Medical Chronicle November/December 2013 | Page 36

PAIN

morning headaches that are
associated with other stigmata of
increased intracranial pressure such
as papilloedema, nausea and vomiting,
should be urgently investigated for a
space-occupying intracranial lesion.
Lower back pain is a major health
issue worldwide. Up to 50% of
patients with chronic low back
pain may have complaints of sleep
dysfunction.
Some physiological studies have
shown arousal disturbances in
patients with back pain. This, in turn,
can make patients feel worse during
the day, emphasising the vicious cycle
of pain-insomnia-pain.

Chronic lower back pain

Fibromyalgia causes chronic pain
and discomfort, often with multiple
tender points. Non-restorative sleep,
generalised body pains, fatigue as
well as cognitive and emotional
disturbances interfering with daily
activities are typical in this condition.

Fibromyalgia

challenging. In patients with pain
and insomnia, it may be worthwhile
to start with non-pharmacological
treatment.

NON-PHARMACOLOGICAL
TREATMENT

Cognitive behaviour treatment
(CBT): Has been shown to be of clear
value in patients with insomnia. In
CBT, patients’ incorrect beliefs and
attitudes about sleep are changed
and relaxation therapy and sleep
restriction (paradoxical approach
where the patient spends less time in
bed to increase sleep efficiency) as
well as stimulus control therapy and
temporal control measures (minimal
daytime napping, wake up at same
time) are used. Up to 70% of people
achieve sustained improvement
after CBT.

Arthritic disorders that interfere with
sleep commonly include osteoarthritis
and rheumatoid arthritis.
Osteoarthritis and ankylosing
spondylitis have been linked to light,
restless sleep, and in rheumatoid
arthritis, sleep disturbances are
common and are associated with
joint pain, depression and functional
disabilities.

Arthritis

Even when healthy, pain-free
individuals are purposefully
sleep deprived in studies, states
of hyperalgesia and reduced
pain thresholds develop. In
polysomnographic studies,
particularly the disruption of
slow-wave sleep has suggested a
relationship with pain sensitivity;
after three consecutive nights of
deprivation of slow-wave sleep,
almost one quarter of healthy
women had decreased mechanical
pain thresholds and an increased
inflammatory skin flare response
was, interestingly, also found. Specific
brain regions - the periaqueductal
gray is an area in the midbrain that
is known to modulate not only sleep
stages but also nociception, and the
thalamus is associated both with
arousal and processing of painful
stimuli to cortical structures.

Insomnia causing pain

APPROACH TO
TREATMENT

Many available pain medications can,
unfortunately, worsen sleep disorders,
and the commonly used hypnotics
have no analgesic effects. In addition,
depression and anxiety often also
co-exist, making treatment even more

PHARMACOLOGIC
TREATMENT

Many different classes of medications
have been used in the treatment of
insomnia and pain. In clinical practice,
opioids, sedative pain medications,
antidepressants and anticonvulsants
are often prescribed.
Analgesics: The non-steroidal
anti-inflammatory agents commonly
used to treat pain may interfere
with restorative sleep and alter
EEG appearance; aspirin and cyclooxigenase-2 inhibitors may depress
slow-wave sleep.
Opioids: The potential for
dependency and respiratory
depression are concerns, making
the careful evaluation of underlying
additional sleep disorders such as
obstructive sleep apnoea mandatory.
Studies have shown that tramadol
may also depress slow-wave sleep, and
opioids in general can fragment sleep
and also decrease REM sleep.

36 MEDICAL CHRONICLE NOVEMBER/DECEMBER 2013

Antidepressants: Antidepressants
such as the tricyclics and serotonin
and noradrenalin reuptake inhibitors
(SNRIs) are commonly used as
therapy in patients with chronic
pain. Evidence exists for their use
in conditions such as neuropathic
pain, fibromyalgia, low back pain and
headache.
Amitriptyline is known to cause
some sedation. In clinical studies,
it has been shown that it increases
total sleep time, decreases sleep
onset latency, increases slow-wave
sleep and suppresses REM sleep.
For this reason, it is often used in
clinical practice as a sleep-promoting
agent. Other antidepressants such
as mirtazapine also have sedative
properties.
SSRIs are of limited use in painful
conditions and most cause sleep
disturbance, especially early in the
treatment.
The newer SNRIs:
venlafaxine, duloxetine
have shown promise in
the treatment of painful
conditions. Duloxetine
increases REM latency
and duration, however,
amitriptyline proved
superior regarding
sleep disturbances in
fibromyalgia.
Anticonvulsants:
Several of the
antiepileptic medications
are used in patients
with chronic pain. Of the
older anticonvulsants,
carbamazepine is
effective in the treatment
of neuralgic conditions
such as trigeminal
neuralgia and gives an
improvement in sleep
continuity, an increase
in total sleep time, less
fragmentation and decreased REM
sleep, and increased slow-wave sleep.
Valproate/valproic acid is
commonly used for the prophylaxis of
migraine with good clinical efficacy
and causes minimal sleep changes in
normal individuals.
Pregabalin and gabapentin are
also used for treating neuropathic
disorders. It caused an increase
in slow-wave sleep and a minor
disruption in arousals and sleep
shifts, making it effective in sleep
disturbances related to pain but
somnolence may occur.

HYPNOTICS

Benzodiazepines: Have no analgesic
properties but have been used to
reduce the fear and anxiety often
found in patients with chronic
pain conditions. In addition,
benzodiazepines reduce sleep-onset
latency and wakefulness during the
night and increase sleep efficiency, but

they also potentiate CNS depression
with alcohol and other sedatives and
may cause respiratory depression.
Generally, the benzodiazepines
influence sleep architecture, have
the potential of development of
dependence and can cause unwanted
daytime somnolence.
Non-benzodiazepines: The
non-benzodiazepine hypnotics, the
‘Z-drugs’, have become popular for
the treatment of insomnia, having
minimal impact on sleep stages and
no REM sleep rebound. The risk for
adverse effects is less than with
the benzodiazepines, but memory
impairment and psychomotor
retardation may occur.
Zolpidem and zopiclone:
Decrease sleep-onset latency and
increase Stage 2 and slow-wave
sleep without causing tolerance or
rebound phenomena; controlledrelease formulations are available for
maintaining sleep, but these should
not be re-administered during the
night. It must be noted that short-term
treatment with benzodiazepine or
non-benzodiazepine hypnotics under
strict adherence to contraindications
is effective in treating insomnia in
most neurological conditions.
Melatonin: In a slow-release
form it has also shown benefit
in older patients with insomnia,
where it improved sleep
continuity and daytime wellbeing.
Antipsychotics: The older
neuroleptic medications
(phenothiazines) have both sedative
and analgesic properties. The
routine use of phenothiazines in
the management of chronic pain
is not advisable due to the serious
side effects such as extrapyramidal
effects, tardive dyskinesia,
anticholinergic effects and
orthostatic hypotension.
The atypical antipsychotics,
olanzapine and quetiapine, increased
sleep time and sleep efficiency in
studies.
Antihistamines: The
antihistamines have sedative
properties, and many are available
as over-the-counter medications
and used as sleep promoters.
Diphenhydramine has modest benefit
in mild insomnia, and promethazine
and hydroxyzine have also been
shown to have effects on sleep in
healthy volunteers, but have a long
half-life with probable daytime
sedation.
There are many medications that
have dual effects of sedation and
analgesia, but there are currently
no guidelines in the literature
on pain and insomnia and more
research in this important area is
needed.

Conclusion

References available on request.