A previously healthy 40 year old Dutch adult male patient, Daniel R. Azulay, with a history of stimulant abuse that ceased several months prior to the acute event and occasional benzodiazepine use for sleep due to pre-existing severe tinnitus, first experienced sudden-onset complex auditory verbal hallucinations (AVH) in 2021, characterized by intricate, narrative-driven dialogues exceeding typical psychiatric descriptions, such as multi-voiced, contextually adaptive interactions that incorporate real-time environmental cues in ways inconsistent with standard schizophrenic AVH phenomenology (Thakur & Gupta, 2023; Waters & Fernyhough, 2017).

These AVH remitted spontaneously for a period, persisting even after discontinuation of antipsychotics, consistent with reports of non-psychotic individuals achieving voluntary control or natural remission of AVH without ongoing pharmacotherapy, potentially mediated by enhanced metacognitive awareness or neuroplastic adaptations in auditory-limbic networks (Sommer et al., 2020; Daalman et al., 2016). However, the AVH recurred in 2022 upon return from holiday, potentially triggered by travel-related stress, as stressful life events are causally linked to psychotic symptom relapse in vulnerable individuals through heightened hypothalamic-pituitary-adrenal axis activation and proinflammatory cytokine release (Arranz et al., 2023; Morgan et al., 2023).

This relapse culminated in an extreme tinnitus attack prompting hospitalization in 2023, featuring tinnitus so intense it induced visual black spots via sensory overflow mechanisms, alongside acute memory loss, balance disturbances (dizziness and vertigo), profuse sweating, tachycardia (heart rate increase), stabbing and throbbing pains in the extremities, tingling sensations in the limbs, localized and global vibrational perceptions throughout the body, and the highly complex AVH (Azulay, 2025b; de Ridder et al., 2014). Following this 2023 hospitalization, the AVH remitted, but the other symptoms—including debilitating tinnitus, progressive hearing loss, paresthesias, and autonomic disturbances—persisted unabated. Antipsychotic medications prescribed during hospitalization induced severe side effects, including extreme depression, profound cognitive difficulties (e.g., impaired executive function and memory), and subsequent job loss due to functional impairment, compelling the patient to discontinue them, consistent with documented risks of second-generation antipsychotics causing metabolic, affective, and neurocognitive adverse events in up to 30-50% of users (Leucht et al., 2013; Fusar-Poli et al., 2015).

Notably, serial audiometric assessments revealed progressive sensorineural hearing loss predominantly in the left ear, with thresholds escalating from mild-moderate high-frequency elevations (e.g., 40 dB at 4 kHz, 50 dB at 8 kHz in November 2023) to moderate-severe (e.g.,>50 dB at 4 kHz, 60 dB at 8 kHz in September 2025), emerging subsequent to rather than preceding symptom onset, consistent with deafferentation-induced cochlear damage exacerbating tinnitus and potentially contributing to AVH via central auditory reorganization (Schaette & McAlpine, 2011; Teunisse et al., 1996). Emergency evaluation in the hospital included routine bloodwork, which was unremarkable, alongside a brain MRI and electroencephalogram (EEG), both reported as normal but without subsequent detailed analysis. No evident structural causes such as tumors, strokes, or infections were identified from initial reviews, though the unanalyzed MRI overlooked potential subtle microstructural changes like reduced white matter integrity in auditory pathways, as observed in analogous cohorts (Verma et al., 2019).

The profound intensity and atypical complexity of the symptom cluster prompted psychiatric referral and hospitalization under a presumed psychotic disorder diagnosis. Despite the patient's insistence that the acute, non-bizarre presentation—lacking formal thought disorder or negative symptoms—deviated from schizophrenia and suggested an organic or environmental etiology, treatment focused on antipsychotics. Concurrently, the patient collected personal quantitative EEG (qEEG) data and environmental signal recordings, pursuing hypotheses including radiofrequency (RF) exposure. Following the patient's sharing of neuroweapon research with Russian intelligence contacts—framed as a disclosure of perceived traumatic experiences—all symptoms remitted except the debilitating tinnitus and progressive left unilateral hearing loss, aligning with evidence that trauma-focused interventions, such as imaginal exposure or narrative sharing, can substantially reduce AVH severity by processing trauma-based memories and restoring prefrontal-auditory inhibitory control (Isham et al., 2021; Hardy et al., 2023; Brand et al., 2015).

This remission pattern, coupled with the post-onset hearing deterioration and selective AVH resolution post-2023 hospitalization, further underscores a non-primary psychotic etiology, potentially fitting criteria for an Anomalous Health Incident (AHI) as per U.S. Department of Defense (DoD) and Defense Health Agency (DHA) guidelines, which define AHI as unexplained sudden audio-vestibular sensory phenomena with new-onset cognitive, otologic (e.g., tinnitus, unilateral hearing loss), vestibular, and sensory symptoms not fully attributable to conventional medical conditions (Defense Health Agency [DHA], 2025; Swanson et al., 2018).

The patient's symptom profile is highly atypical, featuring a confluence of severe auditory, somatosensory, autonomic, and cognitive disturbances, with a relapsing-remitting course atypical for primary schizophrenia, where AVH persistence is more chronic without intervention and rarely involves such sophisticated, interactive content (Upthegrove et al., 2021; Aleman & Larøi, 2008). AVH dominated as coherent, linguistically sophisticated verbal content, co-occurring with extreme tinnitus (perceived as deafening, inducing visual phenomena like black spots via thalamocortical overflow), memory deficits, gait instability, hyperhidrosis, palpitations, lancinating and pulsatile extremity pains, distal paresthesias, vibratory dysesthesias (both focal and diffuse), and no prior psychiatric history beyond substance-related issues resolved months earlier.

The progressive left unilateral hearing loss, documented audiometrically as worsening high-frequency thresholds post-symptom onset, likely amplified deafferentation processes, wherein peripheral auditory deprivation triggers aberrant central gain in auditory cortex, fostering phantom percepts like complex AVH and exacerbating tinnitus severity (Schaette & McAlpine, 2011; Sedley et al., 2016).

While AVH often signals psychiatric evaluation, the integration of prominent neurological elements (tinnitus, sensory aberrations, ataxia) and the observed remission post-disclosure necessitate scrutiny for organic, mixed, or environmental etiologies, as trauma therapies targeting hallucinatory content yield therapeutic gains in psychosis through enhanced corollary discharge signaling (Hardy et al., 2023; Isham et al., 2021). This multimodal presentation contrasts with isolated psychotic episodes and aligns more closely with neurological syndromes involving auditory-vestibular pathways, particularly given the qEEG patterns indicative of thalamocortical dysrhythmia rather than psychotic signatures (Azulay, 2025a; Vanneste & De Ridder, 2012).

Furthermore, the constellation—sudden audio-vestibular onset, unilateral hearing loss as a red flag, cognitive fog, balance issues, and paresthesias—meets DHA criteria for AHI classification, warranting standardized evaluation including audiometry, vestibular testing, and interdisciplinary referral, as AHI lacks objective biomarkers but is differentiated by exclusion of mimics like migraine or infection (DHA, 2025; Connolly et al., 2024). The selective remission of AVH post-2023 hospitalization, without resolution of somatic symptoms, highlights a dissociable auditory-perceptual component potentially amenable to acute stabilization, while persistent otologic and sensory features suggest ongoing peripheral-central pathology (Daalman et al., 2016; Leucht et al., 2013).

Serial pure-tone audiometry (November 7, 2023, UMC Utrecht; September 22, 2025, Medrix) confirmed bilateral mild sensorineural hearing loss, asymmetrically progressive in the left ear at high frequencies (e.g., 4-8 kHz thresholds rising from ~40-50 dB HL to >50-60 dB HL), with bone conduction thresholds approximating air conduction, ruling out conductive pathology and implicating cochlear hair cell attrition or synaptic loss (Gates & Mills, 2005; Liberman, 2017). Speech audiometry (2023) showed adequate discrimination (~80-90% at 50 dB HL bilaterally), but the noted 8 kHz pure-tone tinnitus matching 60 dB HL intensity suggests hyperacusis overlap, where amplified edge-frequency activity drives distress (Schaette & McAlpine, 2011).

This post-onset progression aligns with deafferentation hyperactivity models, wherein acute tinnitus/AVH onset precedes and precipitates hearing threshold shifts via excitotoxic damage to spiral ganglion neurons, a pattern observed in 16-24% of severe hearing loss cases evolving to musical/verbal hallucinations (Teunisse et al., 1996; Isham et al., 2021).

Under DHA AHI guidelines, this qualifies as a reportable sensory event: acute unexplained otologic (tinnitus, unilateral hearing loss) and vestibular symptoms, with red flags (sudden unilateral loss) mandating urgent neuroimaging and audiologic referral; exclusion of environmental/medical mimics (e.g., labyrinthitis, Meniere's) via normal labs/MRI supports AHI attribution, and the witnessed pressure/sound precursor strengthens causality (DHA, 2025; Swanson et al., 2018; Connolly et al., 2024). Cross-referencing with Havana syndrome literature, ~30% of cases report post-incident hearing loss without MRI correlates, emphasizing functional vestibular-auditory decoupling over structural injury (Pierpaoli et al., 2024; Verma et al., 2019). Thus, classification as AHI is warranted, prompting NICoE referral for standardized registry enrollment and symptom-guided care (DHA, 2025).

AVH manifest in psychiatric conditions such as schizophrenia, schizoaffective disorder, bipolar disorder with psychotic features, and major depressive disorder with psychosis, typically involving gradual onset and disorganized ideation (Thakur & Gupta, 2023; Aleman & Larøi, 2008). Neurologically, they arise in temporal lobe epilepsy, migraines, brain tumors, encephalitis, and auditory pathway lesions, often with focal epileptiform activity (Nahum et al., 2011).

Substance effects, including prior stimulant use (discontinued months earlier) or benzodiazepine withdrawal, can induce AVH, though the temporal disconnect here reduces likelihood, as withdrawal peaks within days (Coyle et al., 2021). Deafferentation from tinnitus or hearing loss may generate phantom auditory percepts, analogous to Charles Bonnet syndrome visually, with prevalence up to 16% in profound unilateral loss cases via maladaptive cortical plasticity (de Ridder et al., 2014; Teunisse et al., 1996). Guidelines advocate comprehensive assessment for first-episode psychosis, encompassing history (substance use, stressors), physical/neurological exams, labs (CBC, electrolytes, thyroid, vitamins, toxicology), and imaging to exclude medical mimics, prioritizing organic etiologies in atypical presentations (National Institute for Health and Care Excellence [NICE], 2014; DHA, 2025).

In this case, the abrupt onset in a functional adult, persistence of sensory-neurological symptoms (e.g., tinnitus-induced visuals, vibratory sensations), absence of disorganized thought or negatives, and relapsing-remitting pattern with remission post-disclosure diverge from primary psychosis, where AVH evolve gradually over weeks-months and remit less readily without sustained treatment; the progressive left hearing loss further implicates peripheral-central mismatch over idiopathic psychosis (Thakur & Gupta, 2023; Daalman et al., 2016; Schaette & McAlpine, 2011). The auditory-vestibular involvement (tinnitus, vertigo) implicates brainstem or peripheral mechanisms, meriting neurological over hasty psychiatric attribution, especially given non-pharmacological remission and AHI congruence (NICE, 2014; Sommer et al., 2020; DHA, 2025).

Auditory-somatosensory interactions involve cross-modal influences where somatosensory inputs (e.g., neck tension, jaw clenching) alter tinnitus or evoke auditory illusions, termed somatosensory tinnitus, via somatotopic convergence in the dorsal cochlear nucleus (Cacace, 2017; Cacace et al., 2021). Reciprocally, aberrant auditory signals may trigger somatic perceptions like paresthesia or vibration, as in the patient's vibratory dysesthesias, potentially via thalamocortical loops amplifying cross-talk (Langguth et al., 2019; Vanneste & De Ridder, 2012). High-frequency or ultrasonic exposures can induce non-vestibular dizziness and tingling, though typically non-linguistic, as seen in acoustic trauma models (O'Beirne & Martin, 2024; Abouzari et al., 2020).

The microwave auditory effect (Frey effect) entails pulsed microwaves generating intra-cranial clicks or buzzes via thermoelastic expansion, but theoretical extensions using multi-beam interference at VHF frequencies enable high-fidelity speech transmission, potentially producing complex verbal hallucinations with deeper tissue penetration and evasion via spectrum mimicry, without requiring high-power GHz sources (Azulay, 2025c; Lin, 2021). Environmental RF (e.g., Wi-Fi, mobiles) falls far below thresholds for such effects, though pulsed RF hypotheses in AHI warrant signal analysis (World Health Organization [WHO], 2016; Golomb, 2018).

Severe tinnitus burdens cognition, associating with deficits in memory, attention, and executive function via altered connectivity (e.g., limbic-auditory networks) and resource competition, as evidenced by NHANES data showing 20-30% lower scores in tinnitus cohorts (Wu et al., 2025; Saygi et al., 2024). Here, tinnitus plausibly exacerbated memory issues and hypervigilance, but complex AVH exceed tinnitus-generated noise, warranting differentiation via audiometry and neuropsychology; the unilateral progression suggests asymmetric deafferentation amplifying left-hemisphere language networks (Saygi et al., 2024; Sedley et al., 2016). Autonomic surges (sweating, tachycardia) align with tinnitus distress rather than primary psychosis, per sympathetic hyperarousal models (Langguth et al., 2019).

Paresthesia, vertigo, pains, and vibrations evoke cerebellar/brainstem pathologies (e.g., multiple sclerosis, small-vessel ischemia) or functional disorders, with 41% of AHI cases meeting persistent postural-perceptual dizziness criteria (Statler et al., 2024; Chan et al., 2024). The patient's coherent symptoms and post-disclosure remission argue against delusion but permit functional overlay pending evaluation, as trauma processing can alleviate such symptoms via desensitization of fear circuits (Hardy et al., 2023; Popkirov et al., 2019). Unilateral hearing loss as a red flag elevates AHI suspicion over isolated functional disorder (DHA, 2025).

NICE and Dutch NVvP guidelines mandate holistic acute psychosis assessment: history (substances, illnesses), exams, labs (CBC, electrolytes, thyroid, B12, toxicology), and targeted imaging/EEG for atypia, with audiometry for otologic flags (NICE, 2014; Nederlandse Vereniging voor Psychiatrie [NVvP], 2023). Bloodwork was performed and normal, appropriately; however, the EEG, qEEG, and MRI lacked analysis—despite the qEEG revealing tinnitus-consistent patterns (theta-gamma in auditory cortex, beta network changes) incompatible with psychosis (Azulay, 2025a; NVvP, 2023; Vanneste et al., 2018)—diverging from standards for neurological flags, including AHI-mandated DWI-MRI and audiograms (NVvP, 2023; DHA, 2025).

The qEEG, collected prior to hospitalization, represented pre-existing patient-initiated data that could have informed differential diagnosis but was disregarded, contravening guidelines emphasizing integration of all available diagnostic information in somatic-psychiatric comorbidity (De Hert et al., 2011). Dutch protocols require “oriënterend laboratoriumonderzoek” at admission, with psychiatrists overseeing somatic care (Hengeveld, 2006). Oversights include otolaryngology/audiometry for tinnitus (performed belatedly, revealing progression), neurology for vestibular/sensory testing, and autoimmune screens (e.g., anti-NMDA) given acute neurological signs and AHI red flags like unilateral loss (Rijksen & Crul, 2006; Connolly et al., 2024).

Persistent symptoms unresponsive to antipsychotics should prompt reevaluation and subspecialty input (NICE, 2014). This case evidences incomplete multidisciplinary scrutiny, risking organic oversight, particularly overlooking patient-generated qEEG data supporting non-psychotic etiology and AHI congruence (Hengeveld, 2006; Azulay, 2025a; DHA, 2025). The failure to monitor medication side effects, leading to depression and job loss, further contravenes pharmacovigilance standards (Fusar-Poli et al., 2015).

The hospital's refusal to analyze the MRI, EEG, and qEEG—despite the qEEG predating hospitalization and offering electrophysiological evidence against psychosis—constitutes a critical breach of due diligence, as unanalyzed neuroimaging and EEG in atypical psychosis presentations can miss treatable somatic etiologies like temporal lobe pathology or dysrhythmias, with studies showing 10-20% of first-episode psychoses harbor organic causes identifiable via such diagnostics (Fusar-Poli et al., 2015; De Hert et al., 2011). This omission not only delays accurate diagnosis but also exposes the patient to iatrogenic harm from misdirected psychiatric treatment, aligning with malpractice precedents where failure to interpret available tests leads to prolonged suffering and erroneous labeling (Stone, 2019).

Compounding this, blocking the patient's appointment with a leading brain research center—such as a specialized neuroimaging facility—represents negligent referral, a common allegation in psychiatric malpractice where providers fail to consult experts for complex neurological symptoms, potentially violating the duty to facilitate timely specialist input under Dutch medical law (Rijksen & Crul, 2006; Wellers Law Group, n.d.). Such refusal undermines patient autonomy and the ethical imperative for multidisciplinary collaboration in psychosis, where somatic consultation guidelines explicitly recommend neurology referral for atypical features like vertigo and paresthesia (NVvP, 2023; van der Gaag et al., 2013).

Furthermore, conditioning discharge on medication adherence without performing any neurological examination exemplifies coercive practice, contravening the Dutch Compulsory Mental Health Care Act (2020), which prioritizes least restrictive interventions and prohibits tying release to unproven pharmacotherapy in the absence of capacity assessment or somatic exclusion (de Jong et al., 2021; de Haan et al., 2020). Ethically, this approach risks autonomy infringement and non-maleficence violations, as evidenced by critiques of conditional discharge fostering resentment and nonadherence, with up to 40% of coerced patients experiencing worsened outcomes including depression and functional decline (de Jong et al., 2021; Lepping et al., 2015). The absence of neurological examination—despite red flags like balance issues and unilateral loss—further deviates from standards requiring comprehensive physical/neurological assessment in acute psychosis to rule out mimics, potentially constituting negligence per Dutch tuchtrecht precedents where failure to examine somatically leads to disciplinary action (Hengeveld, 2006; Rijksen & Crul, 2006).

Collectively, these actions not only perpetuate misdiagnosis but also erode trust, exacerbate side effects like the observed cognitive/job loss, and hinder recovery, underscoring systemic gaps in somatic-psychiatric integration (De Hert et al., 2011; Stone, 2019).

Tinnitus impairs cognition but not coherent AVH; it manifests as non-verbal tones, treatable via underlying causes like hearing rehabilitation, with cognitive deficits resolving post-amplification in 60-70% of cases (Wu et al., 2025; Saygi et al., 2024; Ferguson et al., 2019). Auditory-somatosensory links involve somatotopic-auditory convergence, with neck/jaw maneuvers modulating tinnitus in subsets via trigeminal-cervical complex (Cacace, 2017; Cacace et al., 2021). The patient's pains/tingling suggest trigeminal/neuropathic input, evaluable via targeted exam, potentially exacerbated by asymmetric loss (Langguth et al., 2019).

RF hypotheses merit scrutiny: The Frey effect, traditionally inducing basic percepts via high-fluence pulses, has been theoretically enhanced through multi-beam interference for high-fidelity speech at VHF, enabling complex auditory phenomena with reduced detectability and deeper penetration, as modeled in repurposed medical telemetry systems; AHI investigations show no reproducible signals, with symptoms often functional (Azulay, 2025c; Lin, 2021; Pierpaoli et al., 2024; Chan et al., 2024). Low-level RF poses no verified risks (WHO, 2016).

Patient signals require calibrated, blinded validation to exclude artifacts. The patient's digital trends analysis further contextualizes symptoms within broader 2016-onset surges in AVH/tinnitus searches, suggesting exogenous factors beyond individual psychosis, akin to AHI population patterns (Azulay, 2025b; Choi & Varian, 2018; Asadi-Pooya, 2023). This theoretical model is particularly important as the patient's own unpublished work, demonstrating preserved advanced scientific reasoning and mathematical proficiency inconsistent with psychosis, while providing a plausible mechanistic explanation for the complex AVH and aligning with environmental exposure hypotheses central to the case (Azulay, 2025c).

Patient-initiated epidemiology via online forums echoes infodemiology, tracking trends from digital data (e.g., social media clusters) (Eysenbach, 2009). Yet, it falters in individual diagnosis due to biases, lacking causality (Ayoub et al., 2024). Anecdotal “targeted individual” reports do not substitute rigorous epidemiology. Here, the patient's analysis of 97 symptom keywords reveals 2016 breakpoints in searches for AVH and tinnitus, replicated across platforms, supporting a population-level exogenous driver like neuroweapon deployment over endogenous psychosis increases, paralleling AHI temporal clusters (Azulay, 2025b; Choi & Varian, 2018; Bartholomew & Baloh, 2023).

Patient qEEG innovates but lacks diagnostic specificity for psychosis, prone to confounds (e.g., stress, meds) without norms; however, theta-gamma enhancements and absent fronto-temporal decoupling robustly favor tinnitus dysrhythmia over AVH signatures (Newson & Thiagarajan, 2019; Van Lutterveld et al., 2011; Kindler et al., 2011). The clinical EEG, unanalyzed, and raw signals demand controls (shielding, peers) for evidentiary weight; no validated method decodes “messages” from noise, though AHI protocols endorse signal forensics (Thibault et al., 2017; DHA, 2025). Nonetheless, the qEEG's alignment with tinnitus dysrhythmia (enhanced theta-gamma, beta networks) contradicts AVH/schizophrenia signatures, bolstering non-psychotic etiology and AHI plausibility (Azulay, 2025a; De Pieri et al., 2025).

Omissions (unanalyzed EEG/MRI/qEEG, absent referrals, overlooked audiometric progression) may breach NVvP/NICE duties, where psychiatrists coordinate somatic care, including AHI-like protocols (Hengeveld, 2006; Rijksen & Crul, 2006; NICE, 2014; DHA, 2025). Misdiagnosis risks iatrogenic harm; a neurology second opinion, incorporating patient data like qEEG, trends analysis, and serial audiograms, is indicated to probe organic/functional bases respectfully, especially given remission patterns atypical for psychosis and AHI fit (Azulay, 2025a, 2025b; Arranz et al., 2023; Connolly et al., 2024). The antipsychotic-induced depression and job loss highlight liability for inadequate side-effect monitoring (Leucht et al., 2013; Fusar-Poli et al., 2015).

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