The full details of the flow of signaling from the eye to the visual cortex of the brain that result in the experience of vision are incompletely understood. Many aspects are subject to active controversy and the disruption of new evidence.
In the visual system, signals mostly travel from the retina to the lateral geniculate nucleus (LGN) and then to the visual cortex.
In humans the LGN is normally described as having six distinctive
layers. The inner two layers, (1 and 2) are magnocellular cell (M cell)
layers, while the outer four layers, (3,4,5 and 6), are parvocellular cell (P cell) layers. An additional set of neurons, known as the koniocellular cell (K cell) layers, are found ventral to each of the M cell and P cell layers. These layers were named this way because cells in the M layers of the LGN are larger than cells in the P layers.
Visual representation of the parvocellular and magnocellular pathways
From the LGN, the M pathway continues by sending information to the interblob regions of the 4Cα layer of the V1 region of the visual cortex, also called the "striate cortex".
Other cells in the striate are more influenced from signaling from P
cells and yet others from K cells. As signals are passed to other
regions of the cortex, the signals start to be less separate, more
integrated, and more influenced by signals from other parts of the
brain. While classically it is said that signaling through the M
pathway ultimately flow out of the visual cortex through the dorsal stream and signaling through the P pathway ultimately flows to the ventral stream, subsequent studies have shown that both pathways influence both streams.
Human visual pathway
Function
The
magnocellular pathway cannot provide finely detailed or colored
information, but still provides useful static, depth, and motion
information. The M pathway has high light/dark contrast detection, and is more sensitive at low spatial frequencies than high spatial frequencies. Due to this contrast information, M cells are essential for detecting changes in luminance, and performing visual search tasks and detecting edges.
The M pathway is also important for providing information about
the location of objects. M cells can detect the orientation and position
of objects in space, information that is sent through the dorsal stream.
This information is also useful for detecting the difference in
positions of objects on the retina of each eye, an important tool in
binocular depth perception.
Cells in the M pathway have the ability to detect high temporal
frequencies and can thus detect quick changes in the position of an
object. This is the basis for detecting motion. The information sent to the intraparietal sulcus (IPS) of the posterior parietal cortex allows the M pathway to direct attention and guide saccadic eye movements to follow important moving objects in the visual field. In addition to following objects with the eyes, the IPS sends information to parts of the frontal lobe
that allows the hands and arms to adjust their movements to correctly
grasp objects based on their size, position, and location.
This ability has led some neuroscientists to hypothesize that the
purpose of the M pathway is not to detect spatial locations, but to
guide actions related to the position and motion of objects.
Some information has also been found to support the hypothesis that the M pathway is necessary for facial processing.
Clinical significance
Abnormal
magnocellular pathways and magnocellular cells can be associated with
various disorders and ocular impairments, including dyslexia,
prosopagnosia and schizophrenia.
Dyslexia
Dyslexia
is a disability which affects individual’s ability to read. It often
first manifests in childhood, if at all; however, dyslexia can manifest
itself in adulthood because of a brain tumor or lesion on/penetrating M
cells. There is no clear idea of the role of M cells and the magnocellular pathway in dyslexia.
One theory suggests that the nonlinearity, size, and compensation
of miniature eye movements of M cells all help to focus on a single
target and blur the surroundings, which is crucial in reading. This
suggests that M cells are underdeveloped in many dyslexics. This may be
due to genetics, autoimmunity, or nutrition. The KIAA0319 gene on chromosome six controls cell migration to the LGN during development; and studies in transgenic mice
and on brains of people with dyslexia examined after they died, show
malformations in the LGN and cells expressing KIAA0319 growing in the
wrong place.
M cells are vulnerable to antineuronal antibodies which attack and
render them unusable in the magnocellular pathway. This could be a cause
of why dyslexics are more likely to have weakened immune systems.
Another line of research suggests that defective eye movement
caused by M cells is the cause of dyslexia. Since the magnocellular
system is sensitive to image movement, and dyslexia is posited to be
caused by abnormalities in M cells, dyslexics tend to focus on words
longer, take shorter scans when reading, and stop more often per line.
The study postulates that this is not caused by dyslexia but rather, low
comprehension of the text causing abnormal eye movements in M cells.
Therefore, it is difficult to conclude the importance of M cells in
dyslexia from this study.
Schizophrenia
Schizophrenia
is a mental disorder in which people are unable to differentiate what
is real and what is not. It is believed that the magnocellular pathway
may help with facial recognition and discrimination in children, but
when this pathway is not developed completely or correctly, facial
processing is more difficult for individuals later in life. This is seen
in people with schizophrenia and occurs when there are issues in the
integration of information from the M cell and P cell pathways, making
it difficult for individuals with schizophrenia to differentiate between
reality and hallucinations.
This article describes the human visual system, which is representative of mammalian vision, and to a lesser extent the vertebrate visual system.
System overview
This
diagram linearly (unless otherwise mentioned) tracks the projections of
all known structures that allow for vision to their relevant endpoints
in the human brain. Click to enlarge the image.Representation of optic pathways from each of the 4 quadrants of view for both eyes simultaneously
Optical
Together, the cornea and lens refract light into a small image and shine it on the retina. The retina transduces this image into electrical pulses using rods and cones. The optic nerve then carries these pulses through the optic canal. Upon reaching the optic chiasm the nerve fibers decussate (left becomes right). The fibers then branch and terminate in three places.
Neural
Most of the optic nerve fibers end in the lateral geniculate nucleus
(LGN). Before the LGN forwards the pulses to V1 of the visual cortex
(primary) it gauges the range of objects and tags every major object
with a velocity tag. These tags predict object movement.
The LGN also sends some fibers to V2 and V3.
V1 performs edge-detection to understand spatial organization
(initially, 40 milliseconds in, focusing on even small spatial and color
changes. Then, 100 milliseconds in, upon receiving the translated LGN,
V2, and V3 info, also begins focusing on global organization). V1 also
creates a bottom-up saliency map to guide attention or gaze shift.
V2 both forwards (direct and via pulvinar) pulses to V1 and receives them. Pulvinar is responsible for saccade and visual attention. V2 serves much the same function as V1, however, it also handles illusory contours, determining depth by comparing left and right pulses (2D images), and foreground distinguishment. V2 connects to V1 - V5.
V4 recognizes simple shapes, and gets input from V1 (strong), V2, V3, LGN, and pulvinar. V5's outputs include V4 and its surrounding area, and eye-movement motor cortices (frontal eye-field and lateral intraparietal area).
V5's functionality is similar to that of the other V's, however,
it integrates local object motion into global motion on a complex level.
V6 works in conjunction with V5 on motion analysis. V5 analyzes
self-motion, whereas V6 analyzes motion of objects relative to the
background. V6's primary input is V1, with V5 additions. V6 houses the topographical map
for vision. V6 outputs to the region directly around it (V6A). V6A has
direct connections to arm-moving cortices, including the premotor cortex.
The inferior temporal gyrus recognizes complex shapes, objects, and faces or, in conjunction with the hippocampus, creates new memories. The pretectal area is seven unique nuclei. Anterior, posterior and medial pretectal nuclei inhibit pain (indirectly), aid in REM, and aid the accommodation reflex, respectively. The Edinger-Westphal nucleus moderates pupil dilation and aids (since it provides parasympathetic fibers) in convergence of the eyes and lens adjustment. Nuclei of the optic tract are involved in smooth pursuit eye movement and the accommodation reflex, as well as REM.
These are components of the visual pathway also called the optic pathway that can be divided into anterior and posterior visual pathways. The anterior visual pathway refers to structures involved in vision before the lateral geniculate nucleus. The posterior visual pathway refers to structures after this point.
Light entering the eye is refracted as it passes through the cornea. It then passes through the pupil (controlled by the iris) and is further refracted by the lens. The cornea and lens act together as a compound lens to project an inverted image onto the retina.
Rods and cones differ in function. Rods are found primarily in
the periphery of the retina and are used to see at low levels of light.
Each human eye contains 120 million rods. Cones are found primarily in
the center (or fovea) of the retina. There are three types of cones that differ in the wavelengths
of light they absorb; they are usually called short or blue, middle or
green, and long or red. Cones mediate day vision and can distinguish color
and other features of the visual world at medium and high light levels.
Cones are larger and much less numerous than rods (there are 6-7
million of them in each human eye).
In the retina, the photoreceptors synapse directly onto bipolar cells, which in turn synapse onto ganglion cells of the outermost layer, which then conduct action potentials to the brain. A significant amount of visual processing arises from the patterns of communication between neurons in the retina. About 130 million photo-receptors absorb light, yet roughly 1.2 million axons
of ganglion cells transmit information from the retina to the brain.
The processing in the retina includes the formation of center-surround receptive fields
of bipolar and ganglion cells in the retina, as well as convergence and
divergence from photoreceptor to bipolar cell. In addition, other
neurons in the retina, particularly horizontal and amacrine cells,
transmit information laterally (from a neuron in one layer to an
adjacent neuron in the same layer), resulting in more complex receptive
fields that can be either indifferent to color and sensitive to motion or sensitive to color and indifferent to motion.
Mechanism of generating visual signals
The retina adapts to change in light through the use of the rods. In the dark, the chromophoreretinal has a bent shape called cis-retinal (referring to a cis
conformation in one of the double bonds). When light interacts with the
retinal, it changes conformation to a straight form called
trans-retinal and breaks away from the opsin. This is called bleaching
because the purified rhodopsin changes from violet to colorless in the light. At baseline in the dark, the rhodopsin absorbs no light and releases glutamate,
which inhibits the bipolar cell. This inhibits the release of
neurotransmitters from the bipolar cells to the ganglion cell. When
there is light present, glutamate secretion ceases, thus no longer
inhibiting the bipolar cell from releasing neurotransmitters to the
ganglion cell and therefore an image can be detected.
The final result of all this processing is five different
populations of ganglion cells that send visual (image-forming and
non-image-forming) information to the brain:
M cells, with large center-surround receptive fields that are sensitive to depth, indifferent to color, and rapidly adapt to a stimulus;
P cells, with smaller center-surround receptive fields that are sensitive to color and shape;
K cells, with very large center-only receptive fields that are sensitive to color and indifferent to shape or depth;
In 2007 Zaidi and co-researchers on both sides of the Atlantic
studying patients without rods and cones, discovered that the novel
photoreceptive ganglion cell in humans also has a role in conscious and
unconscious visual perception. The peak spectral sensitivity
was 481 nm. This shows that there are two pathways for vision in the
retina – one based on classic photoreceptors (rods and cones) and the
other, newly discovered, based on photo-receptive ganglion cells which
act as rudimentary visual brightness detectors.
The functioning of a camera is often compared with the workings of the eye, mostly since both focus light from external objects in the field of view
onto a light-sensitive medium. In the case of the camera, this medium
is film or an electronic sensor; in the case of the eye, it is an array
of visual receptors. With this simple geometrical similarity, based on
the laws of optics, the eye functions as a transducer, as does a CCD camera.
In the visual system, retinal, technically called retinene1 or "retinaldehyde", is a light-sensitive molecule found in the rods and cones of the retina. Retinal is the fundamental structure involved in the transduction of light into visual signals, i.e. nerve impulses in the ocular system of the central nervous system. In the presence of light, the retinal molecule changes configuration and as a result, a nerve impulse is generated.
The information about the image via the eye is transmitted to the brain along the optic nerve.
Different populations of ganglion cells in the retina send information
to the brain through the optic nerve. About 90% of the axons in the optic nerve go to the lateral geniculate nucleus in the thalamus. These axons originate from the M, P, and K ganglion cells in the retina, see above. This parallel processing is important for reconstructing the visual world; each type of information will go through a different route to perception. Another population sends information to the superior colliculus in the midbrain, which assists in controlling eye movements (saccades) as well as other motor responses.
The optic nerves from both eyes meet and cross at the optic chiasm, at the base of the hypothalamus of the brain. At this point, the information coming from both eyes is combined and then splits according to the visual field. The corresponding halves of the field of view (right and left) are sent to the left and right halves of the brain, respectively, to be processed. That is, the right side of primary visual cortex deals with the left half of the field of view from both eyes, and similarly for the left brain. A small region in the center of the field of view is processed redundantly by both halves of the brain.
Information from the right visual field (now on the left side of the brain) travels in the left optic tract. Information from the left visual field travels in the right optic tract. Each optic tract terminates in the lateral geniculate nucleus (LGN) in the thalamus.
The lateral geniculate nucleus (LGN) is a sensory relay nucleus in the thalamus of the brain. The LGN consists of six layers in humans and other primates starting from catarrhines, including cercopithecidae and apes.
Layers 1, 4, and 6 correspond to information from the contralateral
(crossed) fibers of the nasal retina (temporal visual field); layers 2,
3, and 5 correspond to information
from the ipsilateral (uncrossed) fibers of the temporal retina (nasal
visual field). Layer one contains M cells, which correspond to the M (magnocellular)
cells of the optic nerve of the opposite eye and are concerned with
depth or motion. Layers four and six of the LGN also connect to the
opposite eye, but to the P cells (color and edges) of the optic nerve.
By contrast, layers two, three and five of the LGN connect to the M
cells and P (parvocellular)
cells of the optic nerve for the same side of the brain as its
respective LGN. Spread out, the six layers of the LGN are the area of a credit card and about three times its thickness. The LGN is rolled up into two ellipsoids
about the size and shape of two small birds' eggs. In between the six
layers are smaller cells that receive information from the K cells
(color) in the retina. The neurons of the LGN then relay the visual
image to the primary visual cortex (V1) which is located at the back of the brain (posterior end) in the occipital lobe in and close to the calcarine sulcus. The LGN is not just a simple relay station, but it is also a center for processing; it receives reciprocal input from the cortical and subcortical layers and reciprocal innervation from the visual cortex.
Scheme of the optic tract with image being decomposed on the way, up to simple cortical cells (simplified)
The optic radiations, one on each side of the brain, carry information from the thalamic lateral geniculate nucleus to layer 4 of the visual cortex.
The P layer neurons of the LGN relay to V1 layer 4C β. The M layer
neurons relay to V1 layer 4C α. The K layer neurons in the LGN relay to
large neurons called blobs in layers 2 and 3 of V1.
There is a direct correspondence from an angular position in the visual field
of the eye, all the way through the optic tract to a nerve position in
V1 (up to V4, i.e. the primary visual areas. After that, the visual
pathway is roughly separated into a ventral and dorsal pathway).
The visual cortex is the largest system in the human brain and is
responsible for processing the visual image. It lies at the rear of the
brain (highlighted in the image), above the cerebellum. The region that receives information directly from the LGN is called the primary visual cortex,
(also called V1 and striate cortex). It creates a bottom-up saliency
map of the visual field to guide attention or eye gaze to salient visual
locations, hence selection of visual input information by attention starts at V1
along the visual pathway. Visual information then flows through a
cortical hierarchy. These areas include V2, V3, V4 and area V5/MT (the
exact connectivity depends on the species of the animal). These
secondary visual areas (collectively termed the extrastriate visual
cortex) process a wide variety of visual primitives. Neurons in V1 and
V2 respond selectively to bars of specific orientations, or combinations
of bars. These are believed to support edge and corner detection.
Similarly, basic information about color and motion is processed here.
Heider, et al. (2002) have found that neurons involving V1, V2, and V3 can detect stereoscopic illusory contours; they found that stereoscopic stimuli subtending up to 8° can activate these neurons.
As visual information passes forward through the visual hierarchy,
the complexity of the neural representations increases. Whereas a V1
neuron may respond selectively to a line segment of a particular
orientation in a particular retinotopic
location, neurons in the lateral occipital complex respond selectively
to complete object (e.g., a figure drawing), and neurons in visual
association cortex may respond selectively to human faces, or to a
particular object.
Along with this increasing complexity of neural representation
may come a level of specialization of processing into two distinct
pathways: the dorsal stream and the ventral stream (the Two Streams hypothesis,
first proposed by Ungerleider and Mishkin in 1982). The dorsal stream,
commonly referred to as the "where" stream, is involved in spatial
attention (covert and overt), and communicates with regions that control
eye movements and hand movements. More recently, this area has been
called the "how" stream to emphasize its role in guiding behaviors to
spatial locations. The ventral stream, commonly referred to as the
"what" stream, is involved in the recognition, identification and
categorization of visual stimuli.
In the parietal lobe, the lateral and ventral intraparietal cortex are involved in visual attention and saccadic eye movements. These regions are in the Intraparietal sulcus (marked in red in the adjacent image).
Newborn infants have limited color perception.
One study found that 74% of newborns can distinguish red, 36% green,
25% yellow, and 14% blue. After one month, performance "improved
somewhat." Infant's eyes do not have the ability to accommodate. The pediatricians are able to perform non-verbal testing to assess visual acuity of a newborn, detect nearsightedness and astigmatism,
and evaluate the eye teaming and alignment. Visual acuity improves from
about 20/400 at birth to approximately 20/25 at 6 months of age. All
this is happening because the nerve cells in their retina and brain that control vision are not fully developed.
Childhood and adolescence
Depth perception,
focus, tracking and other aspects of vision continue to develop
throughout early and middle childhood. From recent studies in the United States and Australia
there is some evidence that the amount of time school aged children
spend outdoors, in natural light, may have some impact on whether they
develop myopia.
The condition tends to get somewhat worse through childhood and
adolescence, but stabilizes in adulthood. More prominent myopia
(nearsightedness) and astigmatism are thought to be inherited. Children
with this condition may need to wear glasses.
Adulthood
Vision is often one of the first senses affected by aging. A number of changes occur with aging:
Over time, the lens become yellowed and may eventually become brown, a condition known as brunescence or brunescentcataract. Although many factors contribute to yellowing, lifetime exposure to ultraviolet light and aging are two main causes.
The lens becomes less flexible, diminishing the ability to accommodate (presbyopia).
While a healthy adult pupil typically has a size range of 2–8 mm,
with age the range gets smaller, trending towards a moderately small
diameter.
On average tear production declines with age. However, there are a number of age-related conditions that can cause excessive tearing.
Other functions
Balance
Along with proprioception and vestibular function,
the visual system plays an important role in the ability of an
individual to control balance and maintain an upright posture. When
these three conditions are isolated and balance is tested, it has been
found that vision is the most significant contributor to balance,
playing a bigger role than either of the two other intrinsic mechanisms.
The clarity with which an individual can see his environment, as well
as the size of the visual field, the susceptibility of the individual to
light and glare, and poor depth perception play important roles in
providing a feedback loop to the brain on the body's movement through
the environment. Anything that affects any of these variables can have a
negative effect on balance and maintaining posture. This effect has been seen in research involving elderly subjects when compared to young controls, in glaucoma patients compared to age matched controls, cataract patients pre and post surgery, and even something as simple as wearing safety goggles. Monocular vision
(one eyed vision) has also been shown to negatively impact balance,
which was seen in the previously referenced cataract and glaucoma
studies, as well as in healthy children and adults.
According to Pollock et al. (2010) stroke is the main cause of specific visual impairment, most frequently visual field loss (homonymous hemianopia,
a visual field defect). Nevertheless, evidence for the efficacy of
cost-effective interventions aimed at these visual field defects is
still inconsistent.
Proper function of the visual system is required for sensing,
processing, and understanding the surrounding environment. Difficulty in
sensing, processing and understanding light input has the potential to
adversely impact an individual's ability to communicate, learn and
effectively complete routine tasks on a daily basis.
In children, early diagnosis and treatment of impaired visual
system function is an important factor in ensuring that key social,
academic and speech/language developmental milestones are met.
Cataract
is clouding of the lens, which in turn affects vision. Although it may
be accompanied by yellowing, clouding and yellowing can occur
separately. This is typically a result of ageing, disease, or drug use.
Presbyopia is a visual condition that causes farsightedness. The eye's lens becomes too inflexible to accommodate to normal reading distance, focus tending to remain fixed at long distance.
Glaucoma is a type of blindness that begins at the edge of the visual field and progresses inward. It may result in tunnel vision.
This typically involves the outer layers of the optic nerve, sometimes
as a result of buildup of fluid and excessive pressure in the eye.
Scotoma is a type of blindness that produces a small blind spot in the visual field typically caused by injury in the primary visual cortex.
Homonymous hemianopia
is a type of blindness that destroys one entire side of the visual
field typically caused by injury in the primary visual cortex.
Quadrantanopia
is a type of blindness that destroys only a part of the visual field
typically caused by partial injury in the primary visual cortex. This is
very similar to homonymous hemianopia, but to a lesser degree.
Prosopagnosia,
or face blindness, is a brain disorder that produces an inability to
recognize faces. This disorder often arises after damage to the fusiform face area.
Visual agnosia,
or visual-form agnosia, is a brain disorder that produces an inability
to recognize objects. This disorder often arises after damage to the ventral stream.
Different species are able to see different parts of the light spectrum; for example, bees can see into the ultraviolet, while pit vipers can accurately target prey with their pit organs, which are sensitive to infrared radiation. The mantis shrimp
possesses arguably the most complex visual system of any species. The
eye of the mantis shrimp holds 16 color receptive cones, whereas humans
only have three. The variety of cones enables them to perceive an
enhanced array of colors as a mechanism for mate selection, avoidance of
predators, and detection of prey. Swordfish also possess an impressive visual system. The eye of a swordfish can generate heat to better cope with detecting their prey at depths of 2000 feet. Certain one-celledmicroorganisms, the warnowiiddinoflagellates have eye-like ocelloids, with analogous structures for the lens and retina of the multi-cellular eye. The armored shell of the chitonAcanthopleura granulata is also covered with hundreds of aragonite crystalline eyes, named ocelli, which can form images.
Many fan worms, such as Acromegalomma interruptum which live in tubes on the sea floor of the Great Barrier Reef,
have evolved compound eyes on their tentacles, which they use to detect
encroaching movement. If movement is detected, the fan worms will
rapidly withdraw their tentacles. Bok, et al., have discovered opsins
and G proteins in the fan worm's eyes, which were previously only seen in simple ciliary photoreceptors in the brains of some invertebrates, as opposed to the rhabdomeric receptors in the eyes of most invertebrates.
Biologists have determined that humans have extremely good vision
compared to the overwhelming majority of animals, particularly in
daylight, though a few species have better. Other animals such as dogs are thought to rely more on senses other than vision, which in turn may be better developed than in humans.
History
In the
second half of the 19th century, many motifs of the nervous system were
identified such as the neuron doctrine and brain localization, which
related to the neuron
being the basic unit of the nervous system and functional localisation
in the brain, respectively. These would become tenets of the fledgling neuroscience and would support further understanding of the visual system.
In 2014, a textbook "Understanding vision: theory, models, and data" illustrates how to link neurobiological data and visual
behavior/psychological data through theoretical principles and
computational models.
Psychosis is a condition of the mind that results in difficulties determining what is real and what is not real. Symptoms may include delusions and hallucinations, among other features. Additional symptoms are incoherent speech and behavior that is inappropriate for a given situation. There may also be sleep problems, social withdrawal, lack of motivation, and difficulties carrying out daily activities. Psychosis can have serious adverse outcomes.
Treatment may include antipsychotic medication, psychotherapy, and social support. Early treatment appears to improve outcomes. Medications appear to have a moderate effect. Outcomes depend on the underlying cause. In the United States about 3% of people develop psychosis at some point in their lives. The condition has been described since at least the 4th century BC by Hippocrates and possibly as early as 1500 BC in the Egyptian Ebers Papyrus.
Hallucinations
A hallucination is defined as sensory perception in the absence of external stimuli. Hallucinations are different from illusions
and perceptual distortions, which are the misperception of external
stimuli. Hallucinations may occur in any of the senses and take on
almost any form. They may consist of simple sensations (such as lights,
colors, sounds, tastes, or smells) or more detailed experiences (such as
seeing and interacting with animals and people, hearing voices, and having complex tactile sensations). Hallucinations are generally characterized as being vivid and uncontrollable. Auditory hallucinations, particularly experiences of hearing voices, are the most common and often prominent feature of psychosis.
Up to 15% of the general population may experience auditory
hallucinations (though not all are due to psychosis). The prevalence of
auditory hallucinations in patients with schizophrenia is generally put
around 70%, but may go as high as 98%. Reported prevalence in bipolar
disorder ranges between 11% and 68%. During the early 20th century, auditory hallucinations were second to visual hallucinations
in frequency, but they are now the most common manifestation of
schizophrenia, although rates vary between cultures and regions.
Auditory hallucinations are most commonly intelligible voices. When
voices are present, the average number has been estimated at three.
Content, like frequency, differs significantly, especially across
cultures and demographics. People who experience auditory hallucinations
can frequently identify the loudness, location of origin, and may
settle on identities for voices. Western cultures are associated with
auditory experiences concerning religious content, frequently related to
sin. Hallucinations may command a person to do something potentially
dangerous when combined with delusions.
So-called "minor hallucinations", such as extracampine
hallucinations, or false perceptions of people or movement occurring
outside of one's visual field, frequently occur in neurocognitive
disorders, such as Parkinson's disease.
Visual hallucinations occur in roughly a third of people with
schizophrenia, although rates as high as 55% are reported. The
prevalence in bipolar disorder is around 15%. Content commonly involves
animate objects, although perceptual abnormalities such as changes in
lighting, shading, streaks, or lines may be seen. Visual abnormalities
may conflict with proprioceptive information, and visions may include experiences such as the ground tilting. Lilliputian hallucinations are less common in schizophrenia, and are more common in various types of encephalopathy, such as peduncular hallucinosis.
A visceral hallucination, also called a cenesthetic
hallucination, is characterized by visceral sensations in the absence of
stimuli. Cenesthetic hallucinations may include sensations of burning,
or re-arrangement of internal organs.
Delusions
Psychosis may involve delusional beliefs. A delusion is a fixed, false idiosyncratic belief,
which does not change even when presented with incontrovertible
evidence to the contrary. Delusions are context- and culture-dependent: a
belief which inhibits critical functioning and is widely considered
delusional in one population may be common (and even adaptive) in
another, or in the same population at a later time. Since normative views may contradict available evidence, a belief need not contravene cultural standards in order to be considered delusional.
Prevalence in schizophrenia is generally considered at least 90%, and around 50% in bipolar disorder.
The DSM-5 characterizes certain delusions as "bizarre" if they
are clearly implausible, or are incompatible with the surrounding
cultural context. The concept of bizarre delusions has many criticisms,
the most prominent being judging its presence is not highly reliable
even among trained individuals.
A delusion may involve diverse thematic content. The most common type is a persecutory delusion, in which a person believes that an entity seeks to harm them. Others include delusions of reference
(the belief that some element of one's experience represents a
deliberate and specific act by or message from some other entity), delusions of grandeur (the belief that one possesses special power or influence beyond one's actual limits), thought broadcasting (the belief that one's thoughts are audible) and thought insertion (the belief that one's thoughts are not one's own). A delusion may also involve misidentification of objects, persons, or environs that the afflicted should reasonably be able to recognize; such examples include Cotard's syndrome (the belief that oneself is partly or wholly dead) and clinical lycanthropy (the belief that oneself is or has transformed into an animal).
The subject matter of delusions seems to reflect the current
culture in a particular time and location. For example, in the US,
during the early 1900s syphilis was a common topic, during the Second
World War Germany, during the Cold War communists, and in recent years,
technology has been a focus. Some psychologists, such as those who practice the Open Dialogue
method, believe that the content of psychosis represents an underlying
thought process that may, in part, be responsible for psychosis, though the accepted medical position is that psychosis is due to a brain disorder.
Historically, Karl Jaspers classified psychotic delusions into primary and secondary
types. Primary delusions are defined as arising suddenly and not being
comprehensible in terms of normal mental processes, whereas secondary
delusions are typically understood as being influenced by the person's
background or current situation (e.g., ethnicity; also religious,
superstitious, or political beliefs).
Disorganization of speech/thought or behavior
Disorganization
is split into disorganized speech (or thought), and grossly
disorganized motor behavior. Disorganized speech or thought, also called
formal thought disorder, is disorganization of thinking that is inferred
from speech. Characteristics of disorganized speech include rapidly
switching topics, called derailment or loose association; switching to
topics that are unrelated, called tangential thinking; incomprehensible
speech, called word salad
or incoherence. Disorganized motor behavior includes repetitive, odd,
or sometimes purposeless movement. Disorganized motor behavior rarely
includes catatonia, and although it was a historically prominent
symptom, it is rarely seen today. Whether this is due to historically
used treatments or the lack thereof is unknown.
Catatonia
describes a profoundly agitated state in which the experience of
reality is generally considered impaired. There are two primary
manifestations of catatonic behavior. The classic presentation is a
person who does not move or interact with the world in any way while
awake. This type of catatonia presents with waxy flexibility.
Waxy flexibility is when someone physically moves part of a catatonic
person's body and the person stays in the position even if it is bizarre
and otherwise nonfunctional (such as moving a person's arm straight up
in the air and the arm staying there).
The other type of catatonia is more of an outward presentation of
the profoundly agitated state described above. It involves excessive
and purposeless motor behaviour, as well as an extreme mental
preoccupation that prevents an intact experience of reality. An example
is someone walking very fast in circles to the exclusion of anything
else with a level of mental preoccupation (meaning not focused on
anything relevant to the situation) that was not typical of the person
prior to the symptom onset. In both types of catatonia, there is
generally no reaction to anything that happens outside of them. It is
important to distinguish catatonic agitation from severe bipolar mania,
although someone could have both.
Negative symptoms include reduced emotional expression (flat affect), decreased motivation (avolition), and reduced spontaneous speech (poverty of speech, alogia). Individuals with this condition lack interest and spontaneity, and have the inability to feel pleasure (anhedonia). Altered
Behavioral Inhibition System functioning could possibly cause reduced
sustained attention in psychosis and overall contribute to more negative
reactions.
Psychosis in adolescents
Psychosis is rare in adolescents.
Young people who have psychosis may have trouble connecting with the
world around them and may experience hallucinations and/or delusions. Adolescents with psychosis may also have cognitive deficits that may make it harder for the youth to socialize and work. Potential impairments include the speed of mental processing, ability to focus without getting distracted (limited attention span), and deficits in verbal memory.
If an adolescent is experiencing psychosis, they most likely have
comorbidity meaning they could have multiple mental illnesses.
Because of this, it can be difficult to determine if it is psychosis or
autism spectrum disorder, social or generalized anxiety disorder, or
obsessive-compulsive disorder.
Traumatic life events have been linked with an elevated risk of developing psychotic symptoms. Childhood trauma has specifically been shown to be a predictor of adolescent and adult psychosis.
Individuals with psychotic symptoms are three times more likely to have
experienced childhood trauma (e.g., physical or sexual abuse, physical
or emotional neglect) than those in the general population.[
Increased individual vulnerability toward psychosis may interact with
traumatic experiences promoting an onset of future psychotic symptoms,
particularly during sensitive developmental periods.
Importantly, the relationship between traumatic life events and
psychotic symptoms appears to be dose-dependent in which multiple
traumatic life events accumulate, compounding symptom expression and
severity. However, acute, stressful events can also trigger brief psychotic episodes.
Trauma prevention and early intervention may be an important target for
decreasing the incidence of psychotic disorders and ameliorating its
effects.
A healthy person could become psychotic if he is placed in an empty
room with no light and sound after 15 minutes, a phenomenon known as sensory deprivation.
Neuroticism, a personality trait associated with vulnerability to stressors, is an independent predictor of the development of psychosis.
Psychiatric disorders
From
a diagnostic standpoint, organic disorders were believed to be caused
by physical illness affecting the brain (that is, psychiatric disorders
secondary to other conditions) while functional disorders were
considered disorders of the functioning of the mind in the absence of
physical disorders (that is, primary psychological or psychiatric
disorders). Subtle physical abnormalities have been found in illnesses
traditionally considered functional, such as schizophrenia. The DSM-IV-TR
avoids the functional/organic distinction, and instead lists
traditional psychotic illnesses, psychosis due to general medical
conditions, and substance-induced psychosis.
Primary psychiatric causes of psychosis include the following:
Cycloid
psychosis is typically an acute, self-limiting form of psychosis with
psychotic and mood symptoms that progress from normal to full-blown,
usually between a few hours to days, and not related to drug intake or brain injury.
While proposed as a distinct entity, clinically separate from
schizophrenia and affective disorders, cycloid psychosis is not formally
acknowledged by current ICD or DSM criteria.
Its unclear place in psychiatric nosology has likely contributed to the
limited scientific investigation and literature on the topic.
Postpartum psychosis
Postpartum psychosis is a rare yet serious and debilitating form of psychosis. Symptoms range from fluctuating moods and insomnia to mood-incongruent delusions related to the individual or the infant.
Women experiencing postpartum psychosis are at increased risk for
suicide or infanticide. Many women who experience first-time psychosis
from postpartum often have bipolar disorder, meaning they could
experience an increase of psychotic episodes even after postpartum.
Medical conditions
A very large number of medical conditions can cause psychosis, sometimes called secondary psychosis. Examples include:
disorders causing delirium (toxic psychosis), in which consciousness is disturbed
Various psychoactive substances
(both legal and illegal) have been implicated in causing, exacerbating,
or precipitating psychotic states or disorders in users, with varying
levels of evidence. This may be upon intoxication for a more prolonged
period after use, or upon withdrawal.
Individuals who experience substance-induced psychosis tend to have a
greater awareness of their psychosis and tend to have higher levels of suicidal thinking compared to those who have a primary psychotic illness. Drugs commonly alleged to induce psychotic symptoms include alcohol, cannabis, cocaine, amphetamines, cathinones, psychedelic drugs (such as LSD and psilocybin), κ-opioid receptoragonists (such as enadoline and salvinorin A) and NMDA receptor antagonists (such as phencyclidine and ketamine). Caffeine may worsen symptoms in those with schizophrenia and cause psychosis at very high doses in people without the condition. Cannabis and other illicit recreational drugs are often associated with
psychosis in adolescents and cannabis use before 15 years old may
increase the risk of psychosis in adulthood.
Approximately three percent of people with alcoholism experience psychosis during acute intoxication or withdrawal. Alcohol related psychosis may manifest itself through a kindling mechanism. The mechanism of alcohol-related psychosis is due to the long-term effects of alcohol consumption resulting in distortions to neuronal membranes, gene expression, as well as thiamin
deficiency. It is possible that hazardous alcohol use via a kindling
mechanism can cause the development of a chronic substance-induced
psychotic disorder, i.e. schizophrenia. The effects of an
alcohol-related psychosis include an increased risk of depression and
suicide as well as causing psychosocial impairments. Delirium tremens,
a symptom of chronic alcoholism which can appear in the acute
withdrawal phase, shares many symptoms with alcohol-related psychosis
suggesting a common mechanism.
According to current studies, cannabis use is associated with
increased risk of psychotic disorders, and the more often cannabis is
used the more likely a person is to develop a psychotic illness. Furthermore, people with a history of cannabis use develop psychotic symptoms earlier than those who have never used cannabis.
Some debate exists regarding the causal relationship between cannabis
use and psychosis with some studies suggesting that cannabis use hastens
the onset of psychosis primarily in those with pre-existing
vulnerability.
Indeed, cannabis use plays an important role in the development of
psychosis in vulnerable individuals, and cannabis use in adolescence
should be discouraged. Some studies indicate that the effects of two active compounds in cannabis, tetrahydrocannabinol (THC) and cannabidiol
(CBD), have opposite effects with respect to psychosis. While THC can
induce psychotic symptoms in healthy individuals, limited evidence
suggests that CBD may have antipsychotic effects.
Methamphetamine
induces a psychosis in 26–46 percent of heavy users. Some of these
people develop a long-lasting psychosis that can persist for longer than
six months. Those who have had a short-lived psychosis from
methamphetamine can have a relapse of the methamphetamine psychosis
years later after a stressful event such as severe insomnia or a period
of hazardous alcohol use despite not relapsing back to methamphetamine.
Individuals who have a long history of methamphetamine use and who have
experienced psychosis in the past from methamphetamine use are highly
likely to re-experience methamphetamine psychosis if drug use is
recommenced. Methamphetamine-induced psychosis is likely gated by
genetic vulnerability, which can produce long-term changes in brain
neurochemistry following repetitive use.
Medication
Administration, or sometimes withdrawal, of a large number of medications may provoke psychotic symptoms. Drugs that can induce psychosis experimentally or in a significant proportion of people include:
The first brain image of an individual with psychosis was completed as far back as 1935 using a technique called pneumoencephalography (a painful and now obsolete procedure where cerebrospinal fluid is drained from around the brain and replaced with air to allow the structure of the brain to show up more clearly on an X-ray picture).
Both first episode psychosis,
and high risk status is associated with reductions in grey matter
volume (GMV). First episode psychotic and high risk populations are
associated with similar but distinct abnormalities in GMV. Reductions in
the right middle temporal gyrus, right superior temporal gyrus (STG), right parahippocampus, right hippocampus, right middle frontal gyrus, and left anterior cingulate cortex
(ACC) are observed in high risk populations. Reductions in first
episode psychosis span a region from the right STG to the right insula,
left insula, and cerebellum, and are more severe in the right ACC, right
STG, insula and cerebellum.
Another meta analysis reported bilateral reductions in insula,
operculum, STG, medial frontal cortex, and ACC, but also reported
increased GMV in the right lingual gyrus and left precentral gyrus. The Kraepelinian dichotomy is made questionable
by grey matter abnormalities in bipolar and schizophrenia;
schizophrenia is distinguishable from bipolar in that regions of grey
matter reduction are generally larger in magnitude, although adjusting
for gender differences reduces the difference to the left dorsomedial prefrontal cortex, and right dorsolateral prefrontal cortex.
During attentional tasks, first episode psychosis is associated
with hypoactivation in the right middle frontal gyrus, a region
generally described as encompassing the dorsolateral prefrontal cortex
(dlPFC). In congruence with studies on grey matter volume, hypoactivity
in the right insula, and right inferior parietal lobe is also reported.
During cognitive tasks, hypoactivities in the right insula, dACC, and
the left precuneus, as well as reduced deactivations in the right basal ganglia, right thalamus, right inferior frontal
and left precentral gyri are observed. These results are highly
consistent and replicable possibly except the abnormalities of the right
inferior frontal gyrus.
Decreased grey matter volume in conjunction with bilateral hypoactivity
is observed in anterior insula, dorsal medial frontal cortex, and
dorsal ACC. Decreased grey matter volume and bilateral hyperactivity is
reported in posterior insula, ventral medial frontal cortex, and ventral
ACC.
Hallucinations
Studies
during acute experiences of hallucinations demonstrate increased
activity in primary or secondary sensory cortices. As auditory
hallucinations are most common in psychosis, most robust evidence exists
for increased activity in the left middle temporal gyrus, left superior temporal gyrus, and left inferior frontal gyrus (i.e. Broca's area). Activity in the ventral striatum, hippocampus,
and ACC are related to the lucidity of hallucinations, and indicate
that activation or involvement of emotional circuitry are key to the
impact of abnormal activity in sensory cortices. Together, these
findings indicate abnormal processing of internally generated sensory
experiences, coupled with abnormal emotional processing, results in
hallucinations. One proposed model involves a failure of feedforward
networks from sensory cortices to the inferior frontal cortex, which
normally cancel out sensory cortex activity during internally generated
speech. The resulting disruption in expected and perceived speech is
thought to produce lucid hallucinatory experiences.
Delusions
The
two-factor model of delusions posits that dysfunction in both belief
formation systems and belief evaluation systems are necessary for
delusions. Dysfunction in evaluations systems localized to the right
lateral prefrontal cortex, regardless of delusion content, is supported
by neuroimaging studies and is congruent with its role in conflict
monitoring in healthy persons. Abnormal activation and reduced volume is
seen in people with delusions, as well as in disorders associated with
delusions such as frontotemporal dementia, psychosis and Lewy body dementia.
Furthermore, lesions to this region are associated with "jumping to
conclusions", damage to this region is associated with post-stroke
delusions, and hypometabolism this region associated with caudate
strokes presenting with delusions.
The aberrant salience model
suggests that delusions are a result of people assigning excessive
importance to irrelevant stimuli. In support of this hypothesis, regions
normally associated with the salience network demonstrate reduced grey matter in people with delusions, and the neurotransmitter dopamine, which is widely implicated in salience processing, is also widely implicated in psychotic disorders.
Specific regions have been associated with specific types of
delusions. The volume of the hippocampus and parahippocampus is related
to paranoid delusions in Alzheimer's disease, and has been reported to be abnormal post mortem in one person with delusions. Capgras delusions
have been associated with occipito-temporal damage, and may be related
to failure to elicit normal emotions or memories in response to faces.
Negative symptoms
Psychosis is associated with ventral striatal (VS) which is the part of the brain that is involved with the desire to naturally satisfy the body's needs. When high reports of negative symptoms
were recorded, there were significant irregularities in the left VS.
Anhedonia, the inability to feel pleasure, is a commonly reported
symptom in psychosis; experiences are present in most people with
schizophrenia.
Anhedonia arises as a result of the inability to feel motivation and
drive towards both the desire to engage in as well as to complete tasks
and goals. Previous research has indicated that a deficiency in the neural representation
in regards to goals and the motivation to achieve them, has
demonstrated that when a reward is not present, a strong reaction is
noted in the ventral striatum; reinforcement learning is intact when
contingencies about stimulus-reward are implicit, but not when they
require explicit neural processing; reward prediction errors are what
the actual reward is versus what the reward was predicted to be.
In most cases positive prediction errors are considered an abnormal
occurrence. A positive prediction error response occurs when there is an
increased activation in a brain region, typically the striatum,
in response to unexpected rewards. A negative prediction error response
occurs when there is a decreased activation in a region when predicted
rewards do not occur. Anterior Cingulate Cortex (ACC)
response, taken as an indicator of effort allocation, does not increase
with reward or reward probability increase, and is associated with
negative symptoms; deficits in Dorsolateral Prefrontal Cortex (dlPFC)
activity and failure to improve performance on cognitive tasks when
offered monetary incentives are present; and dopamine mediated functions
are abnormal.
Psychosis has been traditionally linked to the overactivity of the neurotransmitterdopamine. In particular to its effect in the mesolimbic pathway. The two major sources of evidence given to support this theory are that dopamine receptor D2 blocking drugs (i.e., antipsychotics)
tend to reduce the intensity of psychotic symptoms, and that drugs that
accentuate dopamine release, or inhibit its reuptake (such as amphetamines and cocaine) can trigger psychosis in some people (see stimulant psychosis).
NMDA receptor dysfunction has been proposed as a mechanism in psychosis. This theory is reinforced by the fact that dissociativeNMDA receptor antagonists such as ketamine, PCP and dextromethorphan (at large overdoses) induce a psychotic state. The symptoms of dissociative intoxication are also considered to mirror the symptoms of schizophrenia, including negative symptoms.
NMDA receptor antagonism, in addition to producing symptoms
reminiscent of psychosis, mimics the neurophysiological aspects, such as
reduction in the amplitude of P50, P300, and MMNevoked potentials.
Hierarchical Bayesian neurocomputational models of sensory feedback, in
agreement with neuroimaging literature, link NMDA receptor hypofunction
to delusional or hallucinatory symptoms via proposing a failure of NMDA
mediated top down predictions to adequately cancel out enhanced bottom
up AMPA mediated predictions errors.
Excessive prediction errors in response to stimuli that would normally
not produce such a response is thought to root from conferring excessive
salience to otherwise mundane events. Dysfunction higher up in the hierarchy, where representation is more abstract, could result in delusions. The common finding of reduced GAD67 expression in psychotic disorders may explain enhanced AMPA mediated signaling, caused by reduced GABAergic inhibition.
The connection between dopamine and psychosis is generally believed to be complex. While dopamine receptor D2 suppresses adenylate cyclase activity, the D1
receptor increases it. If D2-blocking drugs are administered, the
blocked dopamine spills over to the D1 receptors. The increased
adenylate cyclase activity affects genetic expression
in the nerve cell, which takes time. Hence antipsychotic drugs take a
week or two to reduce the symptoms of psychosis. Moreover, newer and
equally effective antipsychotic drugs actually block slightly less
dopamine in the brain than older drugs whilst also blocking 5-HT2A
receptors, suggesting the 'dopamine hypothesis' may be oversimplified. Soyka and colleagues found no evidence of dopaminergic dysfunction in people with alcohol-induced psychosis and Zoldan et al. reported moderately successful use of ondansetron, a 5-HT3 receptor antagonist, in the treatment of levodopa psychosis in Parkinson's disease patients.
A review found an association between a first-episode of psychosis and prediabetes.
Prolonged or high dose use of psychostimulants can alter normal functioning, making it similar to the manic phase of bipolar disorder. NMDA antagonists replicate some of the so-called "negative" symptoms like thought disorder in subanesthetic doses (doses insufficient to induce anesthesia), and catatonia
in high doses. Psychostimulants, especially in one already prone to
psychotic thinking, can cause some "positive" symptoms, such as
delusional beliefs, particularly those persecutory in nature.
Culture
Cross-cultural
studies into schizophrenia have found that individual experiences of
psychosis and 'hearing voices' vary across cultures. In countries such as the United States
where there exists a predominantly biomedical understanding of the
body, the mind and in turn, mental health, subjects were found to report
their hallucinations as having 'violent content' and self-describing as
'crazy'. This lived experience is at odds with the lived experience of subjects in Accra, Ghana, who describe the voices they hear as having 'spiritual meaning' and are often reported as positive in nature; or subjects in Chennai, India, who describe their hallucinations as kin, family members or close friends, and offering guidance.
These differences are attributed to 'social kindling' or how
one's social context shapes how an individual interprets and experiences
sensations such as hallucinations. This concept aligns with
pre-existing cognitive theory such as reality modelling and is supported
by recent research that demonstrates that individuals with psychosis
can be taught to attend to their hallucinations differently, which in
turn alters the hallucinations themselves.
Such research creates pathways for social or community-based treatment,
such as reality monitoring, for individuals with schizophrenia and
other psychotic disorders, providing alternatives to, or supplementing
traditional pharmacologic management.
Cross-cultural studies explore the way in which psychosis varies
in different cultures, countries and religions. The cultural differences
are based on the individual or shared illness narratives surrounding
cultural meanings of illness experience. In countries such as India, Cambodia and Muslim
majority countries, they each share alternative epistemologies. These
are known as knowledge systems that focus on the connections between
mind, body, culture, nature, and society. Cultural perceptions of mental disorders such as psychosis or schizophrenia are believed to be caused by jinn (spirits) in Muslim majority countries. Furthermore, those in Arab-Muslim societies perceive those who act differently than the social norm as "crazy" or as abnormal behaviour.
This differs from the lived experience of individuals in India and how
they attain their perspectives on mental health issues through a variety
of spiritual and healing traditions. In Cambodia, hallucinations are linked with spirit visitation, a term they call "cultural kindling". These examples of differences are attributed to culture and the way it shapes conceptions of mental disorders. These cultural differences can be useful in bridging the gap of cultural understanding and psychiatric signs and symptoms.
Diagnosis
To make a diagnosis of a mental illness in someone with psychosis other potential causes must be excluded.
An initial assessment includes a comprehensive history and physical
examination by a health care provider. Tests may be done to exclude
substance use, medication, toxins, surgical complications, or other
medical illnesses. A person with psychosis is referred to as psychotic.
Delirium
should be ruled out, which can be distinguished by visual
hallucinations, acute onset and fluctuating level of consciousness,
indicating other underlying factors, including medical illnesses. Excluding medical illnesses associated with psychosis is performed by using blood tests to measure:
MRI or CT scan of the head to exclude brain lesions.
Because psychosis may be precipitated or exacerbated by common classes of medications, medication-induced psychosis should be ruled out, particularly for first-episode psychosis. Both substance- and medication-induced psychosis can be excluded to a high level of certainty, using toxicology screening.
Because some dietary supplements
may also induce psychosis or mania, but cannot be ruled out with
laboratory tests, a psychotic individual's family, partner, or friends
should be asked whether the patient is currently taking any dietary
supplements.
Common mistakes made when diagnosing people who are psychotic include:
Not appreciating medical abnormalities (e.g., vital signs),
Not obtaining a medical history and family history,
Indiscriminate screening without an organizing framework,
Missing a toxic psychosis by not screening for substances and medications,
Not asking their family or others about dietary supplements,
Premature diagnostic closure, and
Not revisiting or questioning the initial diagnostic impression of primary psychiatric disorder.
Only after relevant and known causes of psychosis are excluded, a mental health clinician may make a psychiatric differential diagnosis
using a person's family history, incorporating information from the
person with psychosis, and information from family, friends, or
significant others.
Types of psychosis in psychiatric disorders may be established by formal rating scales. The Brief Psychiatric Rating Scale (BPRS) assesses the level of 18 symptom constructs of psychosis such as hostility, suspicion, hallucination, and grandiosity.
It is based on the clinician's interview with the patient and
observations of the patient's behavior over the previous 2–3 days. The
patient's family can also answer questions on the behavior report.
During the initial assessment and the follow-up, both positive and
negative symptoms of psychosis can be assessed using the 30 item
Positive and Negative Symptom Scale (PANSS).
The DSM-5
characterizes disorders as psychotic or on the schizophrenia spectrum
if they involve hallucinations, delusions, disorganized thinking,
grossly disorganized motor behavior, or negative symptoms.
The DSM-5 does not include psychosis as a definition in the glossary,
although it defines "psychotic features", as well as "psychoticism" with
respect to personality disorder. The ICD-10 has no specific definition of psychosis.
Factor analysis
of symptoms generally regarded as psychosis frequently yields a five
factor solution, albeit five factors that are distinct from the five
domains defined by the DSM-5 to encompass psychotic
or schizophrenia spectrum disorders. The five factors are frequently
labeled as hallucinations, delusions, disorganization, excitement, and
emotional distress. The DSM-5 emphasizes a psychotic spectrum, wherein the low end is characterized by schizoid personality disorder, and the high end is characterized by schizophrenia.
Prevention
The evidence for the effectiveness of early interventions to prevent psychosis appeared inconclusive. But psychosis caused by drugs can be prevented.
Whilst early intervention in those with a psychotic episode might
improve short-term outcomes, little benefit was seen from these measures
after five years. However, there is evidence that cognitive behavioral therapy (CBT) may reduce the risk of becoming psychotic in those at high risk, and in 2014 the UK National Institute for Health and Care Excellence (NICE) recommended preventive CBT for people at risk of psychosis.
Treatment
The
treatment of psychosis depends on the specific diagnosis (such as
schizophrenia, bipolar disorder or substance intoxication). The
first-line treatment for many psychotic disorders is antipsychotic
medication,
which can reduce the positive symptoms of psychosis in about 7 to 14
days. For youth or adolescents, treatment options include medications,
psychological interventions, and social interventions.
Medication
The choice of which antipsychotic to use is based on benefits, risks, and costs. It is debatable whether, as a class, typical or atypical antipsychotics are better. Tentative evidence supports that amisulpride, olanzapine, risperidone and clozapine may be more effective for positive symptoms but result in more side effects. Typical antipsychotics have equal drop-out and symptom relapse rates to atypicals when used at low to moderate dosages.
There is a good response in 40–50%, a partial response in 30–40%, and
treatment resistance (failure of symptoms to respond satisfactorily
after six weeks to two or three different antipsychotics) in 20% of
people.
Clozapine is an effective treatment for those who respond poorly to
other drugs ("treatment-resistant" or "refractory" schizophrenia), but it has the potentially serious side effect of agranulocytosis (lowered white blood cell count) in less than 4% of people.
Most people on antipsychotics get side effects. People on typical antipsychotics tend to have a higher rate of extrapyramidal side effects while some atypicals are associated with considerable weight gain, diabetes and risk of metabolic syndrome; this is most pronounced with olanzapine, while risperidone and quetiapine are also associated with weight gain. Risperidone has a similar rate of extrapyramidal symptoms to haloperidol.
Psychotherapy
Psychological treatments such as acceptance and commitment therapy
(ACT) are possibly useful in the treatment of psychosis, helping people
to focus more on what they can do in terms of valued life directions
despite challenging symptomology. Metacognitive training (MCT) is associated with reduced delusions, hallucinations and negative symptoms as well as improved self-esteem and functioning in individuals with schizophrenia spectrum disorders.
There are many psychosocial interventions that seek to treat the symptoms of psychosis: need adapted treatment, Open Dialogue, psychoanalysis/psychodynamic psychotherapy, major role therapy, soteria, psychosocial outpatient and inpatient treatment, milieu therapy, and cognitive behavioral therapy (CBT).
When these are used without antipsychotic medications, they may be
somewhat effective for some people, especially for CBT, need-adapted
treatment, and soteria.
Early intervention in psychosis
is based on the observation that identifying and treating someone in
the early stages of a psychosis can improve their longer term outcome. This approach advocates the use of an intensive multi-disciplinary approach during what is known as the critical period, where intervention is the most effective, and prevents the long-term morbidity associated with chronic psychotic illness.
Systematic reform
Addressing
systematic reform is essential to creating effective prevention as well
as supporting treatments and recovery for those with psychosis.
Waghorn et al.
suggest that education interventions can be a building block to support
those with psychosis to successfully participate in society. In their
study they analyse the relationship between successful education
attainment and psychosis. Findings suggest proportionately more school
aged persons with psychosis discontinued their education, compared to
those without psychosis.
Waghorn et al.
finds that specialised supported education for those with psychotic
disorders can help lead to successful education attainment.
Additionally, future employment outcomes are relative to such education
attainment. Established approaches to supported education in the US
include three basic models, self-contained classrooms, onsite support
model and the mobile support model. Each model includes the
participation of mental health service staff or educational facility
staff in the student's education arrangements.
Potential benefits of specialised supported education found from
this study include coordination with other service providers (e.g.
income support, housing, etc.) to prevent disrupting education,
providing specialised career counselling, development of coping skills
in the academic environment.
These examples provide beneficial ways for people with psychosis to
finish studies successfully as well as counter future experiences of
psychosis.
History
Etymology
The word psychosis was introduced to the psychiatric literature in 1841 by Karl Friedrich Canstatt in his work Handbuch der Medizinischen Klinik. He used it as a shorthand for 'psychic neurosis'. At that time neurosis meant any disease of the nervous system, and Canstatt was thus referring to what was considered a psychological manifestation of brain disease. Ernst von Feuchtersleben is also widely credited as introducing the term in 1845, as an alternative to insanity and mania.
The term stems from Modern Latinpsychosis, "a giving soul or life to, animating, quickening" and that from Ancient Greek ψυχή (psyche), "soul" and the suffix -ωσις (-osis), in this case "abnormal condition".
In its adjective form "psychotic", references to psychosis can be
found in both clinical and non-clinical discussions. However, in a non-clinical context, "psychotic" is a nonspecific colloquialism used to mean "insane".
Classification
The word was also used to distinguish a condition considered a disorder of the mind, as opposed to neurosis, which was considered a disorder of the nervous system. The psychoses thus became the modern equivalent of the old notion of madness, and hence there was much debate on whether there was only one (unitary) or many forms of the new disease. One type of broad usage would later be narrowed down by Koch in 1891 to the 'psychopathic inferiorities'—later renamed abnormal personalities by Schneider.
The division of the major psychoses into manic depressive illness (now called bipolar disorder) and dementia praecox (now called schizophrenia) was made by Emil Kraepelin, who attempted to create a synthesis of the various mental disorders identified by 19th-century psychiatrists,
by grouping diseases together based on classification of common
symptoms. Kraepelin used the term 'manic depressive insanity' to
describe the whole spectrum of mood disorders, in a far wider sense than it is usually used today.
In Kraepelin's classification this would include 'unipolar' clinical depression, as well as bipolar disorder and other mood disorders such as cyclothymia.
These are characterised by problems with mood control and the psychotic
episodes appear associated with disturbances in mood, and patients
often have periods of normal functioning between psychotic episodes even
without medication. Schizophrenia
is characterized by psychotic episodes that appear unrelated to
disturbances in mood, and most non-medicated patients show signs of
disturbance between psychotic episodes.
Treatment
Early
civilizations considered madness a supernaturally inflicted phenomenon.
Archaeologists have unearthed skulls with clearly visible drillings,
some datable back to 5000 BC suggesting that trepanning was a common treatment for psychosis in ancient times. Written record of supernatural causes and resultant treatments can be traced back to the New Testament. Mark 5:8–13 describes a man displaying what would today be described as psychotic symptoms. Christ cured this "demonic
madness" by casting out the demons and hurling them into a herd of
swine. Exorcism is still utilized in some religious circles as a
treatment for psychosis presumed to be demonic possession.
A research study of out-patients in psychiatric clinics found that 30
percent of religious patients attributed the cause of their psychotic
symptoms to evil spirits. Many of these patients underwent exorcistic
healing rituals that, though largely regarded as positive experiences by
the patients, had no effect on symptomology. Results did, however, show
a significant worsening of psychotic symptoms associated with exclusion
of medical treatment for coercive forms of exorcism.
Bust of Hippocrates
The medical teachings of the fourth-century philosopher and physician Hippocrates of Cos proposed a natural, rather than supernatural, cause of human illness. In Hippocrates' work, the Hippocratic corpus,
a holistic explanation for health and disease was developed to include
madness and other "diseases of the mind". Hippocrates writes:
Men ought to know that from the
brain, and from the brain only, arise our pleasures, joys, laughter, and
jests, as well as our sorrows, pains, griefs and tears. Through it, in
particular, we think, see, hear, and distinguish the ugly from the
beautiful, the bad from the good, the pleasant from the unpleasant....
It is the same thing which makes us mad or delirious, inspires us with
dread and fear, whether by night or by day, brings sleeplessness,
inopportune mistakes, aimless anxieties, absentmindedness, and acts that
are contrary to habit.
Hippocrates espoused a theory of humoralism wherein disease is resultant of a shifting balance in bodily fluids including blood, phlegm, black bile, and yellow bile. According to humoralism, each fluid or "humour"
has temperamental or behavioral correlates. In the case of psychosis,
symptoms are thought to be caused by an excess of both blood and yellow
bile. Thus, the proposed surgical intervention for psychotic or manic
behavior was bloodletting.
18th-century physician, educator, and widely considered "founder of American psychiatry", Benjamin Rush,
also prescribed bloodletting as a first-line treatment for psychosis.
Although not a proponent of humoralism, Rush believed that active
purging and bloodletting were efficacious corrections for disruptions in
the circulatory system, a complication he believed was the primary
cause of "insanity".
Although Rush's treatment modalities are now considered antiquated and
brutish, his contributions to psychiatry, namely the biological
underpinnings of psychiatric phenomenon including psychosis, have been
invaluable to the field. In honor of such contributions, Benjamin Rush's
image is in the official seal of the American Psychiatric Association.
Early 20th-century treatments for severe and persisting psychosis
were characterized by an emphasis on shocking the nervous system. Such
therapies include insulin shock therapy, cardiazol shock therapy, and electroconvulsive therapy. Despite considerable risk, shock therapy was considered highly efficacious in the treatment of psychosis including schizophrenia. The acceptance of high-risk treatments led to more invasive medical interventions including psychosurgery.
Gottlieb Burckhardt (1836–1907)
In 1888, Swiss psychiatrist Gottlieb Burckhardt performed the first medically sanctioned psychosurgery in which the cerebral cortex
was excised. Although some patients showed improvement of symptoms and
became more subdued, one patient died and several developed aphasia
or seizure disorders. Burckhardt would go on to publish his clinical
outcomes in a scholarly paper. This procedure was met with criticism
from the medical community and his academic and surgical endeavors were
largely ignored. In the late 1930s, Egas Moniz conceived the leucotomy (AKA prefrontal lobotomy) in which the fibers connecting the frontal lobes
to the rest of the brain were severed. Moniz's primary inspiration
stemmed from a demonstration by neuroscientists John Fulton and
Carlyle's 1935 experiment in which two chimpanzees were given
leucotomies and pre- and post-surgical behavior was compared. Prior to
the leucotomy, the chimps engaged in typical behavior including throwing
feces and fighting. After the procedure, both chimps were pacified and
less violent. During the Q&A, Moniz asked if such a procedure could
be extended to human subjects, a question that Fulton admitted was quite
startling.
Moniz would go on to extend the controversial practice to humans with
various psychotic disorders, an endeavor for which he received a Nobel Prize in 1949. Between the late 1930s and early 1970s, the leucotomy was a widely accepted practice, often performed in non-sterile environments such as small outpatient clinics and patient homes. Psychosurgery remained standard practice until the discovery of antipsychotic pharmacology in the 1950s.
The first clinical trial of antipsychotics (also commonly known as neuroleptics) for the treatment of psychosis took place in 1952. Chlorpromazine
(brand name: Thorazine) passed clinical trials and became the first
antipsychotic medication approved for the treatment of both acute and
chronic psychosis. Although the mechanism of action was not discovered
until 1963, the administration of chlorpromazine marked the advent of
the dopamine antagonist, or first generation antipsychotic. While clinical trials showed a high response rate for both acute psychosis and disorders with psychotic features, the side effects were particularly harsh, which included high rates of often irreversible Parkinsonian symptoms such as tardive dyskinesia. With the advent of atypical antipsychotics
(also known as second generation antipsychotics) came a dopamine
antagonist with a comparable response rate but a far different, though
still extensive, side-effect profile that included a lower risk of
Parkinsonian symptoms but a higher risk of cardiovascular disease. Atypical antipsychotics remain the first-line treatment for psychosis associated with various psychiatric and neurological disorders including schizophrenia, bipolar disorder, major depressive disorder, anxiety disorders, dementia, and some autism spectrum disorders.
Dopamine is now one of the primary neurotransmitters implicated
in psychotic symptomology. Blocking dopamine receptors (namely, the
dopamine D2 receptors) and decreasing dopaminergic activity continues to
be an effective but highly unrefined effect of antipsychotics, which
are commonly used to treat psychosis. Recent pharmacological research
suggests that the decrease in dopaminergic activity does not eradicate
psychotic delusions or hallucinations,
but rather attenuates the reward mechanisms involved in the development
of delusional thinking; that is, connecting or finding meaningful
relationships between unrelated stimuli or ideas. The author of this research paper acknowledges the importance of future investigation:
The model presented here is based
on incomplete knowledge related to dopamine, schizophrenia, and
antipsychotics—and as such will need to evolve as more is known about
these.
— Shitij Kapur, From dopamine to salience to psychosis—linking biology, pharmacology and phenomenology of psychosis
Freud's
former student Wilhelm Reich explored independent insights into the
physical effects of neurotic and traumatic upbringing, and published his
holistic psychoanalytic treatment with a schizophrenic. With his
incorporation of breathwork and insight with the patient, a young woman,
she achieved sufficient self-management skills to end the therapy.
Lacan extended Freud's ideas to create a psychoanalytic model of psychosis based upon the concept of "foreclosure", the rejection of the symbolic concept of the father.
Psychiatrist David Healy
has criticised pharmaceutical companies for promoting simplified
biological theories of mental illness that seem to imply the primacy of
pharmaceutical treatments while ignoring social and developmental
factors that are known important influences in the etiology of
psychosis.
Society and culture
Disability
The classification of psychosis as a social disability is a common occurrence.
Psychosis is considered to be among the top 10 causes of social disability among adult men and women in developed countries.
And the traditional, negative narrative around disability has been
shown to strongly and adversely influence the pathways through
employment and education for people experiencing psychosis.
Social disability by way of social disconnection is a significant
public health concern and is associated with a broad range of negative
outcomes, including premature mortality. Social disconnection refers to
the ongoing absence of family or social relationships with marginal
participation in social activities.
Research on psychosis found that reduced participation in social
networks, not only negatively effects the individual on a physical and
mental level, it has been shown that failure to be included in social
networks influences the individual's ability to participate in the wider
community through employment and education opportunities.
Equal opportunity to participate in meaningful relationships with
friends, family and partners, as well as engaging in social constructs
such as employment, can provide significant physical and mental value to
people's lives.
And how breaking the disability mindset around people experiencing
psychosis is imperative for their overall, long-term health and
well-being as well as the contributions they are able to make to their
immediate social connections and the wider community.
Research
Further
research in the form of randomized controlled trials is needed to
determine the effectiveness of treatment approaches for helping adolescents with psychosis.
Through 10 randomized clinical trials, studies showed that Early
Intervention Services (EIS) for patients with early-phase schizophrenia
spectrum disorders have generated promising outcomes. EIS are specifically intended to fulfill the needs of patients with early-phase psychosis.
In addition, one meta-analysis that consisted of four randomized
clinical trials has examined and discovered the efficacy of EIS to
Therapy as Usual (TAU) for early-phase psychosis, revealing that EIS
techniques are superior to TAU.
A study suggests that combining cognitive behavioral therapy
(CBT) with SlowMo, an app that helps notice their "unhelpful
quick-thinking", might be more effective for treating paranoia in people
with psychosis than CBT alone.
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