name :rahul.hosi.

charna
roll no:19010
class: m.a part 1
college:r.d . national college
topic psychology perspective on the movie "the machinist"

introduction of self:
Rahul is doing masters in psychology. Rahul is interested in philosophy and
psychology.species of world and life as a big puzzle have and he wants to solve it.solve this
puzzle he requires to see the intricate patterns of the life so that's why he pays a lot of
attention to very small details of everything. this details could be of any person of anything or
just small happening. Rahul religious philosophy which includes the eastern religions like
Buddhism Jainism Hinduism and Sikhism.he just not believe what other person is saying he
wants details and evidences of what exactly it is and he misses his information mostly on
evidence experience them on the other person's opinion. sceptical view of religion and
philosophy.

literature review
1.year of publication:2018

researcher name: flavie waters, vivian chiu,amanda Atkinson,Jan dark blom

review: research found out by doing meta analysis of different and some experimentation
that as the number hours of wakefulness that hours of non sleeping increases subjects
developed hallucinations and some other sensory problems. this article showed that there is
a close link between insomnia and hallucinations

demerits: research could have used more of experimentation

2.year2014

researcher nam:sunil j. wimalwansa

review this was based on insights of author. and recent literature of ptsd . it concluded that
development and sustenance of ptsd is greatly affected by changes in amygdala and
hippocampus. in general because of changes in neuro-endocrine system patient probe to
maladaptive learning of responses.. this is the main cause of development of ptsd. thee also
other causes like childhood upbringing. support after war. individual differences etc.

Demerits:more experimentation could have done

3. year of publication:1982

researcher names:keane ,t.m, kaloupek,d.g

review: they found that imaginal flooding technique of psychotherapy in which client is
exposed to feared . has greatly helped than other forms therapy because . they fear situation
. they are being exposed to situations.

demerits:they could have experimented more with other forms of therapy

theories of ptsd
Emotional processing theory
The earlier network theor) has been elaborated by and Foa and Rothbaum in several ways
in order to take account of
accumulating knowledge, particularly with respect to assault and rape victims. One devel-
opment was to elaborate the relationship between PTSD and knowledge available prior to
the
trauma, during the trauma, and after the trauma. They proposed that individuals with more
rigid pre-trauma views would be more vulnerable to PTSD. These could be rigid positive
views about the self as being extremely competent and the world as extremely safe, which
would be contradicted by the event, or rigid negative views about the self as being extremely
incompetent and the world as being extremely dangerous, which would be confirmed by the
event
Another development was an increased emphasis on negative appraisals of responses and
behaviors which could exacerbate perceptions of incompetence outlined how these
appraisals might relate to events that took place at the time of the trauma, to symptoms that
developed afterwards, to disruption in daily activities, and to the responses of others. Beliefs
that were present before, during, and after the trauma could interact to reinforce the critical
negative schemas involving incompetence and danger that they hypothesized underlie
chronin ptsd

Dual representation theory

In contrast to the proposal of fear network theories that a traumatic memory is an ordinary
memory that has a particular structure (more response elements, stronger inter-element
associations, etc.) is the idea that trauma memories are represented in a fundamentally
distinct
way These authors suggested that pathological responses (for example, vivid and
uncontrollable reexperiencing in the present) arise when trauma memories become disso-
ciated from the ordinary memory system and that recovery involves transforming them into
ordinary or narrative memories. However, they have not made clear whether ordinary
memories of the traumatic event can exist alongside dissociated memories, and exactly
how one form of memory is transformed into another.
One way of understanding this notion of a dissociated memory is to posit that there are two
(or more) memory systems and that trauma information is better represented in one system
than in the other. Several cognitive psychologists have proposed that there is a separate
perceptual memory system that records information that has received little, if any, conscious
attention. For example, even under ordinary conditions of attentional diversion, people
frequently fail to see highly visible but unexpected objects before their eyes, a phenomenon
known as ‘‘inattentional blindness’’ These unattended objects or items
that are not consciously seen in their experiments are nevertheless encoded and analyzed in
considerable detail and can unconsciously affect participants’ responses on tests of indirect
memory. The findings appear to be very relevant to trauma victims, whose attention tends to
be captured by the immediate source of threat and who may report that they simply failed to
hear words that were shouted or shots that were fired in close proximity to them. Whereas in
some models, the perceptual memory system is unable to support conscious experience, in
others, it supports sensory images such as visual scene. Although perceptual
representations are usually thought to be transient or only detectable by indirect probes, it
has
been suggested that experiencing events with high levels of emotion or importance results in
the storage of long-lasting, vivid traces.
According to Brewin et al.’s version of dual representation theory, two memory
systems continue to operate in parallel, but one may take precedence over the other at
different times. Oral or written narrative memories of a trauma reflect the operation of a
‘‘verbally accessible memory’’ (VAM) system, so called to reflect the fact that the trauma
memory is integrated with other autobiographical memories and the fact that it can be
deliberately retrieved as and when required. VAM memories of trauma are therefore
represented within a complete personal context comprising past, present, and future. They
contain information that the individual has attended to before, during, and after the traumatic
event, and that received sufficient conscious processing to be transferred to a long-term
memory store in a form that can later be deliberately retrieved. These memories are
available
for verbal communication with others, but the amount of information they contain is restricted
because they only record what has been consciously attended to. Diversion of attention to
the
immediate source of threat and the effects of high levels of arousal greatly restrict the
volume

In contrast, flashbacks are thought to reflect the operation of a ‘‘situationally accessible

memory’’ (SAM) system, so called to reflect the fact that flashbacks are only ever triggered
involuntarily by situational reminders of the trauma (encountered either in the external
environment or in the internal environment of a person’s mental processes). The SAM
system
contains information that has been obtained from more extensive, lower level perceptual
processing of the traumatic scene, such as sights and sounds that were too briefly
apprehended to receive much conscious attention and hence did not become recorded in
the VAM system. The SAM system also stores information about the person’s bodily
response to the trauma, such as changes in heart rate, flushing, temperature changes, and
pain. This results in flashbacks being more detailed and emotion-laden than ordinary
memories.
Because the SAM system does not use a verbal code, these memories are difficult to
communicate to others, and they do not necessarily interact with and get updated by other
autobiographical knowledge. SAM memories can be difficult to control because people
cannot always regulate their exposure to sights, sounds, or smells that act as reminders of
the
trauma. The emotions that accompany SAM memories are restricted to ‘‘primary emotions’’
that were experienced during the trauma. During some traumatic events, there may be time
for more complex evaluations to take place. A person may experience a range of emotions
such as anger and shame, and these would be coded into a SAM memory along with fear,
helplessness,
One implication of dual representation theory is that PTSD is a hybrid disorder that
potentially incorporates two separate pathological processes, one involving the resolution of
negative beliefs and their accompanying emotions and one involving the management of
flashbacks. Recovery depends on the outcome of both these processes. One requirement is
to reduce negative emotions generated by cognitive appraisal of the trauma, by consciously
reasserting perceived control, reattributing responsibility, and achieving an integration of the
new information with preexisting concepts and beliefs. The second requirement is to
prevent the continued automatic reactivation of situationally accessible knowledge about the
trauma. , it was suggested that this is brought about by creating
new SAMs that block access to the original ones. The new SAMs would consist of the
original trauma images paired with states of reduced arousal and reduced negative affect
brought about by habituation or by cognitive restructuring of the meaning and significance
of the event.
This approach is consistent with the idea that two systems underpin human the One is
associative and automatic, making use of basic principles such as the
similarity between elements or the closeness of two elements in time. It searches for and
bases
conclusions on patterns and regularities between elements such as images and stereotypes.

Anxious apprehension model

argued that variables implicated in the etiology and maintenance
of panic disorder are also involved in PTSD, and that there is a marked similarity between
panic attacks and traumatic flashbacks. While recognizing the role of biological vulnerability,
the trauma itself, and the experience of intense emotions at the time, their key point is the
inclusion of cognitive factors that occur after the trauma and produce a feedback cycle of
anxious apprehension. That is, patients with PTSD focus their attention upon and are
hypervigilant for information about ‘emotional alarms’ and associated stimuli. Although in
the face of actual trauma, the alarm is genuine, false alarms can occur subsequently in the
absence of danger, as described model of panic disorder.
In PTSD, the focus of people’s anxious apprehension is on cognitive and physiological
cues from the time of the actual trauma as they wish to avoid the distress generated by
alarms.
The learned alarms generate hyperarousal symptoms, which through their association to
cues
present at the time of the original trauma (the real alarm) result in a negative feedback loop
ensuring successive reexperiencing symptoms. To prevent the triggering of alarms, the
person
will tend to avoid emotional interoceptive information, for example, through emotional
numbing, as well as avoid external trauma-related stimuli. Jones and Barlow argued that
coping styles and social support can, as in other anxiety disorders, moderate the expression
of
PTSD.
This approach emphasizes the similarity of PTSD to other anxiety disorders and the
importance of distorted information processing in PTSD. Consistent with the model, panic
symptoms are often reported both during and after trauma and may be a risk factor for later
PTSD symptoms have proposed that the content of
intrusive memories corresponds to moments that act as warning signals for the traumatic
event. While Jones and Barlow’s theory draws attention to a potentially important but
neglected aspect of PTSD, it does not discuss in detail the role and variety of cognitions and
emotions arising from the consequences of the event

Conditioning theory
This approach sought to apply conditioning theories developed for other anxiety disorders
to PTSD. Following Mowrer’s two-factor learning theory, an initial phase of fear
acquisition through classical conditioning results in neutral stimuli present in the traumatic
situation acquiring fear-eliciting properties through their association with the unconditioned
stimulus (in this case, those elements of the traumatic situation that directly arouse fear).
Keane, Zimering, and Caddell) proposed that a wide variety of associated stimuli
would acquire the ability to arouse fear through the processes of stimulus generalization and
higher order conditioning. Although repeated exposure to spontaneous memories of the
trauma would normally be sufficient to extinguish these associations, extinction would fail to
occur if the person attempted to distract themselves or block out the memories, rendering
the
exposure incomplete. Avoidance of the conditioned stimuli, whether through distraction,
blocking of memories, or other behaviors, would be reinforced by a reduction in fear, leading
to the maintenance of PTSD.
In their application of conditioning theory to combat veterans, Keane et al. made further
suggestions about the origin of specific symptoms. For example, they proposed that
amnesia
for aspects of the trauma could be due to avoidance of thinking or talking about it, as well as
to being in a different mood state at recall than at the time of the trauma. Anger and
irritability might reflect behaviors acquired during military training and reinforced during
civilian life by the attainment of desired goals or a reduction in anxiety. More recently Orr et
al.have shown that people with PTSD develop conditioned responses more readily to
aversive events in general and that these responses are harder to extinguish. Although this
could be a result of PTSD, it may also reflect genetic or acquired pre-trauma differences in
conditionability.

introduction of movie
Posttraumatic stress disorder (PTSD) is an anxiety disorder that can develop following
exposure to a traumatic event, including terrifying or life-threatening situations such as
sexual assault or natural disasters. The disorder is characterized by a reaction of intense
fear, helplessness, or horror when the individual experiences, testifies about, or is faced with
one or more events that involve death, severe wounds, or a threat to one's own or another's
physical integrity. One of the most important symptoms of PTSD is the revival of the
traumatic event, which has been interpreted as an inability to downregulate negative
emotions. Neuroimaging studies that probed the ability to regulate emotions in healthy
volunteers have found a pattern characterized by activation of the prefrontal cortex
associated with a reduction in amygdala activity. This suggests an inhibitory prefrontal
cortex-amygdala circuit that underlies emotional regulation. The hypothesis that increased
amygdala activation associated with PTSD results from dysfunction in the inhibitory
mechanism exerted by the prefrontal cortex has been the topic of debate. The present
review investigates the validity of dysfunction in the prefrontal-amygdala pathway in PTSD.
The studies provide evidence that the amygdala and prefrontal cortex exhibit distinct
activation patterns in PTSD, thus supporting the model of a dysfunctional circuit.
Inconsistencies in the literature may be attributable to distinct PTSD subgroups, different
experimental approaches, different contrasts employed in neuroimaging studies, and small
sample sizes.

PTSD has been known by many names in the past, such as “shell shock” during the years of
World War I and “combat fatigue” after World War II. But PTSD does not just happen to
combat veterans. PTSD can occur in all people, in people of any ethnicity, nationality or
culture, and any age. PTSD affects approximately 3.5 percent of U.S. adults, and an
estimated one in 11 people will be diagnosed PTSD in their lifetime. Women are twice as
likely as men to have PTSD.

People with PTSD have intense, disturbing thoughts and feelings related to their experience
that last long after the traumatic event has ended. They may relive the event through
flashbacks or nightmares; they may feel sadness, fear or anger; and they may feel detached
or estranged from other people. People with PTSD may avoid situations or people that
remind them of the traumatic event, and they may have strong negative reactions to
something as ordinary as a loud noise or an accidental touch.

A diagnosis of PTSD requires exposure to an upsetting traumatic event. However, exposure

could be indirect rather than first hand. For example, PTSD could occur in an individual
learning about the violent death of a close family. It can also occur as a result of repeated
exposure to horrible details of trauma such as police officers exposed to details of child
abuse cases.

introduction of movie:
"If you were any thinner," Stevie tells him, "you wouldn't exist." Trevor Reznik weighs 121
pounds and you wince when you look at him. He is a lonely man, disliked at work, up all
night, returning needfully to two women who are kind to him: Stevie, a hooker, and Marie,
the waitress at the all-night diner out at the airport. "I haven't slept in a year," he tells Marie.

Christian Bale lost more than 60 pounds to play this role, a fact I share not because you
need to know how much weight he lost, but because you need to know that it is indeed
Christian Bale. He is so gaunt, his face so hollow, he looks nothing like the actor we're
familiar with. There are moments when his appearance even distracts from his performance,
because we worry about him. Certainly we believe that the character, Trevor, is at the end of
his rope, and I was reminded of Anthony Perkins' work in Orson Welles' "The Trial," another
film about a man who finds himself trapped in the vise of the world's madness.

movies plot:
Trevor Reznik (Christian Bale) is a machinist whose insomnia has led to him becoming
emaciated. His appearance and behavior keep his coworkers away, and they eventually turn
against him when he is involved in an accident which causes his coworker, Miller, to lose his
left arm. Trevor, who was distracted by an unfamiliar co-worker named Ivan, is blamed for
the accident. No one at the factory knows of Ivan and there are no records of him. Trevor
seems to find peace only with Stevie, a prostitute with genuine affection for him, and with
Maria, a waitress at an airport diner he frequents. He is haunted by brief flashes of recurring
imagery, and things such as his car cigarette lighter take on a menacing air. A mysterious
series of post-it notes appear on his refrigerator, depicting a game of hangman.

These vague incidents send him further into paranoia, but he nonetheless attempts to
establish a relationship with Maria. Meeting her at an amusement park, Trevor goes with her
son Nicholas on a fun house ride called "Route 666," whose flashing lights cause Nicholas to
suffer an epileptic seizure. No longer able to think clearly, Trevor suspects that the bizarre
events are a concerted effort to drive him insane. These ideas are fed to him in small
random clues. One of them is a picture of Ivan fishing with Trevor's coworker Reynolds,
which he discovers in Ivan's wallet when Ivan leaves it unattended in a pub. Another
near-accident at work causes Trevor to lash out in rage at his co-workers; as a result, he is
immediately fired. Increasingly distracted and alienated, Trevor forgets to pay his utility bills
and his electricity is disconnected. A dark, viscous liquid begins trickling out of the freezer,
coating the refrigerator door with streaks of what appears to be blood.

After several attempts to confront Ivan, Trevor tries to trace his license plate. He follows
Ivan's car to read its license plate, but runs out of gas during the pursuit. When a DMV clerk
insists that personal information cannot be released unless a crime has been committed,
Trevor throws himself in front of a car in order to accuse Ivan of committing a hit and run. He
files a police report with Ivan's plate number on it, only to be baffled when he is told that the
car in question is his own; he had reported the vehicle totaled one year ago. He flees from
the suspicious policemen and goes to Stevie, who clothes and washes him, but he finds the
photo of Ivan and Reynolds framed in her home and accuses her of conspiring against him.
Confused, Stevie says the picture is of Reynolds and Trevor, but he refuses to look at it and
is thrown out after a verbal conflict. He goes to the airport diner, but is told by an unfamiliar
waitress they've never had an employee named Maria. The waitress at the counter tells
Trevor she has served him every day for a year, and in all that time he spoke so little that
she began to think he was a mute.

Trevor sees Ivan take Nicholas into Trevor's apartment and, fearing the worst, sneaks inside.
Nicholas is nowhere to be seen and doesn't respond to Trevor's calls. He confronts Ivan in
the bathroom and kills him after a struggle. He pulls back the shower curtain, only to find the
bathtub empty. He goes to the refrigerator and opens it to find rotting fish and other spoiled
food tumble out. His mind then flashes back to the fishing photo, which actually shows a
healthy Trevor with Reynolds, just as Stevie claimed, and Trevor hallucinating Ivan in it. The
scene returns to one which occurred during the opening credits, in which he tries to dispose
of someone's corpse, presumably Ivan's, by rolling it in a rug and casting it into the ocean.
When the rug unravels, there is nothing inside. Ivan, alive as ever, appears holding a
flashlight and laughs.

Trevor stares into a mirror at home, repeating the words, "I know who you are." It is revealed
that one year prior, Trevor ran over and killed a boy identical to Nicholas after taking his
eyes off the road to use the car's cigarette lighter, which was witnessed by the boy's mother,
identical to Maria. He decided to drive away, and the resulting guilt became the deep-seated
cause of his insomnia, emaciation and repressed memory. Ivan was a figment of Trevor's
imagination and a manifestation of himself before the accident. He fills the missing letters of
the hangman note to spell "killer." He briefly considers going to the airport and escaping, but
instead drives to police headquarters, signifying his "road to salvation," a recurring theme in
the film. He is accompanied by a silent but encouraging Ivan, who bids him an approving
farewell outside the station. At the police station's front desk, he confesses to the hit and run.
Two police officers escort Trevor to a cell, where he states he wishes to sleep and does so
for the first time in a year..

movies cast:
Christian Bale as Trevor Reznik
Jennifer Jason Leigh as Stevie
John Sharian as Ivan
Aitana Sánchez-Gijón as Maria
Michael Ironside as Miller
Lawrence Gilliard, Jr. as Jackson (as Larry Gilliard)
Reg E. Cathey as Jones
Anna Massey as Mrs. Shrike
Matthew Romero as Nicholas
Robert Long as Supervisor Furman
Colin Stinton as Inspector Rogers
Craig Stevenson as Tucker

neurobiological basis of ptsd:

Amygdala-prefrontal cortex model in the pathophysiology of posttraumatic stress disorder

Posttraumatic stress disorder is an anxiety disorder that develops following exposure to a

traumatic event. Events that precipitate PTSD include terrifying or life-threatening situations
such as sexual assault and natural disasters. The disorder is characterized by a reaction of
intense fear, helplessness, or horror when the individual experiences, testifies about, or is
faced with one or more events that involve death, severe wounds, or a threat to one's own or
another's physical integrity. The symptoms include reexperiencing the traumatic event,
avoidance of trauma-related situations, blunted affect (emotional numbness), and
hyperarousal
Posttraumatic stress disorder is one psychiatric condition in which disruption of amygdala
inhibition through prefrontal structures has been proposed to explain the pathophysiology of
the disorder. Studies that investigated negative emotional processing in PTSD patients
demonstrated hypoactivation of the mPFC but hyperactivation of the amygdala . Thus, the
PFC-amygdala dysfunction model comprises two main elements: (i) the emotional distress
that characterizes PTSD arises from amygdala hyperactivity and (ii) amygdala
hyperactivation is caused by defective inhibition from a hypoactive mPFC .

The role of the amygdala in this model is supported by animal studies that emphasized its
implication in memory consolidation. The amygdala modulates memory consolidation with
the storage of emotionally relevant information and plays a critical role in fear and anxiety.
For example, neuronal morphology and neurotransmitter content in the amygdala in rats
exposed to a single prolonged stressor as an animal model for human PTSD has been
investigated Changes in morphology (i.e., an increase in dendritic arborization of pyramidal
neurons in the basolateral amygdala) induced by a single prolonged stressor were mediated
through enhanced neuropeptide Y function. The authors suggested that this structural
plasticity in the amygdala may provide a cellular and molecular basis of psychiatric disorders
such as PTSD.

In neuroimaging and lesion studies in humans, mPFC-mediated inhibition of the amygdala

has been suggested to be a neural mechanism involved in the extinction of fear conditioning.
This is relevant because PTSD symptomatology has been linked to a defect in fear
extinction processes Posttraumatic stress disorder can be seen as a failure in the trauma
recovery process (Yehuda & LeDoux, 2007). The disorder may also result from an enhanced
association between a traumatic event (unconditioned stimulus) and the environment
(conditioned stimulus), such as that seen in aversive conditioning . In fact, studies that used
the aversive conditioning model in patients diagnosed with PTSD found an enhanced
response, indexed by heart rate and skin conductance, during the phases of fear
conditioning and extinction

The neural correlates of fear conditioning and extinction processes in patients with PTSD
were investigated by Bremner et al. using positron emission tomography. Women who were
sexually abused during childhood and subsequently diagnosed with PTSD performed a task
in which the conditioned and unconditioned stimuli were a blue square and electric shock,
respectively. Compared with the control group (i.e., women with no history of sexual abuse),
women with PTSD exhibited increased activation of the amygdala during the acquisition
phase of conditioning, whereas during the extinction phase, a decrease was found in ACC
activity Milad et al. investigated whether the extinction of fear responses is impaired in PTSD
and whether such impairment is related to dysfunctional activation of brain regions known to
be involved in fear extinction. In the PTSD group, greater amygdala activation was observed
during extinction learning, with lesser activation of the vmPFC during extinction recall.
Moreover, the magnitude of extinction across all subjects correlated with vmPFC activation
during extinction recall testing, supporting the hypothesis that fear extinction is impaired in
PTSD.
As described in the following sections, other studies have also observed changes in brain
responses in PTSD patients using diverse trauma- and non trauma-related stimuli.
Brain processing of trauma-related stimuli assessed by script-driven imagery paradigms

The advantage of using stimulation related to the trauma is the possibility of inducing and
reproducing PTSD symptoms in the laboratory, which allows the processing of the traumatic
event to be directly investigated. The best established paradigm for this approach is the
script-driven imagery in which the participants are instructed to carefully listen to a script
specifically related to their trauma and imagine the event as vividly as possible.

Based on this approach, conducted a study on PTSD patients using positron emission
tomography. Increased activation was found in the amygdala, rostral anterior cingulate
cortex, and other paralimbic regions when participants listened to the traumatic script
compared with the neutral script. Shin used a similar methodology and found that patients
with PTSD had increased activity in the orbitofrontal cortex compared with controls (i.e.,
participants with a history of trauma but not diagnosed with PTSD). Moreover, the PTSD
group exhibited decreased activation of the ACC and prefrontal regions in general.
Interestingly, decreased activity in the left inferior frontal gyrus was observed only in PTSD
patients during exposure to the traumatic script, thus suggesting a change in prefrontal
region function and supporting the model of PFC-amygdala dysfunction in PTSD.
Based on this approach, conducted a study on PTSD patients using positron emission
tomography. Increased activation was found in the amygdala, rostral anterior cingulate
cortex, and other paralimbic regions when participants listened to the traumatic script
compared with the neutral script.i
used a similar methodology and found that patients with PTSD had increased activity in the
orbitofrontal cortex compared with controls (i.e., participants with a history of trauma but not
diagnosed with PTSD). Moreover, the PTSD group exhibited decreased activation of the
ACC and prefrontal regions in general. Interestingly, decreased activity in the left inferior
frontal gyrus was observed only in PTSD patients during exposure to the traumatic script,
thus suggesting a change in prefrontal region function and supporting the model of
PFC-amygdala dysfunction in PTSD.

The same group of researchers studied Vietnam veterans and army nurses with and without
a diagnosis of PTSD In the PTSD group, decreased activity of the medial frontal gyrus was
found during exposure to a traumatic script compared with a neutral script. An increase in
amygdala activity was also observed exclusively in the group of veterans who suffered from
PTSD. Notably, both veterans and nurses exhibited an inverse correlation between the
activity levels of the medial frontal gyrus and amygdala. Additionally, symptom severity was
found to positively and negatively correlated with amygdala and medial frontal gyrus activity,
respectively. These findings strongly suggest that PTSD symptoms may be related to
PFC-amygdala circuit dysfunction.
However, some evidence contradicts the PFC-amygdala dysfunction model. Using the
script-driven imagery paradigm, conducted an analysis of connectivity to investigate the
pattern of brain activation in subjects with a history of work or motor vehicle accidents, half of
whom were diagnosed with PTSD. This type of analysis allows one to observe the
relationships between the activation patterns of different cerebral areas, which might indicate
functional connectivity. Such analyses showed a positive relationship between amygdala
activity and the activity of other structures, such as the ACC and sub-callous gyrus, in PTSD
subjects. Because no expected pattern was observed, the proposed model of amygdala
inhibitory circuits through prefrontal structures was not corroborated.

Some research has found peculiar result.studied a sample of war veterans with and without
PTSD and a group of subjects who never fought in wars (controls). In the comparison
between traumatic/stressful and neutral scripts, the three groups exhibited deactivation in
the mPFC but in different regions. Veterans with PTSD exhibited deactivation in the rostral
ACC (rACC), whereas those without PTSD and controls exhibited deactivation in the
vmPFC. With regard to the amygdala, the results were even more intriguing. No results were
found for the amygdala in the group of veterans with PTSD, whereas those without PTSD
(i.e., the resilient group) exhibited deactivation in this region (i.e., heightened response to the
neutral script). The control group, in contrast, exhibited amygdala activation. Additionally,
amygdala activity inversely correlated with the traumatic experience, which disagrees with
the hypothesis of amygdala hyperactivity in PTSD symptomatology.

Two fMRI studies provided relevant evidence that favors the model of a dysfunctional
PFC-amygdala circuit in PTSD. The first study showed a decrease in the activity of medial
prefrontal regions in PTSD subjects compared with controls (i.e., traumatized subjects
without a diagnosis of PTSD) when exposed to traumatic scripts . The second study
investigated whether nontraumatic autobiographic negative scripts produced the same
pattern of brain activity An activation pattern similar to that observed for trauma-related
script-driven imagery was found (i.e., decreased activation in the anterior cingulate gyrus in
PTSD patients compared with controls). studied brain activation patterns in police officers
with and without PTSD using single photon emission computed tomography. In the
comparison between traumatic and neutral scripts, reduced activation in the medial frontal
gyrus was observed in PTSD subjects compared with controls (i.e., police officers without
PTSD), supporting the PFC-amygdala dysfunction model.

Processing of trauma-related stimuli: other paradigms

In addition to script-driven imagery, other paradigms have been used to investigate the
neurobiology of PTSD. These paradigms include other trauma-related stimuli, such as
words, sounds, images, and even smells, that lead to the traumatic experience.

studied the processing of trauma-related words in individuals with PTSD using fMRI. The
work investigated the time course of amygdala activation in response to negative words
(general words and words related to the trauma). Initially, patients with PTSD had increased
activity in the left amygdala only during the processing of trauma-related words. The
response of the amygdala was found to positively correlate with the severity of PTSD
symptoms. These finding also lend support to the hypothesis of PFC-amygdala circuit
dysfunction in PTSD.
investigated the neural correlates of visualization and imagery of war-related pictures and
negative and neutral pictures in war veterans with and without PTSD. The group of veterans
with PTSD exhibited increased activity in the right amygdala and ventral anterior cingulate
gyrus while producing mental images related to combat. also investigated the processing of
images related and unrelated to war in veterans with and without PTSD. The pictures were
or were not presented subliminally. Interestingly, amygdala activation was greater in PTSD
subjects than in controls, regardless of the picture content and level of consciousness at
which the picture was presented, suggesting general amygdala hyperactivity in PTSD.

conducted a study in which Iraqi and Afghanistan veterans were exposed to neutral and war
pictures intercalated with a cognitive task. This task consisted of pushing a key for
recognition of geometric shapes (circles and squares). During the visualization of
trauma-related pictures, a positive correlation was found between the severity of PTSD
symptoms and activation of the vmPFC, inferior frontal gyrus, and anterior cingulate gyrus.
Such a finding was interpreted as a greater prefrontal involvement in an attempt to regulate
affect. Additionally, a negative correlation was found between symptom severity and
activation in cognitive-processing areas (i.e., medial frontal and dorsal anterior cingulate
gyri) during the performance of the cognitive task, suggesting executive function impairment
in PTSD patients. This finding also suggests different patterns of brain activation in PTSD
depending on symptom severity and the type of processing system recruited.

Researchers have also employed sounds to investigate the neural circuits that underlie
PTSD . Three groups of volunteers (veterans with PTSD, veterans without PTSD, and
individuals who never fought in war) were exposed to war-related sounds (e.g., explosions,
helicopters, shootouts) and neutral sounds. The results showed activation in the ACC and
medial prefrontal gyrus in the three groups of subjects. However, increased activation in the
left amygdala was noted only in veterans with PTSD. Thus, although no specific decrease in
prefrontal activity had been identified, amygdala hyperactivity supported the model assessed
in the present article.
In studies that used similar methodologies,reported hyperactivation of the mPFC in response
to trauma-related sounds in war veterans with PTSD, providing contradictory evidence for
the present model. observed that exposure to sounds and images of war resulted in
decreased activity in the mPFC in veterans with PTSD. noted that veterans with PTSD
exhibited increased activity in the right amygdala and periaqueductal gray matter (PAG) in
response to war-related sounds compared with controls (i.e., neutral sounds), supporting the
validity of amygdala activity disruption.

Brain responses to olfactory cues have also been investigated in patients with PTSD. War
veterans with and without PTSD were exposed to odors that might be related to their trauma
(e.g., the smell of fuel), negative non trauma-related odors (e.g., hydrogen sulfide), positive
odors (e.g., vanilla), and neutral stimuli (e.g., odorless air). The study showed that veterans
with PTSD reported that the fuel smell was the most negative and stressful odor compared
with the control odors. The exposure to such an odor was related to increased activity in the
amygdala, insula, and ACC. A decrease in lateral PFC activity was also observed

Two studies that used trauma-related pictures and words reported hyperactivation of the
ACC in patients with PTSD. However, other studies reported increased activation in this
structure during the processing of trauma-related stimuli
Despite these various findings, the main result was decreased activity in medial prefrontal
areas (i.e., ACC) associated with increased activation of the amygdala during trauma-related
stimulus processing. However, some studies also found increased activation in prefrontal
structures including the ACC itself, thus leaving the issue open regarding which specific
prefrontal region plays a key role in the model of PFC-amygdala circuit dysfunction

Processing of nontrauma-related stimuli

Another approach usually used in PTSD neuroimaging studies is nontrauma-related

stimulation, in which emotional facial expressions are taken into account. This approach is
based on the idea that PTSD may be generally linked to changes in the processing of
emotional stimuli and not specifically to trauma-related stimuli. This view widens the
possibility that PTSD involves not only fear conditioning, which has indeed been debated in
the literature

With the aim of observing general fear processing in patients with PTSD, employed facial
expressions as nontrauma-related stimuli. Groups of individuals with and without PTSD were
instructed to pay attention to either neutral or fearful faces. Compared with the control group,
the PTSD group showed a reduction in the activity of the mPFC, particularly the right ACC,
during the visualization of fearful images. Nevertheless, no increase in amygdala activity was
observed . In a similar work that used fearful, neutral, and happy faces, studied firemen and
war veterans with and without PTSD. The group of PTSD subjects exhibited increased
activity in the amygdala and decreased activity in the mPFC in response to fearful faces
compared with happy faces. Additionally, a negative correlation was found between
amygdala and mPFC activity, supporting the idea of failure in the regulation of amygdala
activity in subjects with PTSD.

Although the pattern of prefrontal hyperactivity was previously described in facial expression
paradigms an earlier study reported no significant results for the PFC. These authors found
only an increase in amygdala activity in response to negative faces compared with positive
faces and a positive correlation between PTSD symptom severity and amygdala activity. The
fact that emotional faces were presented for only 33 ms (i.e., without the subject's conscious
awareness of their display) may have minimized the role of the mPFC, justifying the absence
of results regarding these high-order areas However, another work that used masked faces
in a shorter period of time (16.7 ms) found not only amygdala activation in response to
fearful faces but also activation of the mPFC

examined the amygdala response to the visualization of happy and fearful facial
expressions. The sample included individuals who had been recently traumatized and
presented acute PTSD. In the condition in which faces were masked, a positive correlation
was found between amygdala activity and PTSD severity during the visualization of fearful
faces, suggesting that changes in the amygdala may already appear before the
establishment of chronic PTSD itself.
The emotional Stroop test demonstrated decreased activity in the ACC in PTSD patients, a
finding that was not observed in the classic Stroop test (Stroop, 1935), which might indicate
specific cingulate cortex dysfunction for emotional stimuli in PTSD

Under resting conditions, Chung et al. (2006) found increased activity in the amygdala and
other limbic areas in addition to a decrease in the superior frontal gyrus in PTSD patients
compared with controls (i.e., no trauma). These results appear to reflect a generalized failure
in the ability to regulate emotions. Phan, Britton, Taylor, Figure, and , however, studied three
groups of subjects (i.e., veterans with PTSD, veterans without PTSD, and nonveterans
without PSTD) and found differences in the activation of amygdala and mPFC regions that
do not fit the model of amygdala hyperactivity and mPFC hypofunction. The paradigm
consisted of visualizing aversive, neutral, and blank pictures on the screen. Increased
activity in the dorsal area of the mPFC was observed in the three groups in response to the
negative images compared with the neutral images. Importantly, only the group of veterans
without PTSD exhibited activation in the vmPFC, a possible pathway for amygdala
downregulation. These findings indicate the need to identify more precisely the prefrontal
regions involved in emotional regulation.

In summary, studies of nontrauma-related stimuli have also provided various results, with a
predominant reduction in the activity of the mPFC and increased amygdala activation.
Altogether, these results suggest that the general processing of emotions is altered in
individuals with PTSD.

in conclusion​:
Classic studies on fear conditioning and extinction in animals have provided a basis for a
model of the brain circuits involved in anxiety disorders in humans, such as PTSD. The
fundamental hypothesis is that PTSD is characterized by hyperactivity of the amygdala with
concomitant failure in the top-down inhibitory control mediated by PFC regions. Notably,
however, PTSD, despite the similarity, is not restricted to Pavlovian conditioning. PTSD is a
condition with very characteristic symptoms of dissociation and revival, with not only an
enhanced reaction to fear but also a variety of other emotions such as blame, shame,
sadness, and anger . Several human neuroimaging studies noted that the most common
findings are actually hyperactivity of the amygdala and mainly a decrease in the activity of
mPFC structures, although some studies point in other directions.

addressed the hypothesis of enhanced activation of the amygdala in PTSD in which

responses to fear and anxiety were abolished after amygdala lesions. A first possibility is
that amygdala damage abolishes the development of PTSD among combat veterans and
supports the assertion that amygdala hyperactivity plays a causal role in the pathophysiology
of PTSD. A second possibility is that emotional memory enhancement observed in PTSD
relies on amygdala hyperactivity. A third possibility is that the role of the amygdala is related
to the function of the detection and evaluation of environmental cues, which may signal
threats. Such detection appears to be exaggerated in PTSD. Obviously, these hypotheses
are not mutually exclusive. An extensive lesion of the amygdala can impede the
development of PTSD by impairing the detection of threatening cues, impeding the
expression of fear and anxiety and altering the formation of emotional memories.
The role of the medial prefrontal regions in PTSD, such as the anterior cingulate and
ventromedial and orbitofrontal cortices, include various functions of complex and
interconnected structures. The most common proposition is that a hypoactive mPFC would
fail to regulate the responses of the amygdala, thus impairing fear extinction and the
mechanisms of emotional regulation also suggested the hypothesis that a hypoactive mPFC
can result from the chronic stress associated with PTSD or perhaps amygdala dysfunction.
The authors suggested that the role of the mPFC in PTSD may extend beyond amygdala
inhibition, possibly mediating the patients' subjective experience of trauma. A hypoactive
mPFC could lessen the subjective response to the traumatic experience by decreasing
emotional responses, such as blame and shame, and acting to protect against the trauma.
However, some studies of PTSD found a hyperactive mPFC, making the interpretation of the
role of this structure in this disorder difficult. Different mPFC nuclei might be related to
different functions involved in emotion generation and emotional regulation.

found dACC activation and ventral ACC deactivation, supporting the hypothesis that different
subdivisions of the ACC play differential roles in PTSD. Etkin and Wager (2007) mentioned
that the rACC might reflect resilience and emotional regulation mechanisms. Thus,
hypoactivity of this structure would reflect a failure of emotional regulation. The dACC, in
turn, would be related to emotional or conscious experience. Hypoactivation, therefore, could
be related to symptoms of emotional numbness and dissociation, whereas hyperactivation
could be related to increased negative subjective experience.

In conclusion, the diversity of findings may derive from the fact that PTSD is a syndrome with
a considerable heterogeneity of symptoms between individual patients. Some authors
suggested the existence of distinct PTSD subgroups with specific underlying
pathophysiology. In fact, a dissociative subtype of PTSD has been proposed (Lanius et al.,
2010) for the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, a
classification supported by clinical and neuroimaging evidence in which approximately 30%
of PTSD patients presented a preponderance of dissociative/avoidance symptoms instead of
hyperarousal/intrusive symptoms. Grouping patients with different peritraumatic responses
may be another of the factors that impede the full knowledge of this disorder, rendering
contradictory findings on the PFC. Individuals with different peritraumatic reactions may also
have differences in their fear circuitry. Additionally, different paradigms can show not only
opposite results but also different technical approaches. Some inconsistencies in the
findings may be attributable to the use of different contrasts, for example. Another factor
might be the small sample size used by several studies, leading to less accurate results and
poor interpretations.
stated that the inconsistencies observed in the results of studies on anxiety disorders
highlight the importance of addressing the neurobiological heterogeneity within psychiatric
diagnoses. This aim can be achieved through the application of genetic, neuroimaging, and
neurochemical approaches that can refine anxiety disorder phenotypes and elucidate the
genotypes associated with these disorders. The complex influence of factors that mediate
risk and resilience in the development of PTSD and other stress-related psychopathology
was discussed in a recent review Biological factors such as genotype and neurobiology
appear to interact with environmental factors such as childhood background and trauma
load, affecting the pattern of reactivity and recovery in the aftermath of trauma exposure.

Nonetheless, amygdala and prefrontal structures exhibit distinct patterns in PTSD, thus
supporting the model of a dysfunctional circuit (see table 1). Importantly, other structures are
also frequently found to have altered activity in patients with PTSD, such as the
hippocampus and visual cortex . Neuroimaging studies have unquestionably allowed us to
deepen our knowledge of the structural and physiological changes observed in patients with
PTSD. Nevertheless, further studies are needed to better understand the neural correlates of
such a complex and diverse disorder

insomnia​.
Insomnia is a sleep disorder that is characterized by difficulty falling and/or staying asleep.
People with insomnia have one or more of the following symptoms:

Difficulty falling asleep

Waking up often during the night and having trouble going back to sleep
Waking up too early in the morning
Feeling tired upon waking
Insomnia is a sleep disorder that is characterized by difficulty falling and/or staying asleep.
People with insomnia have one or more of the following symptoms:

Difficulty falling asleep

Waking up often during the night and having trouble going back to sleep
Waking up too early in the morning
Feeling tired upon waking
Types of Insomnia
There are two types of insomnia: primary insomnia and secondary insomnia.

Primary insomnia: Primary insomnia means that a person is having sleep problems that are
not directly associated with any other health condition or problem.
Secondary insomnia: Secondary insomnia means that a person is having sleep problems
because of something else, such as a health condition (like asthma, depression, arthritis,
cancer, or heartburn); pain; medication they are taking; or a substance they are using (like
alcohol).

Acute vs. Chronic Insomnia

Insomnia also varies in how long it lasts and how often it occurs. It can be short-term (acute
insomnia) or can last a long time (chronic insomnia). It can also come and go, with periods of
time when a person has no sleep problems. Acute insomnia can last from one night to a few
weeks. Insomnia is called chronic when a person has insomnia at least three nights a week
for three months or longer
Causes of chronic insomnia include:

Depression and/or anxiety

Chronic stress
Pain or discomfort at night and ptsd

Neuroimaging Measures of Insomnia

To date two brain activity studies that evaluatesleep in patients with insomnia have been
under-taken: one using TC-99HMPAO single-photonemission CT (SPECT) and one using
fluorodeoxy-glucose positron emission tomography (PET).Inthe SPECT study, imaging was
conducted aroundthe sleep-onset interval in patients with primaryinsomnia and good sleeper
subjects.Contrary toexpectation,patients with insomnia exhibiteda consistent pattern of
reduced activity acrosseight preselected regions of interest, with themost prominent effect
observed in the basalganglia.61The frontal medial, occipital, and pari-etal cortices also
showed significant decreasesin blood flow compared with good sleepers.Inthe PET study,
imaging data were acquired frompatientswithchronicinsomniaandcontrolsubjects for an
interval during wakefulness
andduringconsolidatedNREM.Patientswithinsomniaexhibitedincreasedglobalcerebralglucose
metabolismduringwakefulnessandNREM sleep.62In addition, it was found thatpatients with
insomnia exhibited smaller declinesin relative glucose metabolism from wakefulnessto sleep
in wake-promoting regions includingtheascendingreticularactivatingsy
hypothalamus, and thalamus.A smaller decreasewas also observed in areas associated with
cogni-tion and emotion including the amygdala,
hippo-campus,insularcortex,andintheanteriorcingulate and medial prefrontal cortices.In
addition to the brain activity studies, there isone study by Winkelman and
colleagues,63usingproton MR spectroscopy, which assess brainGABA levels in 16 patients
with primary insomniaas compared with 16 good sleeper subjects.GABA was measured in
terms of global activitywithinthebasalganglia;thalamus;andthetemporal, parietal, and occipital
cortical areas.Average brain GABA levels were found to be nearly30% lower in patients with
primary insomnia.Given that GABA is the primary inhibitory neuro-transmitter in the brain,
this suggests that therewas less inhibition (ie, more activation) in the insomnia
group.Further, GABA levels were nega-tively correlated with wake after sleep-onset
measures.These data suggest that GABA defi-ciency may be a neurobiologic characteristic
of insomnia and the efficacy of benzodiazepines hypnotics may reside in their potential to
increaseGABA secretion and activity within the brain.

IN INSOMNIAN europhysiologic Measures of Insomnia

To date, there are several studies that have shown that patients with primary insomnia
exhibit more cortical arousal than either good sleepers

specifically, these studies show that patients with primary insomnia exhibit more
high-frequency EEG activity (beta and gamma frequencies) at sleep onset and during
NREMsleep.These EEG frequencies are associated with active mental information
processing during wakefulness,suggesting that patients with insomnia have a failure to
terminate mental processing while otherwise asleep.There is also evidence that patients with
sleep state mispercep-tion (ie, paradoxical insomnia) exhibit more betaEEG activity than
good sleepers or patients with primary insomnia,38and beta activity is
negativelyassociatedwiththeperceptionofsleepquality,39,40and positively associated with
thedegreeofsubjective-objectivediscrepancy.37Taken together, these data suggest that
cortical arousal may occur uniquely in association with primary insomnia (ie, one or more of
the types
ofprimaryinsomniaincludingpsychophysiologicinsomnia,paradoxicinsomnia,idiopathicinsomni
a, and so forth) and that this form of arousal may be associated with the tendency toward
sleep-state misperception.

line of treatment for ptsd

medication
Treatment of Established PTSD – Non-cognitive symptoms
Once the disorder is established, one could consider targeting the emotional response, i.e.,
the expression of fear or other non-cognitive symptoms associated with PTSD, such as
hyperarousal, or the cognitive processes associated with PTSD, such as retrieval of aversive
memories or extinction of fear-related memories. Of note, treatments that suppress
non-cognitive PTSD symptoms are the only currently approved pharmacotherapeutic
strategy.

SSRIs
Selective serotonin re-uptake inhibitors (SSRIs) have shown efficacy in reducing symptom
severity and in relapse prevention in PTSD patients ( although only approximately 60% of
patients respond to the treatment and only about 20 – 30% of patients will achieve full
remission
. However, a recent report from the Institute of Medicine concluded that current evidence to
determine efficacy of SSRIs is at best suggestive (Committee on Treatment of Posttraumatic
Stressand more recent guidelines on the treatment of PTSD question the use of SSRIs for
veterans with combat-related PTSD relative to their therapeutic benefit in patients with
non-combat-related PTSD Thus, while SSRIs can be considered relatively well tolerated and
safe, further studies with higher power are needed before conclusions can be drawn.
Moreover, SSRIs still suffer a number of shortcomings, including delayed onset of action,
partial response with residual symptoms, or non-response, and undesirable side effects
(e.g., loss of sexual drive, gastrointestinal effects, changes in body weight) which limits their
utility and indicates a major unmet medical need for novel treatment approaches in PTSD.

OTHER ANTIDEPRESSANT
Besides SSRIs, a number of other pharmacological approaches have been investigated in
the clinic for treating PTSD patients, including other antidepressants, adrenoceptor
antagonists, anticonvulsants, atypical antipsychotics and benzodiazepines (see Ravindran
and for a review). Antidepressant drugs include dual serotonin and noradrenaline re-uptake
inhibitors, such as venlafaxine ), tricyclic antidepressants such as amitriptyline Andrew
imipramine , monoamine oxidase inhibitors (MAOIs) like phenelzine reversible monoamine
oxidase A inhibitors (RIMAs) such as moclobemide as well as drugs with other mechanism
of action, like the 5-HT2A/2C antagonist/5-HT re-uptake inhibitor nefazodone (, the mixed
α2A/2C adrenoceptor antagonist/5-HT2A/2C/3 antagonist mirtazapine (land 5-HT re-uptake
enhancer/glutamate
There have also been attempts to normalize the noradrenergic hyperreactivity suggested to
underlay PTSD hyperarousal symptoms. Blockade of the α1 adrenoceptor with the α1
adrenoceptor antagonist prazosin has been reported to improve various PTSD symptoms,
but in particular sleep and ameliorate nightmares A recent comparison study of prazosin and
quetiapine for ameliorating night-time sleep disturbance indicates better overall tolerability of
prazosin Ligands acting at the α2 receptor have been less promising. Mirtazapine has
shown positive results in one study of PTSD which suggests that α2A/C adrenoceptor
blockade also has beneficial effects, although mirtazapine’s effects could of course also be
mediated via serotonergic mechanisms In this respect it is of note that mirtazapine increases
NE release in various brain areas via α2A autoreceptor blockade thereby facilitating α1
activity. Stimulation of presynaptic α2A autoreceptors with the α2A adrenoceptor agonist
guanfacine, which should lead to reduced noradrenaline release, on the other hand, failed to
reveal therapeutic benefit . However agonist activity at post-synaptic α2A receptors may
mask effects of presynaptic blockade of NE release, as guanfacine has potent agonist
activity at post-synaptic receptors . Non-selective β adrenoceptor blockade with propranolol
was ineffective when given to prevent the development of PTSD in a recent study by
although there is some resurgence of interest in using propranolol in conjunction with
therapy (see below). Thus, while there is some evidence that manipulations of noradrenergic
activity may have utility specifically for sleep disturbances, efficacy for overall symptom
reduction is not supported thus far.

ANTIPSYCHOTICS
Atypical antipsychotic drugs are largely used as adjunctive therapy to e.g. antidepressant
drugs in the treatment of PTSD. Only a limited number of randomized, double-blind,
placebo-controlled clinical trials have been reported with risperidone and olanzapine, leading
to mixed results (e.g., Butterfield et al.,

Thus, although there is evidence that pharmacological approaches using psychoactive drugs
that are currently in the clinic have some beneficial effects in PTSD, with the most
convincing data generated for antidepressant drugs, this evidence must be considered
mixed. Almost all of the drug classes examined for efficacy in PTSD suffer from a dearth of
adequately powered studies to support definitive conclusions either for or against efficacy.
Along these lines, the Committee on Treatment of Posttraumatic Stress concluded that for all
the drug classes mentioned above, the evidence is inadequate to determine efficacy in the
treatment of PTSD. Overall the field clearly requires more efficacious pharmacological
approaches to treat this disorder, as well as a more concentrated effort to adequately test
potential therapeutics in large randomized clinical trials

self review of the movie the machinist

merits
movie shows the journey of trevor reznik .if you are not aware of the movie and we have not
read about the movie so what movie is all about so we will not be able to guess exactly what
the movie is trying to tell us. this is the status of the director. that is Brad Anderson.till the
end we are not able to guess it is the hallucinations are because of the psychosis at a
sizofreniya or because of insomnia. but in the end we come to know that the guy and killed a
small boy with his speeding car that trauma is not allowing him to sleep well so that's why he
develops insomnia and because of the insomnia for one year he develops hallucinations. in
hallucinations he sees the dead boy but without face and a guy named ivan.
you also develops delusions that the guy who in accident lost his arm because the
negligence of Trevor is plotting the same with the trevor.the movie scenes and hallucination
are made such that we are also in the mindset of forever and we also believe that it is true
that the guy is trying to do the same with trevor.
before developing ptsd the character is shown to be with the healthy weight but after the
incident it has shown to to reduce weight significantly so every time which exercise weight
there are 1 to 2 pounds of less weight compared to last time this shows that that is a
significant amount of stress and non self care in the character is subconscious mind is
playing a game with him like in the end the guy ivan takes into his own house and never
believe that aiven is plotting to kill Trevor. that's why when when ever get to his house and
gets a chance he kills ivan.but when he is hallucination about dumping is body in water s.
there comes a guy with the torch and when the traveller looked sides is face the guy is same
ivan. at that moment travel comes to know hallucinations of this personality which is his own
unconscious. when travel talk talk to the guy ivan trevor ask him what to do then ivan says
he knows that. and driver goes to to police station and tell police about his committed crime
and he is convicted and taken to the present as he is now in present I can have a peaceful
sleep because close now it doesn't has to to bother about it is killed of committing a crime
because he is prison.
movie greatly poultries how exactly a person with ptsd she is the world and how real the aalu
solutions feel and what exactly is the body's condition when under extreme stress and how
emotionally engaging are the particular and oscillations and delusions.it is very difficult for
the person without ptsd to understand how exactly they have hallucination. with the help of
this movie we can understand the condition of the person with ptsd. the main cause of the
stress that is ptsd is is hidden from the audience for very long time but insomnia and
hallucinations are portrayed for a very long time
is relationship with the call girl was going peaceful but because of his hallucinations he
thought that ivan is the ex lover of the call girl and the call girl is with the friends with that
ivan and plotting to harm the trevor. trevor is also having hallucinations of meeting the
mother II of a dead child who he killed. he remembers how the mother looks sped over the
child. he saw his mother running towards the child and he was scared so that's why he ran
away from the spot to not get caught. movie greatly portrays that the image of the mother
and the child.trevor has as illusion that there is a waitress at an airport and almost every
evening he goes to that airport and he has a hallucination the same person is standing as a
waitress as of child mother and he is flirting with the waitress.when we see the last scene
where the mother was running towards the child we come to know that the waitress
hallucination was because of the image of this mother and he is not able to cope up with
stress that a mother has lost her child and that's why his mind builds up the image that he is
flirting or in the sense loving the mother by giving gracious tips and and going to their home
and spending the time like ok father and having intimate closeness with the the waitress.
according to me this shows that he is feeling the the guilt of hurting the mother with his love
towards that mother in the image of the waitress so he does not feel the guilt because he is
giving love to the woman. the accident it happened not because of the willingness of the
character but because of the negligence
demerits​ : movie could have been little long

references:​https://www.psychcongress.com/article/circuitry-fear-understanding-neurobiology-
ptsd

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1983-32882011000200004

https://www.verywellhealth.com/can-sleep-deprivation-cause-hallucinations-3014669

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6048360/

https://www.mayoclinic.org/diseases-conditions/post-traumatic-stress-disorder/symptoms-ca
uses/syc-20355967