When worlds collide: Vivid visual hallucinations, cerebral granulomas, and familial risk – A case study and discussion

INTRODUCTION

Hallucinations are sensory experiences without external stimuli, profoundly altering one’s perception of reality.^[1] While auditory hallucinations are a hallmark of schizophrenia, visual hallucinations (VH) have a broader etiology, appearing in psychiatric disorders like schizophrenia or bipolar disorder, as well as neurological conditions.^[2,3] These include Lewy body dementia, Parkinson’s disease (affecting up to 50% of patients), delirium, Charles Bonnet syndrome (linked to visual impairment), Anton syndrome, epilepsy, migraines, brain tumors, peduncular hallucinosis, substance-induced states, metabolic disorders, and prion diseases.^[3,4]

The nature of VH provides diagnostic clues: Simple VH (e.g., lights or shapes) often relates to occipital lobe pathology, while complex VH (e.g., figures or scenes) suggests temporal lobe involvement, delirium, or psychosis.^[4] In schizophrenia, VH is less frequent but increasingly noted, potentially tied to specific symptom profiles.^[5] Neuroimaging studies highlight abnormal activity in visual processing areas, including occipital and temporal cortices, and networks governing attention and reality testing.^[2] Structural imaging may reveal lesions like calcified granulomas, often from past infections such as neurocysticercosis or tuberculosis, which can disrupt neural circuits and contribute to neuropsychiatric symptoms, including psychosis.^[6]

A genetic predisposition, such as a family history of schizophrenia, combined with organic brain changes, may create a “dual-hit” scenario, unmasking psychotic symptoms.^[3,6] Treatment is further complicated by sensitivity to side effects like extrapyramidal side effects (EPSE), often requiring atypical antipsychotics or clozapine.^[7] This report details a woman with complex VH, paranoid ideation, calcified granulomas, cerebral atrophy, and a family history of schizophrenia, complicated by EPSE during treatment.

CASE REPORT

A 41-year-old single woman, belonging to lower socioeconomic status (LSES), presented with a 1-year history of vivid VH occurring during wakefulness. She presented with a 12-month history of VH. She reported seeing clear and distinct images that no one else could perceive. These visions appeared when she was fully awake and conscious, seeming entirely real. The hallucinations often took the form of a small child who would converse with her, ask for food, and express gestures of crying if food was not provided promptly. She believed that the figure sometimes manifested as the goddess Krishna, leading her to leave small amounts of food either next to the vision or in a temple, convinced that the food amount would decrease afterward.

Despite recognizing these figures as real, she did not find them distressing. Initially, the hallucinations occurred once or twice daily, but their frequency gradually increased to four times a day, lasting up to 2 min each. The appearances were more frequent during the day and ceased with eye closure or sleep. There were no perceptual disturbances in other sensory modalities. Ten days before evaluation, she developed fearfulness, suspicion of family harm, and sleep disturbances, without other sensory hallucinations.

Clinical and imaging findings

Mental status examination confirmed VH and paranoid delusions. A computed tomography scan showed [see figure 1]:

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Figure 1:

Computed tomography scan of brain: axial sections show multiple chronic calcified granulomas (marked by yellow arrow) in (a) Left ganglio-capsular region, (b) Right occipital region (largest: 3.6 x 2.5 mm), (c) Right occipito-parietal region, (d) Right occipital region with diffuse cerebral and cerebellar atrophy with enlarged ventricles and sulci. Orange colour arrow shows additional physiological calcifications, i.e., of the pineal gland (a and d) and the choroid plexus (b and d).

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1. Multiple chronic calcified granulomas in the right parietal, bilateral occipital, and left gangliocapsular regions (largest: 3.6 × 2.5 mm in right occipital).

2. Diffuse cerebral and cerebellar atrophy with enlarged ventricles and sulci.

Neurology opinion was sought and it was advised neuroimaging but was not done citing financial constraints. Moreso, no other or specific intervention was advised by neurology.

The positive and negative syndrome scale (PANSS) yielded a baseline score of 49.^[8] Trifluoperazine (TFP) (5 mg twice daily) and trihexyphenidyl (2 mg twice daily) were initiated but caused restlessness, slurring of speech, difficulty in sleeping, and, on examination, revealed postural tremors and cogwheel rigidity. Clozapine was initiated due to the patient poor tolerance to TPF despite being on central anti-cholinergic, restlessness (possibly akathisia), and insomnia. Clozapine was introduced at 12.5 mg nightly, with cross-tapering of TFP. Within 3 weeks, the patient showed marked clinical improvement with resolution of VH and reduction in suspiciousness, fearfulness, and better sleep profile. PANSS score at follow-up was 33.^[8]

DISCUSSION

This case illustrates the convergence of organic brain changes (granulomas and atrophy) and genetic predisposition in VH and psychosis. The occipital granulomas likely contribute to VH, despite their chronic nature.^[4,6] Diffuse atrophy suggests a broader neurodegenerative process, while the family history of schizophrenia indicates genetic vulnerability.^[9] A “dual-hit” model, where organic lesions unmask a genetic predisposition, is plausible.^[3]

The differential includes schizophrenia with prominent VH, organic psychosis, or a combined presentation.^[5,6] EPSE with TFP reflects treatment sensitivity, common in patients with neurological abnormalities.^[7] TFP-related EPSE could also be explained by individual susceptibility. Clozapine’s lower EPSE risk and efficacy justified its use, with rapid symptom improvement supporting this choice.^[7,10] This case emphasizes the need for comprehensive neuroimaging and careful treatment selection, as the boundary between organic and functional psychosis is often unclear.^[3] Clozapine’s role in complex cases warrants further exploration.^[10]

CONCLUSION

We report a case of a woman with VH, paranoid delusions, calcified granulomas, cerebral atrophy, and a family history of schizophrenia, where EPSE necessitated clozapine, leading to significant improvement. This underscores the importance of integrating organic and functional etiologies, managing treatment side effects, and adopting a tailored neuropsychiatric approach.