateral frontal, parietal and ipsilateral hippocampus. Adjacent cortex around the NCC evaluated in 6 cases, revealed inflammation, gliosis, axonal disruption/ beading, and variable synaptic/ neuronal dystrophic changes. There was a single case of NCC with Focal cortical dysplasia (FCD) type IIb (double pathology). In 11/12 cases Engel's post-surgery outcome was available with all having class I outcome. CONCLUSION: HS was most common pathology associated with cysticercosis (Dual pathology), localised ipsilateral to the cysticercal cyst, suggesting that HS is a secondary/ epiphenomenon. Perilesional changes such as inflammation, gliosis, dystrophic synaptic and axonal pathology play a role in inducing or perpetuating the epileptiform activity. The association of FCD IIb with NCC in one case is likely to be a chance occurrence.

Varied aetiology of acute acquired comitant esotropia: A case series.

This is an observational case series of five cases of acute acquired comitant esotropia (AACE) with diplopia, aged between 5 and 12 years. The duration of presenting complaints ranged from 4 days to 2 months. A detailed ophthalmic evaluation and neuroimaging were done on all patients. Three patients were found to have intracranial pathology. Two patients had pontine glioma and one patient had benign intracranial hypertension. One patient was diagnosed as accommodative spasm and one patient was diagnosed as having Type 2 AACE.We would like to conclude that AACE can be of a varied aetiology ranging from convergence spasm to those harboring serious intracranial diseases. We reiterate that AACE has a small but significant association with intracranial disorders. Neuroimaging is a definite need in cases which cannot be proved to be either Type 1 or 2.