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Nociceptive
considerations
in
treating
with
counterstrain
MARK BAILEY,
PhD
LORANE DICK,
DO
The
proprioceptive
mechanis-
tic
model
of
somatic
dysfunction
proposed
by
Korr
is
accepted
as
the
neurophysiolo-
gic
basis
of
counterstrain
by
the
developer
of
that
manipulative
technique.
We
sug-
gest
that
the
physician
should
also
take
into
account
the
physical
damage,
if
any,
that
the
original
trauma
produced.
We
pro-
pose
that
with
tissue
injury,
nociceptive
reflexes
could
produce
patterns
of
motion
restriction
opposite
that
predicted
by
a
solely
proprioceptive
model.
A
nociceptive
component
is
suggested
as
an
explanation
for
the
origin
and
maintenance
of
somatic
dysfunction
and
its
response
to
the
coun-
terstrain
technique.
In
actuality,
both
pro-
prioceptive
and
nociceptive
responses
may
occur
in
dysfunctional
states.
Other
physiologic
responses
also
may
be
in-
volved.
These
views
are
consistent
with
clinical
experience.
(Key
words:
Counterstrain,
osteo-
pathic
manipulative
treatment,
nocicep-
tive
reflexes,
somatic
dysfunction.)
Counterstrain
is
a
passive
,
positional-re-
lease
manipulative
technique, developed by
Lawrence
Jones.l
·
2
Counterstrain
techniques
place
somatic
systemic
elements
into
the
posi-
tion
of
greatest
perceived ease,
or
comfort, by
passively
approximating
the
attached
surfaces
of those elements. Osteopathic physicians have
demonstrated
time
and
again
that
counter-
strain
is
a clinically
valid
and
useful
entity.
However,
the
theoretical
physiologic mecha-
Dr
Bailey,
currently
a senior
student
at
the
College of
Osteopathic Medicine of
the
Pacific, Pomona,
Calif
, will
be
starting
a neurology residency
at
the
University of
Alabama
at
Birmingham.
Dr
Dick,
past
chairman
of
the
Department
of
Osteopathic Principles
and
Practice, Col-
lege
of
Osteopathic Medicine of the Pacific, is currently
in
private
practice
in
San
Dima
s,
Calif.
Reprint
requests to
Mark
Bailey, PhD, 2128 South-
wood Rd,
Jackson
, MS 39211.
334
•
JAOA
•
Vol
92 •
No
3 • March 1992
nism
by which
counterstrain
techniques ame-
liorate
somatic dysfunction
has
not
been ex-
plained
conclusively. (Somatic dysfunction is
defined
3
as
"Impaired
or
altered
function of
re-
lated
components of
the
somatic [body frame-
work] system: skeletal, arthrodial,
and
myofas-
cial
structures,
and
related
vascular,
lym-
phatic,
and
neural
elements."
Korr
4•5
has
de-
scribed a proprioceptive
mechanism
of somatic
dysfunction
that
Jones
2
accepts
as
underlying
counterstrain.
This
explanation
is compatible
with
personal clinical impressions of changes
observed
during
counterstrain
treatment
.
However,
it
seems
unlikely
that
propriocep-
tive
reflexes
represent
the
sole
element
in-
volved
in
how
counterstrain
works, a position
with
which
Korr
agrees (conversation, May
1989). Advances
in
physiologic knowledge of
the
proprioceptive functions
have
not
changed
Korr's concepts. These advances,
in
fact,
have
clarified
the
theoretical
basis for somatic dys-
function
and
explanations
for response to
ma-
nipulative
treatments
.
In
this paper, we (
1)
sug-
gest
an
updated
theoretical
basis for somatic
dysfunction involving nociceptive
stimuli,
and
(2)
examine
the
responses to counterstrain
treat-
ment.
Our
proposed theoretical role of nocicep-
tive
mechanisms
in
initiating
or
maintaining
somatic dysfunction (or both)
and
proposed ba-
sis for effects of
counterstrain
treatment
ex-
tend
the
concepts related to proprioceptive func-
tions. •
Basic
reflexes
First,
let
us
apply
Korr
's proprioceptive model
to a simple hinge-type joint,
the
elbow.
To
fa-
cilitate
the
discussion,
let
us
concern ourselves
with
only two
antagonistic
muscles
that
act
across
the
elbow joint:
the
lateral
head
of
the
triceps
brachii
muscle,
an
extensor of
the
fore-
arm
,
and
the
brachialis
muscle
, a
forearm
flexor
(Figure 1).
Now
let
us
assume
that
while
the
elbow is semiflexed, a weight is placed
in
(continued on page 337)
Brief
report
• Bailey
and
Dick
recommended starting dose
for
Calan
SR
Is
180
mg
once daily.
Dose
titration
will
be
required
in some patients
to
achieve
blOOd
pressure control. A
lower
Initial starting dosage
of
120
mg/day
may be warranted In some patients leg,
the
elderly, patients
of
small staturel. Dosages above
240
mg
daily should
be
administered in divided doses.
Calan
SR
should
be
administered
with
food
.
i
t01~st11patiion
.
whlcn
Is
easily
managed
In
most patients. Is tne most commonly reported side
effect
ot
talan
SR
.
i
Vetram1m11
snould
be
administered
cautiouSly
to
patients wltn Impaired
renal
function.
Please
see
references
and
brief summary
Of
prescribing InfOrmation
on
next
page
Of
tn
ls advertisement.
1992
Searle
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·
References:
1.
Data on file. Searle . 2. Edmonds D, Wurth
JP
, Baumgart P.
et
al.
Twenty-four-hour
monitoring
of
blood pressure during calcium antagonist
therapy.
tn
: Fleckenstein A, Laragh
SH
. eds.
Hypertension-the
Next Decade:
Verapamllln Focus. New York .
NY
: Churchill Livingstone; 1987:94-100 . 3.
Midtbl2l
KA.
Effects
of
tong-term verapamil therapy on serum lipids and
other
metabolic
parameters.
Am
J Card/of. 1990;
66:131-151.
4.
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her
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SUMMARY
Contraindications
:
Severe
LV
dysfun
c
tion
(see
Warnings)
,
hypotension
(systolic
pres
sure
<
90
mm
Hg)
or
cardiogenic
shock
,
sick
sinus
syndrome
(if
no
pacemaker
is
present)
,
2nd-
or
3rd-degree
AV
block
(if
no
pacemaker
is
present),
atrial
flutter/fibrillation
with
an
accessory
bypass
tract
(eg
,
WPW
or
LGL
syndromes).
hypersensitivity
to
verapa
m
il.
Warnings:
Verapamil
should
be
avo
ide
d
in
patients
wi
th
severe
LV
dysfunction
(eg,
ejection
fraction
<
30
%)
or
moderate
to
severe
symptoms
of
ca
rdia
c
failure
and
in
patients
with
any
degree
of
ventricular
dysfunct
ion
if
they
are
receiving
a
beta-blocker
.
Control
milder
heart
failure
with
optimum
digitalization
and
/
or
diuretics
before
Calan
SA
is
used
.
Verapamil
may
occasionally
produce
hypotension
.
Elevations
of
liver
enzymes
have
been
reported
.
Several
cases
have
been
demonstrated
to
be
produced
by
verapamil.
Periodic
monitoring
of
liver
funct
io
n
in
patients
on
verapamil
is
prudent.
Some
patients
with
paroxysmal
and/or
chronic
atrial
flutter
/
fibrillation
and
an
accessory
AV
pathway
(eg,
WPW
or
LGL
syndromes)
have
developed
an
increased
antegrade
co
nduct
io
n
across
the
accessory
pathway
bypassing
the
AV
node
,
producing
a
very
rap
id
ventricular
response
or
ventricular
fibrillation
after
receiving
I.V
.
verapamil
(o
r
digital
i
s)
.
Because
of
th
is
risk,
oral
verapamil
is
contraindicated
in
such
patients
.
AV
block
may
occur
(2nd-
and
3rd
-
degree
, 0.
8%)
.
Deve
lo
pment
of
marked
1st-degree
b
lock
or
progression
to
2nd-
or
3rd-
degree
block
requires
reduct
ion
in
dosage
or,
rarely
,
discontinuation
and
institution
of
appropriate
therapy
.
Sinus
bradycard
ia,
2nd-degree
AV
block
,
sinus
arrest,
pulmonary
edema
and
/
or
seve
re
hypotension
were
seen
in
some
critically
ill
patients
with
hypertrophic
cardiomyopathy
who
we
re
treated
with
verapamil.
Precautions
:
Verapamil
should
be
given
cautiously
to
patients
with
i
mpaired
hepatic
function
(in
severe
dysfun
c
tion
use
about
30%
of
the
normal
dose)
or
im
pa
ir
ed
renal
fun
ctio
n,
and
patients
should
be
monitored
for
abnormal
prolongation
of
the
PR
interval
or
other
si
gns
of
overdosage
.
Verapamil
may
decrease
neuromuscular
transmission
in
patients
with
Duchenne
's
muscular
dystrophy
and
may
prolong
reco
ve
ry
from
the
neuromuscular
blocking
agent
vecuronium
.
It
may
be
necessary
to
decrease
verapamil
dosage
in
pat
ients
with
attenuated
neuromuscular
transmis-
sion
.
Combined
therapy
wi
th
beta-adrenergic
blockers
and
verapamil
may
result
in
additive
negative
effects
on
heart
rate,
atr
ioventricul
ar
conduc
tion
and
/
or
cardiac
contractility
;
there
have
been
reports
of
excessive
bradycard
ia
and
AV
block
, i
ncluding
complete
heart
block
.
The
r
isks
of
such
combined
therapy
may
outweigh
the
benefits
.
Th
e
combination
shou
ld
be
used
only
with
caution
and
close
monitoring
.
Decreased
metoprolol
and
propranolo
l
clearance
may
occur
when
either
drug
is
adm
iniste
red
concomitantly
with
verapamil.
A
variable
effect
has
been
seen
with
combined
use
of
atenolol.
Chronic
verapamil
treatment
can
incre
ase
serum
d
igoxin
levels
by
50%
to
75
%
during
the
first
week
of
therapy
,
which
can
result
in
di
gitalis
toxicity
.
In
patients
with
hepatic
cirrhosis,
verapamil
may
reduce
total
body
cleara
n
ce
and
extrarenal
clearance
of
digitoxin
.
The
digoxin
dose
shou
ld
be
reduced
when
verapamil
is
given
,
and
the
patient
carefully
A92CA6507T
1a-n®
·
l
veraoami
l
HCIIW
SU
STA
IN
ED-RELEASE
CAPLETS
(
240:mg
)
For
the
many
faces
of
mild
hypertensio
n
et
al.
Antihypertensive and renal effects
of
enalapril and slow-release verapamil
in essential hypertension.
Eur
J
Clln
Pharmacal. 1990;39:<suppl 11:541-543.
s. Schmieder
RE
, Messerli
FH
, Garavaglia
GE
.
et
al.
cardiovascular effects
of
verapamil in patients
with
essential hypertension. Circulation. 1987;75
:1
030-
1036. 6. Midtbl2l K, Lauve o .
Hats
o.
No
metabolic side effects
of
tong-term
treatment
with
verapamil in hypertension. Angiology. 1988;39:1025-1029.
monitored
.
Verapamil
will
usually
hav
e
an
additive
effect
in
patients
receiving
blood
-
pressure
-
lowering
agents
.
Disopyramide
should
not
be
given
within
48
hours
before
or
24
hours
after
vera
pam
il
administration
.
Concomitant
use
of
fle
cainide
and
verapamil
may
have
additive
effects
on
myocard
ial
con
tra
ctility,
AV
conduction
,
and
repolar
i
zat
ion
.
Combined
verapamil
and
qu
inidine
therapy
in
patients
with
hypertroph
ic
cardio
myopath
y
should
be
avoided
,
since
significant
hypotension
may
result
.
Concomitant
use
of
lithium
and
verapamil
may
result
in
a
lower
i
ng
of
serum
lithium
levels
or
increased
sensitivity
to