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Hallucination

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An hallucination is a sensory perception experienced in the absence of an external stimulus, as distinct from an illusion, which is a misperception of an external stimulus. Hallucinations may occur in any sensory modality - visual, auditory, olfactory, gustatory, tactile, or proprioception (sense of balance and position in space).

Prevalence and types of hallucinatory experience

Studies have shown hallucinatory experiences take place across the population as a whole. Previous studies, one as early as 1894[1], have reported that approximately 10% of the population experience hallucinations. A recent survey of over 13,000 people[2] reported a much higher figure with almost 39% of people reported hallucinatory experiences, 27% of which reported daytime hallucinations, mostly outside the context of illness or drug use. From this survey, olfactory (smell) and gustatory (taste) hallucinations seem the most common in the general population.

Hypnagogic hallucinations and hypnopompic hallucinations are considered normal phenomena. Hypnagogic hallucinations can occur as one is falling asleep and hypnopompic hallucinations occur when one is waking up.

Auditory hallucinations (particularly of one or more talking voices) are particularly associated with psychotic disorders such as schizophrenia, and hold special significance in diagnosing these conditions despite the fact that 'hearing voices' is not a sign of mental illness[1].

Florid hallucinations are usually associated with drug use (particularly hallucinogenic drugs), sleep deprivation, psychosis or neurological illness.

Scientific explanations

Various theories have been put forward to explain the occurrence of hallucinations. When psychodynamic (Freudian) theories were popular in psychiatry, hallucinations were seen as a projection of unconscious wishes and desires. As biological theories have become orthodox, hallucinations are more often thought of (by psychiatrists at least) as being caused by functional deficits in the brain. With reference to mental illness, the function (or dysfunction) of the neurotransmitter dopamine is thought to be particularly important[3].

Psychological research has argued that hallucinations may result from biases in what are known as metacognitive abilities[4]. These are abilities that allow us to monitor or draw inferences from our own internal psychological states (such as intentions, memories, beliefs and thoughts). The ability to discriminate between self-generated and external sources of information is considered to be an important metacognitive skill and one which may break down to cause hallucinatory experiences.

Visual Hallucination Subtypes

Hypnagogic Hallucination

These hallucinations occur just before falling asleep and affect a surprising number of people in the population. The hallucinations can last from seconds to minutes, all the while the subject usually remains aware of the true nature of the images. These are usually associated with narcolepsy, but can also affect non-narcoleptics. Hypnagogic hallucinations are sometimes associated with brainstem abnormalities, but this is rare. [5].

Peduncular Hallucinosis

Peduncular means pertaining to the peduncle, which is a name given to a neural tract running to and from the pons. These hallucinations occur most often in the evenings, but not during drowsiness as in the case above. The subject is usually fully conscious and can interact with the hallucinatory characters for extended periods of time. As in the case of hypnagogic hallucinations, insight into the nature of the images remains intact. The false images can occur in any part of the visual field, and are rarely polymodal. [6].

Delirium Tremens

One of the most enigmatic forms of visual hallucinations are the highly variable, possibly polymodal Delirium Tremens. As the name suggests, the subject is usually agitated and confused, especially in the later stages of this disease. Insight is gradually reduced with the progression of this disorder. Sleep is disturbed and short, with REM overflow. [7].

Parkinson's disease and Lewy body Dementia

Parkinson's disease is linked with Lewy body Dementia for their similar hallucinatory symptoms. The symptoms strike during the evening in any part of the visual field and are rarely polymodal. The segue into hallucinations may start with illusions [8] where sensory perception is greatly distorted, but no novel sensory information is present. These typically last for several minutes, during which time the subject may be either conscious and normal or drowsy/inaccessable. Insight into these hallucinations is usually preserved and REM sleep is usually reduced. Parkinson's disease is usually associated with a degraded substantia nigra pars compacta, but recent evidence suggests that PD affects a handful of other sites in the brain. Some places of noted degradation include the median raphe nuclei, the noradrenergic parts of the locus coeruleus and the cholinergic neurons in the parabrachial and pedunculopontine nuclei of the tegmentum. [9].

Migraine Coma

This type of hallucination is usually experienced during the recovery from a comatose state. The migraine coma can last for up to two days and a state of depression is sometimes comorbid. The hallucinations occur during states of full consciousness and insight into the hallucinatory nature of the images is preserved. It has been noted that ataxic lesions accompany the migraine coma.[10].

Charles Bonnet Syndrome

Charles Bonnet Syndrome is the name given to visual hallucinations experienced by blind patients. The hallucinations can usually be dispersed by opening or closing the eyelids until the visual images disappear. The hallucinations usually occur during the morning or evening, but are not dependent on low light conditions. These prolonged hallucinations usually do not disturb the patients very much as they are aware that they are hallucinating. [11].

Focal Epilepsy

The visual hallucinations from focal epilepsy are characterized by being brief, and stereotyped. They are usually localized to one part of the visual field and last only a few seconds. Other epileptic features may present themselves between visual episodes. Consciousness is usually impaired in some way, but nevertheless insight into the hallucination is preserved. Usually this type of focal epilepsy is caused by a lesion in the posterior temporoparietal. [12].

Paranormal theories

A rarely expressed but persistent alternate explanation of hallucinations, espoused by non-materialists, is that people prone to hallucinations can sometimes perceive non-physical phenomena such as angels, visions or the voices of departed spirits or demons. For this reason, a hallucination may also be classified as an anomalous phenomenon, when no suitable scientific explanation is verified.

See also

Further reading

The Anatomy of Hallucinations by Fred H. Johnson, Nelson-Hall, 1978

References

  1. ^ Sidgwick, H., Johnson, A, Myers, FWH et al (1894) Report on the census of hallucinations. Proceedings of the Society for Psychical Research, 34, 25-394.
  2. ^ Ohayon MM. (2000) Prevalence of hallucinations and their pathological associations in the general population. Psychiatry Research, 97(2-3), 153-64.
  3. ^ Kapur S. (2003) Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia. American Journal of Psychiatry, 160(1), 13-23.
  4. ^ Bentall RP. (1990) The illusion of reality: a review and integration of psychological research on hallucinations. Psychological Bulletin, 107(1), 82-95.
  5. ^ http://brain.oxfordjournals.org/cgi/content/abstract/121/10/1819 Manford and Andermann (1998)] Complex visual hallucinations. Clinical and Neurobiological insightsBrain, 121(10), 1819-1840.
  6. ^ Manford and Andermann (1998) Complex visual hallucinations. Clinical and Neurobiological insightsBrain, 121(10), 1819-1840.
  7. ^ Manford and Andermann (1998) Complex visual hallucinations. Clinical and Neurobiological insightsBrain, 121(10), 1819-1840.
  8. ^ Mark Derr (2006) Marilyn and Me, "The New York Times" Feb. 14th, 2006
  9. ^ Manford and Andermann (1998) Complex visual hallucinations. Clinical and Neurobiological insightsBrain, 121(10), 1819-1840.
  10. ^ Manford and Andermann (1998) Complex visual hallucinations. Clinical and Neurobiological insightsBrain, 121(10), 1819-1840.
  11. ^ Manford and Andermann (1998) Complex visual hallucinations. Clinical and Neurobiological insightsBrain, 121(10), 1819-1840.
  12. ^ Manford and Andermann (1998) Complex visual hallucinations. Clinical and Neurobiological insightsBrain, 121(10), 1819-1840.