Challenging the canon: Neurocysticercosis without seizures in alcohol-dependent patients deserves deeper neuroimmunological scrutiny

To Editor,

We read with great interest the recent case series by Alam et al.,[1] which described three patients with alcohol dependence, who developed disseminated neurocysticercosis (NCC) in the absence of seizures—a hallmark clinical symptom in most NCC cases. The authors offer a compelling hypothesis that chronic alcohol use may alter immune or neuronal excitability, preventing the typical seizure manifestation. We commend the authors for their clinical rigor, but believe several critical dimensions warrant further discussion and elaboration.

SEIZURE-FREE NEUROCYSTICERCOSIS: A RARE YET RECOGNIZED PHENOMENON

While NCC is indeed the most common preventable cause of adult-onset epilepsy in endemic areas,[2] seizure-free presentations, though rare, are not unprecedented. Prior reports—particularly those focused on extra parenchymal NCC—have documented neuropsychiatric manifestations in the absence of seizures.[3] However, what distinguishes the present series is the parenchymal involvement evidenced on neuroimaging, typically associated with epileptogenic activity due to mass effect, inflammation, or calcification-induced gliosis.[4]

IMMUNOMODULATION BY ALCOHOL: A DOUBLE-EDGED SWORD

The authors’ proposition—that chronic alcohol consumption modulates host immunity and neuronal excitability, thus altering disease expression—is plausible. Experimental and human studies support alcohol’s biphasic impact on immunity: low doses may suppress inflammatory cytokines, whereas chronic intake enhances systemic inflammation and immune dysregulation.[5,6] The idea that alcohol-induced immune modulation may reduce perilesional inflammation and limit seizure genesis is fascinating but remains speculative. Immunophenotyping in similar patients could elucidate cytokine profiles, T-cell responses, or microglial activation states as mechanistic clues.

ALTERNATIVE EXPLANATIONS AND DIAGNOSTIC CONFOUNDERS

An alternative consideration is that the patients’ subclinical seizures or nonconvulsive status epilepticus may have gone undetected. Electroencephalography (EEG), not reported in the original article, would be critical in confirming the absence of epileptiform activity. Moreover, in Case 2, the psychotic features during alcohol withdrawal (e.g., hallucinations and agitation) may overlap with NCC-induced neuropsychiatric symptoms, blurring the diagnostic clarity.

IMPLICATIONS FOR SCREENING AND MANAGEMENT

This case series also raises an important clinical implication: the underdiagnosis of NCC in alcohol-dependent populations. In endemic regions like India, where pork consumption and poor sanitation co-exist with high alcohol use, routine neuroimaging for atypical neuropsychiatric symptoms could uncover occult NCC.[7] This approach may enable early intervention with cytocidal therapy and secondary seizure prevention.

RECOMMENDATIONS FOR FUTURE RESEARCH

To build upon the insightful work by Alam et al.,[1] we recommend the following research directions:

1. Prospective studies comparing seizure prevalence in NCC patients with and without alcohol dependence.

2. EEG monitoring to rule out subclinical epileptiform activity in similar clinical scenarios.

3. Immunological profiling to assess the role of alcohol-induced modulation in NCC pathophysiology.

4. Longitudinal imaging studies to correlate cyst stage with clinical evolution and seizure onset in alcohol-using vs. non-using cohorts.

CONCLUSION

The authors should be commended for highlighting an atypical but clinically meaningful presentation of NCC in alcohol-dependent individuals. This intersection of parasitic neuroinfection, substance use, and immunology presents a fertile ground for deeper inquiry, both to improve clinical recognition and to advance our understanding of host–pathogen–substance interactions in neuropsychiatric disease.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.