Hallucinations are an occasional side effect of

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Try out PMC Labs and tell us what you think. Learn More. Have you ever encountered a patient who reported isolated visual hallucinations but did not have any other symptoms of delirium or psychosis? Have you wondered which medical and neurologic illnesses may present with visual hallucinations? Have you deliberated about how best to work up and treat patients with visual hallucinations? If you have, then the following questions and answers should serve to frame the differential diagnosis of visual hallucinations and to explore the available options for diagnostic testing and treatment.

Hallucinations, defined as the perception of an object or event in any of the 5 senses in the absence of an external stimulus, are experienced by patients with conditions that span several fields e. When noted by nonpsychiatrists, visual hallucinations, one type of sensory misperception, often trigger requests for psychiatric consultation, although visual hallucinations are not pathognomonic of a primary psychiatric illness.

Visual hallucinations have numerous etiologies. Here, we discuss possible mechanisms and offer a differential diagnosis of visual hallucinations, with an emphasis placed on conditions that arise in the context of medical and surgical illness. Treatment typically rests on the underlying etiology, so timely recognition and an understanding of causative mechanisms are crucial.

Numerous hypotheses have been suggested to explain the genesis of visual hallucinations. These have been summarized and categorized by Asaad and Shapiro 1 : psychophysiologic i. Visual hallucinations can be the result of all 3 processes, given the interplay among disturbances of brain anatomy, brain chemistry, prior experiences, and psychodynamic meaning. To date, no single neural mechanism has explained all types of visual hallucinations; however, the similarity of visual hallucinations that are associated with seemingly diverse conditions suggests a final common pathway.

Manford and Andermann 2 summarized 3 pathophysiologic mechanisms thought to for complex visual hallucinations. The first mechanism involves irritation e. Irritation of the primary visual cortex Brodmann's area 17 causes simple elementary visual hallucinations, while irritation of the visual association cortices Brodmann's areas 18 and 19 causes more complex visual hallucinations. Lesions that cause deafferentation of the visual system may lead to cortical release phenomenon, including visual hallucinations.

It has been further suggested that deafferented neurons undergo specific biochemical and molecular changes that lead to an overall increase in excitability similar to the denervation hypersensitivity seen in phantom limb syndrome experienced by amputees. A multitude of lesions can cause this loss of input and inhibit other cognitive functions. One study reported visual hallucinations in 10 of 13 healthy subjects blindfolded for a period of 5 days; this finding lends strong support to the idea that the simple loss of normal visual input is sufficient to cause visual hallucinations.

Finally, due to its role in the maintenance of arousal, the reticular activating system has been implicated in the genesis of visual hallucinations. Lesions of the brainstem have led to visual hallucinations as in peduncular hallucinosis. Further, visual hallucinations are common in those with certain sleep disorders, and occur more frequently in those who are drowsy.

The observation that visual hallucinations occur more frequently in those who are drowsy even in the absence of frank sleep pathology suggests that the reticular activating system plays a role in visual hallucinations, although the precise mechanism has not yet been established.

The Diagnostic and Statistical Manual of Mental Disorders , Fourth Edition DSM-IV lists hallucinations as a primary diagnostic criterion for various psychotic disorders including schizophrenia and schizoaffective disorder. While the majority of hallucinations reported in primary psychotic disorders are auditory, they may also be visual, olfactory, tactile, or gustatory. They found that the global severity of illness was ificantly higher in patients with schizophrenia and visual hallucinations as compared to those without visual hallucinations.

This finding may help explain widely varying estimates of prevalence of visual hallucinations in those with schizophrenia, as patients with more severe illness e. Visual hallucinations in those with schizophrenia tend to involve vivid scenes with family members, religious figures, and animals.

The hallucinations are usually described as colorful and involving normal-sized people and objects; however, visual hallucinations of giants have also been reported. Delirium, a syndrome that involves an acute disturbance of consciousness as well as a diminished ability to sustain attention, is caused by myriad medical conditions, metabolic disturbances, infections, drug effects, and intracranial processes.

It is often manifest by symptoms e. Indeed, several studies have shown that in general hospitals, many patients seen by psychiatric consultants for sensory misperceptions were initially referred for evaluation of a primary psychiatric disorder most often depression. They also noted a strong positive correlation between visual hallucinations and the of active somatic diagnoses. Delirium from alcohol withdrawal i. Patients with these conditions often report seeing crawling insects, perhaps as a result of contemporaneous tactile disturbances.

Dementia with Lewy bodies DLB is the second most common form of dementia after dementia of the Alzheimer's type. Patients may have insight into their hallucinatory content. Visual hallucinations are an important clinical clue indicating that dementia may be associated with Lewy bodies rather than with another subtype of dementia. Tiraboschi et al. Harding and colleagues 20 reported a strong correlation between Lewy bodies located in the temporal structures specifically in the amygdala and the parahippocampus and well-formed visual hallucinations.

Visual hallucinations also occur in up to half of patients with Parkinson's disease. Posterior cortical atrophy is another neurodegenerative syndrome associated with visual hallucinations and parkinsonian symptoms. The chief pathologic features of posterior cortical atrophy are neurofibrillary tangles and senile plaques similar to those seen in dementia of the Alzheimer's type but with a distribution limited to the occipital and parietal lobes. Patients with posterior cortical atrophy may present with visual agnosia, anomia, apraxia, and features of Gerstmann syndrome. The Charles Bonnet syndrome CBS involves the occurrence of visual hallucinations in the visually impaired.

Any cause of visual impairment including macular degeneration, glaucoma, cataracts, cerebrovascular disease, and tumors may be associated with CBS. Charles Bonnet syndrome has been thought of as a nonpsychiatric cause of visual hallucinations; while this remains true, there is growing evidence that preexisting dementia or cognitive impairment may predispose a patient to the development of CBS. The visual hallucinations in CBS have been described as clear and detailed; they often involve people, faces, animals, and inanimate objects.

While patients may initially be unaware that these images are indeed hallucinations, one of the hallmarks of CBS is the eventual development of insight regarding their visual hallucinations. The strongest risk factors for CBS include bilateral visual impairment, declining visual acuity, cerebral damage, cognitive defects, social isolation, and sensory deprivation.

Antipsychotics and selective serotonin reuptake inhibitors have been used to treat CBS, but there is no clear evidence to support this approach. Anton's syndrome is a rare condition in which patients with cortical blindness deny that they have visual loss. This presentation has been described as a combination of anosognosia and confabulation. The problem may only be discovered when the patient is found running into or falling over objects while reporting odd or fantastical reasons why they did not see the object with which they collided.

The mechanism that underlies Anton's syndrome remains unclear, but it is thought to be related to infarction of the primary visual cortex Brodmann's area 17 with preserved function of the visual association cortices.

These patients may have alterations in emotional reactivity that predispose them to denial. Another hypothesis suggests that there may be a synesthetic translation of the remaining senses into mental images that are perceived by the patient as vision. Visual hallucinations caused by seizures have often been described as simple, brief, and consistent for each patient; they usually consist of small, brightly colored spots or shapes that flash.

Those that remain isolated in 1 visual field suggest seizure activity that originates on the contralateral side. Complex visual hallucinations due to seizures are thought to require the involvement of the visual association cortex. Since occipital seizures are frequently accompanied by a postictal headache, they may be difficult to distinguish from migraines, creating confusion and the delay of appropriate treatment.

While neurologic literature indicates that visual hallucinations associated with seizures are simple, there is a growing body of work that describes complex, formed visual hallucinations as ictal, peri-ictal, and intra-ictal phenomena. The occurrence of complex visual hallucinations as a symptom of epilepsy can be a point of disagreement between neurologists and psychiatrists.

Visual hallucinations associated with migraine headaches can be a classic aura of migraine as well as a less common manifestation such as migraine coma and familial hemiplegic migraine. Variations of this classic picture such as colored patterns also occur. The simple visual hallucinations described above are the most common, but more complex hallucinations can occur in migraine coma and familial hemiplegic migraine.

Hadjikhani and colleagues 43 used functional magnetic resonance imaging fMRI to show that migraine aura is likely caused by spreading cortical depression. This phenomenon involves a brief period of hyperperfusion followed by a slow spreading wave of hypoperfusion. These events are thought to be due to a neuronal dysfunction rather than to a primary vascular event. Peduncular hallucinosis is characterized by visual hallucinations that arise following an infarct of the midbrain. It was originally described in by Lhermitte and has since been the topic of many case reports.

The mechanism has been difficult to pinpoint since the literature features a wide variety of lesions. Lesions may involve the cerebral peduncles, but most often involve the reticular formation or its targets. Each hallucination may last from minutes to hours, often occurring in the evening. Patients eventually develop insight into their hallucinations, and they may find them interesting or amusing.

Hypnagogic hallucinations are visual and auditory perceptions that occur during sleep onset, while hypnopompic hallucinations occur on awakening. They are usually visual and may be bizarre and dreamlike, but with some preservation of consciousness. It was also shown that patients with insomnia, excessive daytime sleepiness, or mental disorders were more likely to experience hallucinations.

Many drugs are labeled as hallucinogens because they alter perceptions, 48 although true hallucinations are perceptions in the absence of any actual stimulus. Hallucinogenic drugs including mescaline, psilocybin, and lysergic acid diethylamide [LSD] are agonists of serotonin 5-HT 2A receptors; they do not always produce true hallucinations unless they are used at high doses. The effects also depend to some degree on the mood of the user and the situation in which the drug is used.

Other drugs often considered to be hallucinogenic include phencyclidine PCP , ecstasy, atropine, and dopamine agonists. Tumors that lie along, or compress, the optic path may cause visual hallucinations. In one case series, 13 of 59 patients with temporal lobe tumors experienced visual hallucinations. The majority of these visual hallucinations are thought to be related to seizure activity caused by the tumor. A handful of inborn errors of metabolism may cause visual hallucinations.

While these are quite rare, they are nonetheless important to consider because patients with inborn errors of metabolism may present with hallucinations at a time when their disease is treatable and when serious neurologic damage has not yet occurred.

Creutzfeldt-Jakob disease CJD is a fatal progressive neurodegenerative illness caused by central nervous system prion infection. Symptoms of CJD may also include visual hallucinations, especially in the Heidenhain variant of the illness.

Visual effects may include color changes, visual field defects, visual agnosia, cortical blindness, metamorphopsia, and micropsia that progresses to the frank visual hallucinations characteristic of the Heidenhain variant. Given the broad variety of potential etiologies of visual hallucinations outlined ly, it is clear that an accurate diagnosis is required before effective treatment can be initiated.

A thorough history and clinical examination are the most vital elements of a workup for visual hallucinations. Associated symptoms and characteristics of the visual hallucinations themselves may help direct diagnosis Table 1. The elicitation of s or symptoms of psychosis, inattention, parkinsonism, impaired vision, or headache will narrow the diagnosis and prompt further diagnostic studies. An EEG is potentially the most revealing diagnostic study, since it can not only highlight seizure activity, but also detect delirium with theta-delta slowing , delirium tremens with rapid beta activity , and CJD with occipital periodic non-generalizing complexes.

Since effective treatment of visual hallucinations see Table 2 is entirely dependent on the underlying cause, care should be taken to ensure diagnostic accuracy, especially since treatments that may be beneficial for one cause of visual hallucinations may exacerbate another. For example, benzodiazepines are the treatment of choice for delirium tremens, but they will almost certainly worsen a delirium due to any other cause. Neuroleptic medications i. These medications are also beneficial for the management of delirium in which hallucinations are thought to be due to release of endogenous dopamine , with intravenous haloperidol having the most evidence for safety and efficacy.

Unfortunately, due to their dopamine-blocking activity, most neuroleptics will ificantly exacerbate parkinsonian symptoms in patients with DLB or dementia associated with Parkinson's disease. Quetiapine and clozapine have a niche role in the treatment of these patients, since their very low affinity for dopamine receptors renders them less likely to cause this serious adverse effect. More focal causes of visual hallucinations may require more focal treatment. Unfortunately, some causes of visual hallucinations e.

For these patients, neuroleptics may minimize visual hallucinations and distress. Most patients with visual hallucinations, regardless of cause, will benefit from the reassurance of their caregivers. Some may also benefit from more formal psychotherapeutic interventions e. Lessons Learned at the Interface of Medicine and Psychiatry. Such consultations require the integration of medical and psychiatric knowledge.

During their thrice-weekly rounds, Dr. Stern and other members of the Psychiatric Consultation Service discuss the diagnosis and management of conditions confronted. These discussions have given rise to rounds reports that will prove useful for clinicians practicing at the interface of medicine and psychiatry.

Hallucinations are an occasional side effect of

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Hallucinations and hearing voices