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IN CONCLUSION | MOSKOVITZ
Comorbidities Decrease Resilience and
Increase Suffering
EVERY CLINICIAN KNOWS that patients are more likely to lack
resilience in the face of pain if they “suffer” from other emotions
or drive states. Pre-existing depression or any of the
hyper-arousal syndromes—obsessive compulsive disorder, generalized
anxiety, panic disorder, focal phobias, post-traumatic
stress disorder—will exacerbate the experience of pain, and any
of these impairments can be caused by the suffering of chronic
pain (12). Distinguishing cause from effect is difficult. When a
drive state alone causes suffering, it might be sufficient to
address the physiologic need: for example, rehydrate a person
suffering from thirst. This is seldom the case in medical practice,
least of all in pain management. Treating the disease
without addressing the suffering that it causes will not suffice.
A complete discussion of ethics and morality as they apply to
the role of the practitioner is not possible here. It is well presented
by Giordano in his work, cited earlier.
Suffering as Disequilibrium of
Frustrated Appetites and Emotions
ANOTHER WAY TO VIEW THE VARIETY of the precursors of suffering
is in terms of equilibrium and disequilibrium. I propose
that suffering is the result of disequilibrium in any form: dehydration
from thirst, starvation from hunger, shortness of breath,
the ennui of confinement, prolonged separation from a friend
or loved one. Although it is possible that each of these drive
states, alone, is sufficient to cause suffering, I propose that suffering
is mediated by fear and grief when the drive state is prolonged
or severe, not unlike the suffering when chronic pain
evokes fear or grief. We do not suffer from mild thirst; we simply
get a glass of water. Thirst that evokes bodily pain, exhaustion,
and fear of injury or death is another matter and thus a
cause of suffering.
PREMISE 4
The neural substrate for the experience of suffering
requires, in part, the anterior cingulate cortex.
A NUMBER OF OBSERVATIONS persuade me to think that the
anterior cingulate cortex (ACC) and its connectivities to the
posterior cingulate cortex, the ventromedial prefrontal cortex,
the amygdala, the hippocampus and the anterior insula, play an
important, if not central, role in the experience of suffering.
The central nervous system is not merely computational; yet, I
choose a useful, if not precise, analogy of the ACC as the
“CPU” that processes internal and external information that
results in the experience of suffering. The physiologic process
by which these structures, circuits, networks, and systems operate
to produce suffering is unknown. Neuroscientists use such
concepts as synergy, resonance, reverberation, synchrony, and
synchronous oscillation when trying to explain the hypothetical
mechanisms underlying suffering or certainty.
As a medical student, I was fascinated by a patient whose
midline brain tumor involving the ACC 7 produced a curious
insensitivity to pain. The young man felt pain after his surgery,
and reacted protectively to it, but it didn’t “bother” him. What
was thought to be a type of “insensitivity to pain” was, I now
propose, the elimination of the experience of suffering that
would be caused by pain in the presence of an intact ACC. I
propose that the patient’s experience was more than an inability
to “interpret” pain, as in “asymbolia” (13).
Anterior cingulotomy or prefrontal leucotomy relieves the
suffering of chronic pain without eliminating the pain itself.
Such neurosurgical procedures decrease pain behavior and disability
without eliminating nociception (14). Damasio reports
the experience of a man with intractable, totally disabling
trigeminal neuralgia and quotes his response the next day after
undergoing anterior, prefrontal leucotomy: “...the pains are the
same, but I feel fine now (4).”
Neuroimaging has validated the neural basis of semantic
and sensory parameters of pain that are assessed through the
McGill Pain Questionnaire (MPQ), almost 30 years after its
development by Ronald Melzack and Warren S. Torgerson (15,
16 ). Such findings further suggest the role of the ACC in the
experience of suffering. Scoring of the MPQ divides the list of
descriptive words for pain into distinct “sensory” and “affective”
pain rating indices. Neuroimaging of subjects with chronic
pain, when challenged with words from the sensory word list,
revealed activation of areas associated with processing of
somato-sensory nociception. When subjects heard words from
the affective word list, there was increased activity in the insula
and ACC (16, 17, 18). Melzack did not use the word “suffering”
in his extensive, statistical validation of the MPQ,
although I think that the word applies to the affective list. One
observation by Melzack illustrates how the prejudices of clinicians
affected pain assessment, then as now: “… patients are
pleased to see (or hear) words which they use to describe their
pain to family and friends but which they would not tell the
physician because he may consider them psychologically
unsound; the administrator thus often senses the patient’s relief
at seeing such words in a list, implying that they are acceptable
and sound descriptors” (19). Those “taboo” words were ones
that describe suffering (splitting, exhausting, cruel, frightful,
excruciating, etc.), as opposed to the sensory words (burning,
stabbing, throbbing, pressing, stinging, etc.).
7 The famous neurologist Houston Merritt made the diagnosis—
without CT or MRI.
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