INSOMNIA now elaborated by both cognitive and physiological models


is measured as a symptom as well as a disorder due to which standard definition
is hard to explain. Recently ,there have been significant advancement  in organization, evaluation and treatment of
insomnia to build more consensus on its definition and measurement.(Summers, Crisostomo et al. 2006)

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falling, initiating or maintaining a sleep is termed as insomnia.
Nonrestorative sleep that’s chronic or low quality sleep may be indicated as
insomnia.(Soldatos, Dikeos et al. 2000)

sleep characterized by difficulty initiating or staying a sleep is called
insomnia.(Roth 2007)


is considered to be a disorder of hyper arousal that is experienced during the complete
day. This hyper arousal might display itself as a state of hyper vigilance
during the day and difficulty in  initiating and keeping sleep at night.(Roth 2007)

arousal is now elaborated by both cognitive and physiological models of

cognitive model tells that fear, anxiety and contemplation about life stresses,
disturbs sleep, producing acute episodes of insomnia, mainly in initiating
sleep and going back to sleep after an awakening.(Roth 2007)

by it, a person commences to experience sleep problems, worry and thoughts
about life problems changes their direction and person starts worrying about
sleep itself and about the daytime consequences of not getting enough sleep.
this negative feeling effect the intellectual activity of a person and it is
increased if sleep related problem is sensed or a sleep deficit is felt.(Roth 2007)

model of the evaluation of insomnia tells that physiological or neuro-physiological
factors are the main factors of hyper arousal. Physiological arousal has been
examined through dimensions of the total body metabolic rate, heart rate
variability, neuro-endocrine measures, and functional Neuro-imaging. Oxygen
consumption may be used to measure the whole body metabolic recent
studies patients who were suffering from insomnia were compared with people
having healthy sleep cycle. It was observed that insomniac patients were
having   metabolic rates (calculated at intervals
across the 24-hour day) greater than the healthy controls. Heart rate
variability may provide a measure of arousal in that it is controlled by both
sympathetic and para-sympathetic nervous system activities. It is found in  36-hour study that compared to healthy normal
sleepers , average heart rates were increased and irregularity was decreased in
all phases of sleep in insomnia patients.(Roth 2007)

neuro-endocrine system may also plays a role in arousal as confirmed by chronic
activation of the stress response system. It is  revealed in many studies that in people having
 insomnia, free cortisol urinary
excretion was higher in  Urine  free cortisol levels is positively linked with
total time in which person remain awake, wake time after sleep onset and stage
1 sleep percentage are effected by  catechol
amines level in urine . When plasma level of cortisol and adrenocorticotropic
hormones (ACTH) have been measured in insomnia patients and healthy normal
sleepers. although the evidence is somewhat diverse, it is found that primary
insomniacs have higher levels of these compounds in their plasma, and the most
significant difference is seen in the evening and the first half of the night .urinary
and plasma measures of cortisol and ACTH suggest that the HPA (Hypothalamus,
Pituitary, and adrenal) axis is linked with the chronic disease of insomnia. (Roth 2007)

last, measurement of cerebral glucose metabolism through positron emission
tomography (PET) has been used (through it whole brain metabolism is measured
indirectly) in patients suffering from insomnia. When insomnia patient were
compared to the healthy persons it was seen that insomniac patient showed
higher metabolism of glucose in cerebral region during waking and non rapid eye
movement sleep. In addition to it, the patients suffering from insomnia established
minor reductions in relative metabolism from waking to non-REM sleep in the
wake-promoting regions of the brain. These result propose interacting neural
networks involved in the failure to fall asleep, which consist of a cognitive
system ,general arousal system, and an emotion-regulating system.(Roth 2007)


has been revealed in research over the past 30 years that two different but
interconnected processes control human sleep wake cycle, the circadian rhythm
control the sleep cycle in a way that after 24 hours person sleeps at the same time,
and the homeostatic or recovery process, where when we sleep less the drive to
sleep more increases. When person does not sleep about 16 hours then he feels
enough desire to sleep. If these two drives, circadian rhythm and homeostatic process
are in synchrony, and then sleeping will be initiated. on the other hand, there
is another factor which can overcome these two process , and this is the state
of physiological arousal, when someone is worry or  does physical or mental work near bed time
then state of physiological arousal is affected.(Wilson and Nutt 2014)


order to help in diagnosis of short-or long-term insomnia, it is very important
to take a sleep history, having a conversation with bed partner, if any
(pointers such as snoring or strange movements may point out other sleep
disorders), and make the patient to keep a sleep diary. And if patient bedtime
and rising time is  recorded with
qualitative score for time to fall sleep , amount of  awakening  during the sleep and feeling of being
refreshed  after the sleep in the morning
is crucial for evaluating ,scheming and monitoring treatment, and  the adequate timing and time-span of sleep
opportunity.(Wilson and Nutt 2014)

patient complains sometimes that they have deprived sleep, but their history shows
the problem is uncommon behaviors at night like heavy snoring, nightmares or
sleepwalking and pauses in breathing.  Patient
may have circadian rhythm problem if sleeps adequately but  not on proper time .if someone has sleep
habit  irregular  say, between 4 am  and noon and when try to go to sleep before
that timing because of important obligation 
like work and lectures  , so cannot
do it earlier than this time so patient is suffering from insomnia . It is
named as delayed sleep phase syndrome and demands a different approach of
treatment. It is very important to find whether the sleep is related with
another disorder.(Wilson and Nutt 2014)


purpose of treatment of insomnia is to lessen suffering and to get efficient
daytime job. The patient guided treatment should be preferred, should consider the
particular pattern of problem, like beginning of sleep or continuing asleep,
and evidence based treatment should be preferred. (Wilson and Nutt 2014)

a diagnosis has been completed, if it possible the cause which is speeding up
the problem should be taken care   and ameliorated. For example, if pain or depression
is cause of insomnia, then it should be efficiently treated. (Wilson and Nutt 2014)

is seen that fear of insomnia is common so patient should need clarification
and encouragement. Patient has to know that no serious harm will come to them
in short period. If they think , they are sleeping less than they need , and
they are also worry about  their
performance due to it  or they think they
are not fresh  because of lack of sleep ,
these things are itself a common cause of insomnia.(Wilson and Nutt 2014)

patients sleep habits are good and   they
activating cause to solve their problem, then hypnotic drug is suitable for
short term solution. The time to fall sleep is decreased, awakening is reduced
and sleeps efficiency and continuity is increased due hypnotic drug.

the patient has a chronic problem, then CBTI (cognitive behavioral therapy for
insomnia) is a psychological intervention designed for insomnia is first line
treatment for chronic problem. This is collective educational, behavioral and mental
therapies that lead to improvement of insomnia. (Wilson and Nutt 2014)

have been many researches of CBTI, this therapy cannot be blinded that is why it
is difficult to design a randomized controlled trial, and getting in touch with
professionals is hard to match with the comparator group. There have been numerous
randomized (but not blinded) studies of physiological in comparison to
pharmacological treatment, and a new research meta-analysis  it is found that when the treatment is going
on , it produces improvement similar to sleeping tablets and important
beneficial long-term effects is produced by it. It also tells studies that
short term pharmacotherapy does not produced long term  effects .(Wilson and Nutt 2014)

the basis of wide available evidence, nine reviews, the State of the Science
Statement and the National Institute of Health (NHS) found out that a CBT therapy
which is set of cognitive and behavioral therapy is as good as prescription medications
are for short-term treatment of chronic insomnia. In addition, it is seen that
beneficial effect of CBT lasts beyond the termination of active treatment in
contrast to medication. (Wilson and Nutt 2014)

the other hand, in |UK psychological therapy for insomnia is an issue that is
why this therapy may not be available, with a rare skilled therapist, and insomnia
is not a main concern for psychologist in the NHS. However, there are patients
who are not capable or reluctant to involve in these treatments, and as a
result drug treatments need to be considered.(Wilson and Nutt 2014)


are few aspects that is to be considered when drug is being prescribed are safety,
efficacy and duration of action. Some Other factors should be considered like
either  drug is effective on patient or
not, adverse drug reaction and history of patients  substance abuse and dependence .(Wilson and Nutt 2014)

drugs enhance the effects of the gamma-aminobutyric acid (GABA)
neurotransmitter at the GABA-A receptor. The state of excitability is regulated
by GABA in all brain areas and the predominantly of neuronal activity is
governed by the equilibrium between excitatory inputs and inhibitory GABAergic
activity. If the balance is heavier in favor of GABA then muscle relaxation, sedation,
amnesia, and ataxia shows up and nervousness and anxiety are reduced. The slightest
reduction of GABAergic activity excites restlessness, arousal, anxiety, insomnia
and exaggerated activity.(Wilson and Nutt 2014)

effectiveness of GABA is enhanced by benzodiazepines and also by the ‘Z’ drug;
zolpidem, zopiclone and Zaleplon, it act at a site on GABA-A receptor hence permit
GABAergic circuits to produce a great inhibitory effect. They have different
timing of action comparing the  pharmacokinetic properties of each and those
with a duration of action lasting longer than the night are accountable to cause
morning sedation, and that is why  patient should be warned   about
driving.(Wilson and Nutt 2014)

 Three Zs’- zopiclone, zolpidem and zaleplon
are the safest GABA-acting hypnotics currently available. These drugs have
half-lives sufficiently short to be free of remaining hangover in most
patients. The half-life of Zaleplon is so short, that if drug is taken at night
still it will be eliminated by the morning. (Wilson and Nutt 2014)

all drugs will help in dealing with insomnia, but zolpidem and zaleplon are not
as good as other drug (hypnotics) for maintain the sleep continuity at night. (Wilson and Nutt 2014)

drugs have less undesirable effect than older drugs, but it should be kept in mind
that the effects of hypnotic agents are increased by simultaneous alcohol.
Also, they are safest because all of the possible unsafe effects such as ataxia
happen during bedtime, but few people get up late at night like old people so it
may be problem for them. (Wilson and Nutt 2014)

and Z drugs interact and enhance sedation when interact with other sedative drug
and sometime it is risk to take it in combination. This is factual in case of alcohol
and have revealed a problem with clozapine.(Wilson and Nutt 2014)

interactions of benzodiazepines rely on their metabolic pathway. the largest
part of the drug  is metabolized in the
liver through the enzyme CYP450 3A4,so any drug which effects these enzyme ,if  co administered with  benzodiazepines will change its concentration
 .(Wilson and Nutt 2014)

mentioning interactions are with calcium-channel-blockers, it increases its
plasma level and carbamazepine  decreases
its concentration.(Wilson and Nutt 2014)

drugs are not indicated  such as chloral
hydrate , clomethiazole and barbiturates due to their very less therapeutic
ration  (the ratio of the maximum
tolerated dose to minimum effective dose) and its  abuse potential.(Wilson and Nutt 2014)

it is seen that short acting benzodiazepines are
very successful  , temazepam one of it
is  misused in UK   , so while prescribing it should be noticed
that patient is not having history of alcohol 
or drug abuse .(Wilson and Nutt 2014)