Dincolo de sevrajul alcoolic: delirium persistent asociat cu leziuni cerebrale sugestive pentru metastaze

Introduction

Delirium represents an acute neuropsychiatric syndrome characterized by fluctuating disturbances of attention and awareness, accompanied by additional cognitive deficits and visual hallucinations⁽¹⁾. Its diagnosis is primarily clinical and relies on a thorough medical history and careful clinical examination, together with the identification of potential differential diagnoses and underlying causes⁽¹⁾. The fluctuating nature of delirium may complicate its recognition, particularly when patients are assessed during periods of relative lucidity⁽¹⁾.

Delirium represents an important clinical complication in patients with cancer and occurs across different oncological settings⁽²⁾. Recent evidence confirms a substantial burden of delirium in this population, although its occurrence varies according to cancer type, clinical setting and the methods used for its assessment⁽²⁾. The diagnostic evaluation of an acute confusional state may become challenging when several potential precipitating conditions coexist, making continued clinical reassessment essential when the course of symptoms is not adequately explained by the initially suspected cause^(1,2).

Chronic alcohol use may further complicate the diagnostic evaluation of acute neuropsychiatric manifestations. Delirium tremens, also referred to as alcohol withdrawal delirium, is a severe complication of alcohol withdrawal resulting from neurophysiological disturbances following alcohol cessation in chronically dependent individuals⁽³⁾. Its clinical presentation includes delirium in the context of alcohol withdrawal, and it is associated with neuropsychiatric manifestations and autonomic dysregulation⁽³⁾. Consequently, when an acute confusional state occurs following alcohol cessation, a withdrawal-related etiology may initially appear clinically plausible. However, the coexistence of alcohol withdrawal with other medical conditions capable of causing delirium may complicate both diagnosis and management.

This diagnostic challenge becomes relevant in patients with lung cancer, because of the tendency of this malignancy to metastasize to the central nervous system^(4,5). Brain metastases are a major complication of non-small cell lung cancer, and they may already be present at the initial diagnosis or develop during the subsequent course of the disease^(4,5). Their clinical manifestations are variable and may include headache, seizures, motor dysfunction, gait disturbances, cognitive impairment and disturbances of mental functioning⁽⁴⁾. Therefore, the development or persistence of neuropsychiatric manifestations in a patient with lung cancer, particularly when accompanied by neurological abnormalities, should raise the possibility of intracranial involvement, warranting appropriate neurological assessment⁽⁴⁾.

The coexistence of chronic alcohol use and a recently diagnosed malignancy may create a complex clinical scenario when acute neuropsychiatric manifestations occur. We present the case of a 39-year-old patient with chronic alcohol use and recently diagnosed non-small-cell adenocarcinoma, who was initially admitted with moderate alcohol withdrawal syndrome. Although withdrawal manifestations resolved following specific treatment, fluctuating disturbances of attention and awareness, perceptual abnormalities and neurological signs persisted. Subsequent cerebral imaging revealed multiple brain lesions suggestive of metastases associated with significant vasogenic oedema and mass effect.

Case presentation

We present the case of a 39-year-old man with no documented history of psychiatric hospitalization or previous psychotropic treatment, admitted as an emergency to the psychiatric department on 29 May 2026. His medical history was significant for pulmonary tuberculosis diagnosed in 2023, with subsequent post-tuberculosis pulmonary fibrosis, and non-small cell lung adenocarcinoma, diagnosed in March 2026. He reported chronic alcohol consumption for approximately 10 years, consisting of four to five 500 mL beers daily with occasional consumption of spirits, as well as active smoking of one to two packs of cigarettes per day for approximately 15 years. No use of other psychoactive substances was reported by the patient or his relatives.

The patient presented approximately 72 hours after cessation of alcohol consumption with generalized tremor, profuse sweating, marked anxiety, irritability, episodes of psychomotor restlessness, mixed insomnia, alcohol-seeking behavior and persistent fronto-occipital headache. The Clinical Institute Withdrawal Assessment for Alcohol Revised (CIWA-Ar) score was 18, supporting the diagnosis of moderate alcohol withdrawal syndrome.

Routine laboratory investigations, including complete blood count, serum biochemistry, electrolytes, glucose, hepatic and renal function tests and urinalysis, showed no significant abnormalities.

The pharmacological treatment administered during psychiatric hospitalization is summarized in Table 1. The manifestations attributed to alcohol withdrawal progressively resolved during the first four days. However, the fluctuating impairment of attention and awareness, visual hallucinations, headache and neurological abnormalities persisted, prompting further diagnostic evaluation. Key clinical milestones leading to etiological assessment are summarized in Table 2.

Despite remission of the withdrawal syndrome, the patient continued to exhibit fluctuating disturbances of attention, vigilance and awareness, with episodes of temporospatial disorientation alternating with periods of relative lucidity. During periods of relative lucidity, he was cooperative and able to provide relevant answers, whereas during confusional episodes the communication became difficult and the responses were delayed or inappropriate. Marked hypoprosexia, distractibility, hypovigilance, bradypsychia and bradylalia were observed.

Memory impairment, involving fixation and recall, became apparent during confusional episodes but improved substantially during periods of lucidity. Brief cognitive assessment performed outside the confusional episodes provided a Mini-Mental State Examination (MMSE) score of 28/30.

Perceptual disturbances consisted predominantly of elementary visual hallucinations, initially accompanied by partial insight and becoming more prominent during confusional episodes. His behavior occasionally became bizarre, with a reduced ability to perform activities of daily living. A particularly notable finding was dressing apraxia, manifested by an inability to correctly orient his clothing while dressing. These manifestations were accompanied by persistent fronto-occipital headache.

Abbreviations: CIWA-Ar – Clinical Institute Withdrawal Assessment for Alcohol, Revised; CT – computed tomography

Key clinical milestones leading to etiological reassessment

Neurological examination provided additional evidence of an underlying organic neurological disorder. Bilateral horizontal nystagmus, a wide-based ataxic gait and postural instability were observed. Deep tendon reflexes were decreased bilaterally in the lower limbs, with mild distal impairment of tactile sensation. Muscle strength was mildly reduced globally, without focal motor deficit, and no pyramidal, extrapyramidal or meningeal signs were identified.

Heteroanamnestic data were particularly important in reconstructing the temporal course of the disorder. Relatives reported that fluctuations in the patient’s level of consciousness had already been present for approximately one to two weeks before hospitalization and, importantly, preceded alcohol cessation. This temporal relationship, together with the persistence of the confusional syndrome after resolution of the withdrawal manifestations, the recently diagnosed lung adenocarcinoma, persistent headache and objective neurological abnormalities, prompted reconsideration of the etiology and investigation for a structural intracranial cause.

Contrast-enhanced cranial computed tomography revealed a large right parietal expansive lesion measuring approximately 47×40 mm, surrounded by extensive vasogenic edema and producing mass effect on the right lateral ventricle, with an approximately 10-mm leftward midline shift. Additional lesions included two cerebellar lesions measuring approximately 10 mm and 8 mm, respectively, and an approximately 4-mm lesion in the left centrum semiovale (Figure 1).

The overall clinical course, together with the neurological and neuroimaging findings, supported the diagnosis of delirium in the context of multiple intracranial lesions radiologically consistent with brain metastases, associated with extensive vasogenic edema and with significant mass effect. The patient was transferred to a neurosurgical department. Corticosteroid therapy was initiated for cerebral edema, and surgical excision of the right parietal lesion was performed. Consequently, the histopathological findings, the postoperative evolution and the long-term psychiatric, neurological and oncological outcomes were not available.

Discussion

The present case illustrates a clinically relevant diagnostic overlap between two simultaneously occurring conditions: a moderate alcohol withdrawal syndrome and a persistent delirium in the context of structural intracranial lesions. At admission, the temporal relationship with alcohol cessation, together with generalized tremor, profuse sweating, anxiety, irritability, psychomotor restlessness and insomnia, supported the diagnosis of alcohol withdrawal syndrome. These manifestations are consistent with the clinical spectrum of alcohol withdrawal, which includes tremor, autonomic activation, anxiety, insomnia, perceptual disturbances, seizures and, in its most severe form, delirium tremens^(3,6,7). Benzodiazepines remain the standard treatment for clinically significant alcohol withdrawal^(6,7). In the present case, the progressive resolution of the manifestations during the first four days of treatment further supported the presence of alcohol withdrawal syndrome.

Importantly, alcohol withdrawal syndrome should be distinguished from alcohol withdrawal delirium, which represents a severe manifestation of alcohol withdrawal. Delirium tremens represents a severe complication of alcohol withdrawal characterized by delirium in the context of withdrawal and accompanied by marked neuropsychiatric and autonomic abnormalities^(3,6). The initial diagnosis of moderate alcohol withdrawal in our patient should not be regarded retrospectively as incorrect. The subsequent clinical course demonstrated that alcohol withdrawal represented only one component of a more complex neuropsychiatric presentation.

The major diagnostic turning point was the persistence of a fluctuating confusional syndrome after the manifestations attributable to alcohol withdrawal had resolved. Delirium is characterized by an acute disturbance of attention and awareness with a fluctuating evolution and may additionally involve cognitive deficits and visual hallucinations⁽¹⁾. Because its manifestations fluctuate, patients may appear substantially improved or relatively lucid during individual assessments, making longitudinal observation particularly important⁽¹⁾. In the present case, episodes of temporospatial disorientation, impaired attention and hypovigilance alternated with periods of relative lucidity. The MMSE (Mini-Mental State Examination) score of 28/30 obtained outside the confusional episodes illustrates the limitations of relying on a single cognitive assessment in a syndrome fundamentally characterized by fluctuation. The diagnosis of delirium remains primarily clinical and depends on the overall temporal pattern, history and examination rather than on an isolated cognitive score⁽¹⁾.

Informant history data were valuable in reconstructing the temporal pattern. Relatives reported that fluctuations in the patient’s level of consciousness had already been present for approximately one to two weeks before admission, and they had preceded alcohol cessation. This chronology could not be fully explained by alcohol withdrawal alone. Current literature on alcohol withdrawal in hospitalized patients emphasizes the importance of reassessment for differential diagnoses, particularly in medically complex patients in whom withdrawal manifestations may coexist with other acute conditions⁽⁶⁾. In the present case, the onset of fluctuations before alcohol cessation, together with persistence of delirium after resolution of the withdrawal manifestations, warranted further investigation for an additional etiology.

Reassessment became particularly important in the context of the patient’s recently diagnosed lung adenocarcinoma. Brain metastases represent a major complication of non-small cell lung cancer, and their clinical manifestations may include headache, seizures, motor dysfunction, gait disturbances, cognitive impairment and alterations in mental functioning^(4,5,8). In the present case, persistent fronto-occipital headache, dressing apraxia, horizontal nystagmus, a wide-based ataxic gait and postural instability represented neurological warning signs accompanying the psychiatric presentation and strengthened the indication for cerebral imaging.

The association between intracranial neoplasia and delirium has recently been quantified more precisely. In a 2025 systematic review and meta-analysis including 27 studies and 35,958 patients with brain tumors, Tentor et al. reported an overall delirium occurrence of approximately 17%, increasing to 31% among patients with brain metastases⁽⁹⁾. Hypoactive delirium was more frequent than hyperactive delirium in the included studies⁽⁹⁾. These findings are particularly relevant to the present case, in which the clinical picture was not characterized exclusively by agitation: periods of psychomotor restlessness alternated with hypovigilance, bradyphrenia and reduced responsiveness. The patient’s fluctuating neuropsychiatric presentation is therefore consistent with the heterogeneous clinical expression of delirium described in patients with intracranial lesions.

The importance of delirium extends to the wider oncological population. An updated 2026 systematic review and meta-analysis comprising 43 studies and 242,923 patients with cancer reported an overall delirium prevalence of 27.1% and an incidence of 14.4%, with considerable variation according to cancer type, clinical setting and assessment method⁽²⁾. These findings reinforce the need for active etiological assessment when delirium occurs in patients with cancer, in whom several precipitating factors may coexist⁽²⁾. In the present case, the identification of one plausible precipitant, alcohol withdrawal, was therefore insufficient to explain a confusional syndrome whose subsequent course became increasingly discordant with the initial diagnosis.

Neuroimaging identified a major structural intracranial abnormality capable of explaining the persistent neuropsychiatric syndrome. Contrast-enhanced CT demonstrated a large right parietal lesion radiologically suggestive of a metastatic lesion and associated with extensive vasogenic oedema, compression of the right lateral ventricle and an approximately 10-mm leftward midline shift, together with additional cerebellar and supratentorial lesions. Perilesional vasogenic edema is a common complication of brain metastases and may contribute substantially to neurological symptom burden⁽⁸⁾. Furthermore, evidence indicates that neurocognitive impairment may already be present in patients with brain metastases before treatment and, therefore, cannot be attributed exclusively to subsequent radiotherapy or systemic therapy⁽¹⁰⁾. In our patient, multifocal lesions consistent with metastatic disease and associated with extensive edema and significant mass effect provided a clinically coherent structural explanation for the delirium and neurological abnormalities.

Strict symptom-to-lesion mapping should be avoided. Although the large parietal lesion could plausibly have contributed to higher-order cognitive and praxis disturbances, and cerebellar involvement to gait and postural abnormalities, multiple lesions, extensive vasogenic edema and a substantial mass effect were simultaneously present. The available findings therefore support a multifocal structural intracranial process rather than allowing each neuropsychiatric or neurological manifestation to be assigned confidently to an individual lesion.

Wernicke encephalopathy represented an important competing diagnosis, because chronic alcohol use, altered mental status, nystagmus and gait ataxia overlap with its characteristic clinical spectrum. Wernicke encephalopathy typically manifests through varying combinations of confusion, ocular abnormalities, including nystagmus, and gait ataxia, while the complete classical triad is not invariably present⁽¹¹⁾. Early intravenous thiamine administration is recommended when the disorder is suspected, because the delayed treatment may result in significant neurological morbidity⁽¹¹⁾. Thiamine administration in the present patient was therefore clinically appropriate. However, specific investigations directed toward Wernicke encephalopathy were not performed, and this diagnosis cannot retrospectively be considered formally excluded. The subsequent demonstration of multiple intracranial lesions with extensive edema and mass effect identified a major structural abnormality capable of accounting for the persistent neurological and neuropsychiatric syndrome.

Other organic causes of delirium remained part of the broader differential diagnosis. Routine laboratory investigations did not identify a major metabolic abnormality; however, EEG, brain MRI and an extended metabolic, infectious or paraneoplastic work-up were not performed during the six-day hospitalization. These potential contributors should therefore not be described as definitively excluded. This distinction is relevant in interpreting the case, because the identification of a highly significant structural intracranial abnormality does not establish the absence of every other potential contributing factor.

The subsequent therapeutic approach was consistent with current principles for symptomatic brain lesions suggestive of metastases. Vasogenic edema represents an important neurological complication of brain metastases, for which corticosteroids are used when clinically symptomatic⁽⁸⁾. Current oncological guidelines recommend that patients with symptomatic brain metastases should receive local therapy, indicating that patients with large tumors producing mass effect are among those more likely to benefit from surgical intervention⁽¹²⁾. In the present case, the large symptomatic parietal lesion was associated with extensive edema and substantial midline displacement, corticosteroid therapy was initiated, and the patient subsequently underwent neurosurgical excision of the parietal lesion.

From a psychiatric perspective, one of the most important aspects of this case is the potential for diagnostic anchoring. Alcohol cessation provided an immediately plausible explanation for the initial neuropsychiatric presentation. The diagnostic risk would have arisen from allowing a confirmed withdrawal syndrome to account for manifestations that subsequently followed a different clinical trajectory. Persistence of delirium after withdrawal resolution, onset of fluctuations before alcohol cessation, persistent headache, neurological abnormalities and the recent diagnosis of lung adenocarcinoma supported the presence of an additional organic process.

The case also highlights the diagnostic value of longitudinal observation and informant history in delirium. Because delirium is fluctuating, an individual examination may underestimate the severity of cognitive and attentional dysfunction⁽¹⁾. In this patient, information provided by relatives established that the altered mental state predated alcohol cessation, while repeated clinical assessments demonstrated that the confusional syndrome persisted independently of the withdrawal manifestations. These observations were decisive in challenging a single-cause interpretation of the presentation and prompted the investigation that identified the underlying intracranial disease.

The particular value of this case lies in illustrating the coexistence of two clinically relevant processes with different temporal trajectories. Moderate alcohol withdrawal was present at admission and responded to specific treatment, whereas persistent delirium was associated with multiple brain lesions suggestive of metastases, extensive vasogenic edema and significant mass effect. This case emphasizes that persistence of delirium beyond the expected course of an identified precipitating condition warrants reevaluation of the underlying etiology, particularly when the temporal history, neurological examination and underlying medical disease suggest an additional organic cause.

Conclusions

This case illustrates the diagnostic complexity of delirium when two clinically relevant conditions with overlapping neuropsychiatric manifestations coexist. Moderate alcohol withdrawal was present at admission and responded to specific treatment; however, the persistence of fluctuating disturbances of attention and awareness after alcohol withdrawal resolution, associated with symptoms preceding alcohol cessation, persistent headache and neurological abnormalities, indicated an additional organic process.

Neuroimaging subsequently revealed multiple brain lesions with extensive vasogenic edema and significant mass effect.

The particularity of this case lies in the divergent clinical trajectories of the two conditions: alcohol withdrawal resolved, whereas delirium persisted, warranting further investigations. Informant history, longitudinal clinical assessment and repeated neurological examination were essential in recognizing this discrepancy. Persistent or atypically evolving delirium should lead to further etiological evaluation, particularly in patients with known malignancy or associated neurological signs, even when an apparently plausible precipitating factor has already been identified.

Limitations

This case report has several limitations. The histopathological confirmation of the presumed metastatic nature of the intracranial lesions was not available to the authors. Their interpretation was therefore based on the neuroimaging findings and on the clinical context of recently diagnosed lung carcinoma. Because the patient was transferred to a neurosurgical department, detailed information regarding corticosteroid therapy, postoperative management and subsequent oncological treatment could not be obtained. Brain MRI, EEG and additional metabolic, infectious or paraneoplastic investigations were also not available within the period covered by the report. Finally, the authors had no further clinical contact with the patient after the transfer. Therefore, the long-term course of the delirium and the neurological, psychiatric and oncological outcomes could not be assessed.

Conflict of interests: none declared

Financial support: none declared

consent: The patient provided written informed consent

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