These two patients presented with complex visual hallucinations after surgical resection of cerebral metastases located in the occipital lobe (case 1) and parietal lobe (case 2), without any relevant neurological, ophthalmological, or psychiatric disorders in the past medical history, and under no opioid pain medication or steroid treatment during the clinical manifestation of the hallucinations.

In the work-up of hallucinations, other competing etiologies of the symptomatology have to be eliminated [10]. From a neurological point of view, it was important to exclude secondary structural epileptic activity of the affected regions, which could also present as polymorphic visual manifestations [11]. However, the multiple EEGs showed no ictal activity in our patients. Paradoxically, antiepileptic drugs such as levetiracetam sometimes potentiate behavioral problems, including visual hallucinations, particularly when combined with steroids [12]. On the other hand, anticonvulsive medication, as used during surgical management of brain tumors, protects against cortical spreading depression (CSD), which also clinically manifests as visual phenomena including photophobia or scintillating scotoma [13]. Only patient 2 had received steroids before the resection, which were then discontinued. High-dose steroids can provoke severe psychiatric complications like delirium, mania, and hallucinations in between 5% [14] to 60% [15] of patients. However, under corticosteroids, hallucinations are part of a psychiatric tableau and do not present alone. Neither of our patients suffered from schizoaffective disorders, neither did they suffer from dementia, which are both also possible etiologies of complex hallucinations [16]. A sudden cortical lesion in the primary visual areas may lead to an unremarked “cortical blindness” or Anton–Babinski syndrome, when the bilateral affection stays filled with clinically manifest hallucinations [17]. In visually impaired individuals, complex hallucinations occur in only 1% of patients, for example as “phantom eye syndrome” [18] or Charles Bonnet syndrome.

More than 250 years ago, the Swiss biologist Charles Bonnet described the hallucinatory experiences of his grandfather, who was suffering from bilateral cataracts [9, 19]. His name has since been linked to the occurrence of visual hallucinations predominantly in elderly individuals with normal mental health and cognitive performance, but with a degree of visual loss as a consequence of a disease of the visual system [8]. This type of complex visual hallucination has been conceptualized as “phantom vision” due to deafferentation, similar to phantom-limb syndrome [8].

Regarding the localization of the metastatic lesions in our patients, postoperative sites in the occipital and parietal regions do not necessarily lead to deafferentation of the basic visual pathways such as in case 1, but can also affect the higher visual association cortices, such as in case 2. Visual inputs are assumed to be regulated by the inhibition processes of higher cortical areas, and damage to these cortical structures leads to impaired suppression of neuronal excitation, which is followed by biochemical changes and an increase in excitability with a releasing of the visual symptoms [10]. Some authors describe that brainstem lesions may also lead to impairment of the ascending cholinergic and serotonergic pathways, which can be manifest with complex visual phenomenon (called “peduncular hallucinosis”) [7].

Phantom vision due to deafferentation is a real symptom, explained by a phenomenologic and neuroscientific concept. However, it is formally impossible to decide the exact pathomechanism at the neuronal level between interruption, micro-epileptic activity, or CSD within the postsurgical lesions, but there is also no need to do so. There is currently no evidence for any treatment of Charles Bonnet syndrome, in particular after surgical tumor resection. According to the literature, the pharmacological targets in the management of the hallucinations modulate predominantly GABAergic, dopaminergic, cholinergic pathways or even apply a reduction of the cortical excitation. Antipsychotic drugs are frequently used to alleviate the visual hallucinations in Parkinson’s disease and delirium [20]; whether they are also useful in patients with structural cerebral lesions remains open. Some authors describe a beneficial use of antiseizure drugs to reduce the frequency and intensity of the symptoms in similar cases [7, 21], but this reduction of the cortical excitation with levetiracetam did not diminish the symptoms in our patients; thus, it also sustains our hypothesis of a nonepileptic origin of the hallucinations. Generally, previous studies concluded that there is no need for pharmacologic treatment unless the patient is particularly bothered and intimidated by the hallucinations. Most important is that the healthcare provider recognizes the syndrome to avoid misdiagnosing mentally healthy individuals, which can lead to unnecessary and potentially harmful treatment. The duration of Charles Bonnet syndrome is in most cases self-limited, and the information about the benign course is also reassuring for the patient [7,8,9, 20, 21].