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5 Tyrer P,
Rutherford
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propranolol.
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1981;i:520-2.
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Dawling S. Gradual
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1983;i:
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Gunderson JG, Singer
MT.
Defining borderline patients:
an overview.
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Tyrer P,
Alexander
J.
Classification
of
personality
disorder.
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163-7.
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Casey P, Gall J. The relationship between
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1988;ii:
235-40.
Boxing
and
the brain
J
A N
Corsellis
The
American
pathologist
Martland wrote a paper
entitled "Punch
drunk"
in 1928, in
which
he drew
attention for
the
first time
to a
"peculiar
condition
among
prize fighters."
"Many
cases
remain
mild,
but
in
severe cases," he wrote, "there may develop a
peculiar
tilting
of
the
head,
a marked
dragging
of
one
or
both legs,
a
staggering, propulsive gait with the
facial characteristics of
the
parkinsonian
syndrome, or
a
backward
swaying of
the
body,
tremors, vertigo,
or
deafness. Finally,
marked
mental
deterioration
may
set in
necessitating
commitment
to an
asylum."
Such
changes,
even
when
mild,
are now rarer.
Control of the
sport,
while
varying
greatly
from
country
to
country,
has
been
considerably tightened
up,
and
the authorities
in
the United
Kingdom
have
worked hard
to
minimise
the
dangers. Nevertheless,
hitting
people
on
the
head
must
always
carry
some
risk
to
the
brain,
and
as
long
as
the
sport
is
encouraged
as a
noble
activity
by
some
its existence is bound
to
be
questioned by
others.
Two
forms
of
damage
may
occur.
Firstly,
there is
the
remote
risk
ot
death
in
the
ring
or
within
a
few
days
after
the
fight-a
catastrophe
usually
caused
by
bleed-
ing
inside
the
head.2
This risk
in
boxing
seems
to
be no
greater
than that
in
other
sports,
although
accurate
mortality figures
do
not
exist.3
Indeed, McCunney
and
Russo
found
that
the threat
to
life
was less than that
in
sports
ranging
from
college
football
and horse
racing
to
hang gliding
and
scuba
diving.4
Sammons, however,
uncovered
a
greater
risk
to
American
boxers
during
the
1970s.5
Secondly, and perhaps more
importantly,
there is the
risk
of
unremitting
disease
in those who
survive a
career
in
boxing, and it is
this
kind of
damage
that
is least
discussed.
Repeated sublethal blows to
the
head,
whether
or not they cause a
knockout,
may lead
to
insidious
changes that
may
underlie
the punch
drunk state'
or
Millspaugh's
dementia pugilistica.6
The many
neurological facets
of the
punch
drunk state
have been
reported
by neurologists
in
the United
Kingdom7-"
and,
more
recently, the United
States.3
12
The
pathological
aspects,
however,
have been
less
often
studied.
Perhaps
an
element
of
serendipity
enters
into the
supply
of
brains of former
boxers,
for most
studies
have been based on the
microscopical
exam-
ination
of
a
single
or a
few
brains.
The
pathological
focus
has
consequently
tended
to
fall
on one
or
other
kind
of change
to
the detriment
of any more com-
prehensive
pattern that
might
underlie
the
features of
"punch drunkenness."
The
ethical criticisms of
boxing
have
been
smoulder-
ing
in
Britain for
some
years. In 1956
Edith Summer-
skill
published
a
polemic
entitled The Ignoble Art,
in
which
she
warned
of
the
dangers
to
the
brain and
eye. 3
In 1964 a
symposium
on the medical
aspects
of
boxing
was
held in
London,
when
the
arguments
were
outspoken
but
inconclusive.
14
Neuropathology
was
scarcely touched
on, and
by
the end
most
lay
experts
and some doctors
cast
doubt,
and
even
scorn,
on
the
14
JANUARY
1989
idea that
the brain could be at
risk in
such
a
worthy
and
enjoyable
sport.
Four
years later, before
his
clinical
assessment of
over
200 former boxers,
Roberts wrote
that
"there has been
no
specific
pathological evidence
to
confirm
the
assumption
that boxing
is
causally
related
to the
clinical
syndrome
described."'"
Saffron
Walden,
Essex
CB1O
IBY
J
A
N Corsellis, FRCPSYCH,
emeritus
professor of
neuropathology
BrMedJ
1989;298:
105-9
Neuropathological
observations
In
his
prescient
way
Martland noted
that
"the
late
manifestations of punch drunk
will be
seen
chiefly
in
the
neurologic
clinics
and asylums and
such
material
will
practically
fall
to
the
neuropathologist connected
with
such institutions."'
Cases
did
begin
to
become
available-in
1957-to
the
neuropathological
depart-
ments
of
Runwell
Psychiatric Hospital,
Essex, and
the
Institute
of
Psychiatry
in
London.
The
findings
added
weight
to
the
critical view
of
Summerskill,'3 although
the
original
project
had
begun
merely
as a
clinical
and
pathological
inquiry
into
the
late effects
on
movement,
memory,
and mental
state
of
repeated
blows
to
the
heads
of
15
men,
all
of
whom
had
boxed
in
their
youth.'5
The pros and
cons
of
the sport
became
of
interest only
after
the
findings had
been
analysed.
These
findings
were
often
complex,
and
they
varied
in
severity;
in
one
case
no
neurological
damage
was
found.
Four
main
sites
of
change
were
described.
Septal
regions-The
most
obvious
abnormality,
seen
in
11
of
13 cases,
was
centred
on
the
deep
mid-
line
structures. The septa
were
wide
apart, torn,
and
fenestrated, and often
only
tags
survived.
The
ventricles
were
enlarged
and the
fornices
atrophied.
Spillane
had first
illustrated
these
anomalies
by
air
encephalography.'
On
microscopy
the tissue
in
this
area,
including
the thalamus and
hypothalamus,'6
showed
severe
gliosis
partially
reminiscent of
the
Wernicke-Korsakoff
syndrome.
Cerebellum
and substantia
nigra-Perhaps
the
most
striking clinical
features
of
punch
drunkenness lie
in
the
disordered
movement,
summarised
by Roberts
as
forming
"a
relatively
stereotyped
pattern.
At
its
mildest,
this
consisted
of
dysarthria
with
or
without
disequilibrium
and
spasticity,
or
rigidity
and
striatal
tremor
associated
with
varying
degrees of
dementia.
All
grades
of
disturbed
neurological
function
in
cere-
bellar,
pyramidal and
extra-pyramidal
systems
were
apparent
between these
extremes."'"
The
motor
path-
ways
in
the
cerebellum and
the
substantia
nigra
were
affected.
In
the
cerebellum atrophy
and
glial
fibrosis
affected
those
folia
that
were
encircled by
the foramen
magnum.
In
addition
there
was
a
pronounced
loss
of
Purkinje
cells
(confirmed
by
cell
counts)
in the undersurface of
the cerebellum.
In
the
substantia
nigra
the
most
obvious lesion, often
apparent
to
the naked
eye, was
the
lack
of
the
large
pigmented
neurones, which
is the
clas-
sical
neuropathological
feature
of
a
parkinsonian
state.
Neurones-The
most inexplicable
alteration
in
the
105
BMJ
VOLUME
298
Normal
septum.
No
cavum;
fornix
and thalamus normal
Died
in
ring
during
third
fight.
Normal
septum;
no
cavum
or
tears.
Former
champion.
Anterior view:
large
caval
remnant
and
septal
tags.
Posterior
view:
flattened
fornix,
detached sheet
Cavum,
fragmented
septum, shredded
strands
Anterior
view:
normal
septum
Posterior
view:
septum
lost;
flattened fornix
Wide
cavum,
torn
walls;
enlarged
anterior horns
Anterior
view:
wide
cavum
torn
septa.
Posterior
view:
thin
sheet
of fornix
detached
1
mm
Former
world
champion.
Large
vents,
no
cavum,
only
remnant
of
septal
tags
Anterior
view:
cavum.
Posterior view:
flattened
fornix
floor
of
hypothlanrrius
thin
and
stretched
Anterior
and
posterior
vtews
(left)
and
antenior/middle
viezv
(right)
of
a
normal brain and
brains
of
nine
former
boxersfixed
in
formalin.
The
importance of
the
septal
cava
has
been
reported
previously's
Septal
tags,
cavum;
pathological
appearance
of
the
brain of
a
boxer,
first
found
by
Constantinidis
and
Tissot,7
is
a
bizarre
tendency
for
many
neurones,
mainly
in
the
deep
temporal
grey matter,
to
develop
abnormal
neurofibrils
(the
so
called
Alzheimer
tangle)
without
neuritic
(senile) plaques. Tangles
and
plaques
are
common,
particularly
in the
elderly
and the
demented;
tangles
without
neuritic
plaques
are
rare.
Why
these
two
structures
should
develop
in
any
condition
is
unknown.
These
abnormalities,
within
a
general
trend
to
cerebral
atrophy,
together
form
a
pattern
that
has
not
been
described
in
any
other
condition.
Indeed,
this
BMJ
VOLUME
106
298
14
JANUARY
1989
combination ofabnormalities
seems to be
characteristic
of
people
who have
had blows
to the head
delivered
over
a
period
of
years.
Three other-changes
have
also
been
found. Firstly,
a
trend
to
excessive
meningeal
and
subpial
siderosis
was
reported.
8
Secondly,
Lampert
and
Hardman,"9
extending
the work of
Strich
on
dementia
after
injury
to
the
head,20
described how
nerve
fibres
may be
torn
by
the
swirling
of
the
brain
within
the
boxer's
skull. The
consequent
reduction of
axons
and the
appearance
of
distorted
end
swellings
scattered
in
the
boxer's
white
matter
are
now
being
studied
immunocytochemically
at
the
Johns
Hopkins
University
School of Medicine. Thirdly, widespread
deposition
of
13-protein
in the
cortex
that is reminiscent
of,
and
yet
distinct from,
the
neuritic form
of
plaque
has
been
identified,
also
immunocytochemically
(G
Roberts,
personal
communication).
Years
must
pass
before
the
long
term
effects
of
punch
drunkenness
on
the
structure
of
the
brain
can
be
studied. Computed
tomography
and
magnetic
resonance imaging
may
help
by showing
early
changes
during
life.
A
report on
boxing
in
1984
described
the
results
of
scanning
and
other laboratory
studies
as
disturbing.2'
The results
showed
what doctors
had
begun
to
suspect
from
the
experimental
and
psy-
chological
investigations-that
is,
that pronounced
brain
damage
in
boxers
may go
completely
undetected
if
an
examination
is
limited
to
traditional
tests. Jordan
commented
that
the
"frequent
finding
of atrophy
on
the CT
scan
cannot
be
overlooked
in
young.
boxers,"
but he
was
cautious
over
the
importance
of
this
if
seen
alone.3
Magnetic
resonance
imaging
has
the advantage
that it
can
detect
damage
to
white
matter
in
a
closed
head
injury.
The only report
of
the
use
of
magnetic
resonance
imaging
in
young
boxers that
I could
trace
recorded normal
results.22
To
the
neuropath-
ologists
the
worrying
thing about
the
more
advanced
techniques,
such
as
positron
emission
tomography,
is
the
difficulty
of
applying
them
routinely
to
identify
the
incipient
disintegration of
living
fibre pathways
or
groups of neurones,
particularly
at a
stage
when
-'use
nervous
tissue
recovery
may
still be
possibi
once
destroyed
ca1.not
be
rel,
Dedicated
spectators
may well
enjoy
this
scene,
but
the
frankness
of
its
description begins
to show why so
many
medical people
with
knowledge
of the brain are
finding
fault
with the
sport.
The
American
Medical
Association
and
comparable
societies
in
Australia,
Britain,
Canada, and some
Scandinavian
countries,
as
well
as
the
World Medical
Association,
have
all
come
out
against boxing
during
the
last
few
years.
The
reasons
for
this
rejection
by
a
profession
not
widely known
for reckless decisions
are
complex
but
would
seem
to
include
a
growing
reaction
against
gratuitous
violence.
For
what
it
is
worth,
my
opposition
to
the
sport
derives,
in
a
more
prosaic
way,
from
having
spent
many years
examining
human
brains,
some
of
which
were
intact
but most
of
which had
been
damaged
by
disease
or
trauma.
The
irreparable
scarring
and
degeneration
in the
brains of
boxers
was
unnecessary
and
the
effects
catastrophic.
The
prevention of
such
damage
seems
all
too
reasonable,
but
the
essence
of
a
contest
is
that
it
takes
place between
consenting
adults,
and thus whether
it
has
anything
to
do
with
anyone
else is
debatable.
On the other
hand,
prevention
is better than
cure,
particularly
when the
disease
in
question
is incurable.
The
virility,
or
any
other
virtue,
shown
by
one
man
hitting
another
on
the head
in
a
boxing
ring
cannot
transform
the
act
into
an
accident;
the blows
are
intended.
Similarly,
an
agreement
to
fight,
however
amiable,
cannot
alter
the
fact
that
hitting
one
another
is
deliberate.
This
point,
however
trite,
distinguishes
boxing
from all other
sports.
Racing
car
drivers do
not
drive
at
each
other
in order
to
collide,
nor
is
the
primary
aim
of
soccer or
rugby
to
score
hits
rather than
goals
or
points.
Certainly fights
break
out,
but
the
referee
is
there
to
stop
rather
than
to assess
them.
To
estimate
the
risks
of
neurological
damage
in
other
sports
a
postal
inquiry
designed
to
find
punch
drunk
sportsmen
and
women
was
sent to
162
British neurol-
ogists
in
1976
and
produced
five
soccer
players
(in-
cluding
one
"much
given
to
heading
and
able
to
do
so
even
if
the
ball
were
blasted
at
him
from
about six
yards"),
twelve
steeplechasers,
two
amateur
rugby
players,
possibly
two
wrestlers,
and
a
parachute
jumper.2
Boxers,
but
not
necessarily
different
ones,
were
mentioned
290
times.
Virile sport
Of
course
brain
damage
can
occur
in other
sports,
Most
boxing
enthusiasts
agree that
the
British and
at
times
injuries
are
inflicted
deliberately.
To
Boxing
Board
of Control
supervises
the
sport in
as
boxing
enthusiasts,
therefore,
the
separation
of their
responsible
and devoted
a
way
as
is
practicable.
This sport
from others
seems
unfair,
and
some
maintain that
voluntary body
acts on
the
advice
of
the
senior medical
all
contact
sports
carry
the
same
risk.
"Why pick
on
officer,2'
area
medical
officers,
and
expert
advisers,
boxing?"
one
critic
wrote.
To him the
boxer's
sole
who
are
required
to warn the keen and
often
im-
aim
was to
score
points.
When he
achieved this
poverished
young
hopefuls
of
the
hidden dangers in
a
through
his
skill,
as
by
knocking
the
other
man
out, he
virile
sport
that is
made more
popular, and
perhaps got
full
marks.
A
vagary
of
the
law in
the
United
more
glamorous,
by the
coverage
of
press and
tele-
Kingdom
is that
no
offence
to a
boxer
is committed
vision.
One
of
the
most
interesting
paradoxes
is
during
a
fight
because
both
parties
have
agreed
to
it.
the
increasing
social condemnation of violence
and
The
validity of
the
contest
is
beyond
question
because
brutality
while
money
and
effort
are
poured
into the British
Boxing
Board of
Control,
at
least in
1981,
encouraging
men to
batter
one
another
into
a state
of
was
made
up
not
only
of
businessmen,
dental
surgeons,
confusion
if
not
unconsciousness.
An
experimental
and
ex-professional
boxers,
but
also
of
solicitors
and
punch
delivered
by
Frank
Bruno
was
measured
by
judges.'3
Atha
et
al and
represented
a
transient
blow to
the head
of
about half
a
ton.24
Television
cameramen
have
learnt
to
exploit
the art,
Tighter
rules
or
abolition?
Although
boxing
has
had,
and
still
has,
its
ups
the drama,
and the
blood
so
skilfully
that
few
viewers
stop
to
think what
might
be
at
risk
behind the boxer's and
downs,
there
seems
good
reason
to
agree
with
face;
fewer
still
are
inclined
to
find
out.
Joyce
Carol Whiteson's claim that
the British
Boxing
Board
of
Oates,
a
boxing
buff,
was
quoted
by
Wills
as
describing
Control
has
greatly improved
the
lay
and medical
"the
electrifying
effect
upon
a
typical
fight
crowd when control
of
the
sport.23
The
incidence of cerebral
fighting
suddenly
emerges
out
of boxing-when,
for
damage
is
considerably
less than
it
was
in
the
days
of
instance,
a
boxer's face begins
to bleed and the
fight booth
boxing
and
when
the
overall
supervision
of
enters
a
new
and
a more
dangerous
phase.
The
flash of
contests
and
contestants
was
far
more
lax.
Paradoxically,
as
the rules
were
tightened
up
the
red is the
visible
sign
of the
fight's
authenticity
in
the
of
many spectators
and boxers
are
justified
in
opposition
became
more
strident.
Lady Summerskill,
eyes
being
proud,
as
many
of
them are,
of their
scars."25
26
both
as
doctor and
as
politician,
was
outspoken
in
107
BMJ
VOLUME
298
14
JANUARY
1989
Dempsey and Firpo
1924,
by
George
Bellaus.
(Oil
on canvas.
1295x
1607
cm.)
Reproduced
by pernission of
the
Whitney
Museum
ofAmerican
Art (gift of
Gertrude
Vanderbilt
Whitney,
31.95)
damning
the
sport.'3
In
1959
an
editorial
on
boxing
in the Lancet
claimed that
"as
doctors
we
have
a
clear moral
duty
to
fight
for
its total abolition"28
and
Critchley, after his earlier clinical study of
69
boxers,"
commented
more
diplomatically
that "there is
ample
justification
on
medical
grounds
for its dis-
continuation.
By
the
1970s,
with further medical evidence of
damage,
the
Lancet
conceded that "those who control
boxing
have made
considerable
progress
in their
efforts
to
protect
men
from excessive
damage,
especially
in
amateur
contests,"
but,
the editorial
continued,
"it
remains
inescapable
that
boxing
is
the
only
sport
in
Britain
where there is
consistently high
risk
of head
injury
and where
repeated
minor
trauma to
the brain
is
inevitable.
It
remains for
the
protagonists
of
boxing
to
produce
more
clinical and
neuropathological
evidence
that the
hazards
are
slight."29
On
the
same
evidence
the
British
MedicalJournal
affirmed
more
boldly
that
"the
argument
for stricter
regulation
is
overwhelming."30
Interest
had
also
been
growing
in
the United
States,
and the
American Medical
Association
held
an
inquiry
by
its council for
scientific
affairs,
which
advised
in
1983
that
banning boxing
was not
a
realistic
solution.3'
Many
practical proposals
were
made,
but
several
seemed
utopian:
all
bouts,
amateur
or
professional,
should be held where
adequate
neurosurgical
facilities
were
immediately
available for
skilled
emergency
treatment;
advanced life
support systems
should be
available
at
the
ringside;
and
a
comprehensive plan
for
evacuating
any
seriously
injured
boxer
to
hospital
should
be
ready.
In
most
countries
it
might
be
easier
to
hold
contests
in
a
neurosurgical
operating
theatre!
Within
a
few
years
the
ultimate
sanction
was
revived
when outspoken editorials
in
theJ7ournal
of
the
American
Medical
Association called
for
boxing
to
be banned and
the editor
went
on to
foretell
its
doom.32
33
To
compare
the views
of
one
country
with those
of
another
may be
misleading.
Sammons
quoted
how
in
New
Jersey
(where
Martland had
worked)
in
1984
108
"despite
the
appearance
of
a
modern,
bureaucratic
system
of
control in
sport,
prizefighting
was conducted
under barbaric conditions
and control was lax or
non-existent."5
On the other
hand,
in
New York
state
strict
rules
were
enforced3
(although the New
York State Medical
Society
favours
a
ban34).
These
local
variations
led
Jordan,
as
well
as the American
Medical
Association3'
and
JAMA,32
to
emphasise
how
American "professional
boxing
desperately needs a
national regulatory
agency
to
enforce uniform
medical
standards."3
After
these
outspoken
criticisms the
many
independent boxing
bodies
are now
forming
one
association while legislation is
planned for
a
single,
federally
chartered
United States
Boxing Commission;
amateur
boxing
has also
responded.35
Perhaps
it is
no
coincidence
that Jordan
and Sammons
have
forecast
a
secure
future
for
the
sport
in
the United
States.35
In
contrast
Sweden
and other
countries have
already
stopped
professional
boxing without
disaster,
the ban
in Sweden having been
imposed
in
1969.
Since
then
"very
strict
medical
supervision
of
amateur
boxing has
been well
accepted."36
Many
British
doctors
now
accept
that boxing is
a
risky business and
so,
presumably, do those
doctors
attached
to
the British
Boxing
Board
of
Control for
there would
otherwise
be
no
need
to
emphasise the
ever
improving
conditions.
Indeed, it
appears to a
concerned
outsider
that the
medical
influence of
the
board
has
spread, along with Whiteson's
advice,
even
beyond
the
United
Kingdonm,
and the rules
of
boxing
(if
boxing
there
must
be)
will
be able
to
develop
on as
humane
a
base
as
practicable.
The
board,
moreover,
seems
best
placed
to
cope
with
those who
might
want to
promote
the odd
contest
while
perhaps
rewriting
the
odd
rule.
For those who
cannot
compromise
the
honourable
action would be
to
vote
against the
sport.
A
few
years
ago
the proposal
to
ban
boxing
was
debated
on
the
radio
programme
You The
Jury.
The final
vote,
from
a
panel
of
around
100
people,
was
split
evenly
at
42%,
with
16%
abstaining.
Obviously
boxing
is popular,
and
BMJ
VOLUME
298
14
JANUARY
1989
many boxers have
done well,
though
their triumphs
have
often
helped others more than
themselves.
Success
sits
at
the
ringside
but many there are not boxers.
My
opinion
is
that
the
brain should
not
be a target
in
any
sport,
and
no
amount of juggling
with the
regulations
can
take away the risk.
Experienced
and
outstanding
boxers
are
themselves
aware
of
this,
difficult
as
it
may
be
for
them
eventually
to
call
a
halt.
Barry
McGuigan
said: "Boxing damages
your brain.
Don't
let
anybody tell you
different,"3
while Terry
Marsh
remarked drily:
"I
don't
need the
British
Medical
Association
to tell
me
getting
hit
on
the head
can't
do
me
any
good."38
Because the
present
evidence
is
incomplete
or has
been
unconvincingly
presented there
may
well be
those
who
see
no wrong
in
one
man
freely
damaging
another
man's brain.
Others
may
consider
that the present
risks
are
justified.
For
these
people
one
suggestion
might
be to read
Beyond the Ring:
the Role
ofBoxing
in
American
Society5;
another
might
be
to
recall
the
remorse
of Garry
Wills,
a
former boxing
fan:
"I
stood
talking
to
Muhammad
Ali,
embarrassed
by
his
inarticulateness,
and
deeply
ashamed,
as
it
was
not
his
own
superb
body
that had
done
this
terrible
thing
to
his
superb
mind.
I
had
done
it
too,
as
part
of
the
crowd
urging
him
on,
applauding
the
blood.
I
have
not
watched a
boxing
match
since
then."'5
Sammons
merely
wrote:
"In
boxing parlance,
Ali
was
punch
drunk.''5
1
Martland
HS.
Punch
drunk.
JAMA
1928;91:1103-7.
2
Cruikshank
JK,
Higgens
CS,
Gray
JR.
Two
cases
of intracranial
haemorrhage
in young
amateur
boxers.
Lancet 1980;i:626-7.
3 Jordan
BD.
Neurologic aspects
of
boxing.
Arch Neurol
1987;44:453-9.
4
McCunnev
WJ,
Russo PK. Brain
injuries
in
boxers.
Phvsician
Sports
Medicine
1984;12:53-67.
5
Sammons
JT.
Beyond
the
ring:
the role
of
boxing
in
American
societe.
Urbana and
Chicago:
University
of Illinois
Press,
1988.
6
Millspaugh JA.
Dementia
pugilistica.
United States
Naval
Bulletin
1937;35:
297-302.
7
Critchley
M.
Medical
aspects
of
boxing, particularly
from
a
neurological
8
Spillanie
1).
Five boxers.
Blrled,7
1962;ii:1205-1(0.
9
Mawdslev C,
Fergusoni
FR.
Netirological
disease
in
boxers.
Lancet
1963;ii:
795-80
1.
10
Roberts
AH.
Brain damage
in
boxers.
A
studs
of
prevalence of traumatic
encephalopaths'
among
ex-professional
boxers.
London:
Pitman, 1969.
11
Harvey
PI'RP,
Newsom
Dasies
J.
Traumatic
encephalopathv
in
a
young
boxer.
Lancet 1974;ii:928-9.
12
Guterman
A, Smith
RWV.
Neurological
sequelae.
Sposrts
Meldicine
1987;4:
194-2
10.
13 Summerskill
E.
'hth
ignoble
art.
London:
Heinemann,
1956.
14
Bass
AL, Blonstein
J1,_
James
RI), Williams JGP,
eds.
Mledical
aspects
of
boxin¢g.
Oxford:
lPergamon
Press,
1964.
15
Corsellis
JAN,
Bruton
CJ,
Freeman-Browne
D.
The
aftermath
of
boxing.
P.svholetMed
1973;3:270-303.
16
Corsellis JAN. Post-traumatic
dementia.
In:
Katzman
R,
Terry
RD,
$lick
KL,
eds. Alzheimer's disease:
senile dementia
and
related disorders.
New
York:
Rasen
P'ress,
1978:125-33.
17
Constantinidis
J,
'Tissot
R.
Lesions
neurofibrillaires d'Alzheimer
gen6ra1is&es
sans
plaques
seniles. Archives Suisse
Neurologie
Neurochirurgie
Psychtatrie
1967;100:
1 17-30.
18
Adams
CWM,
Bruton
CJ.
The
cerebral
vasculature
in
dementia pugilistica.
,
,Veu2rol
Neurosurg
I'ssvchiatrv
(in
press).
19
Lampert
PW,
Hardman
JM.
MIorphological
changes
in
boxers.
7AMAA
1984;251:2676-8.
20
Strich
S.
Diffuse
degeneration
of
the
cerebral white
matter
in
ses-ere
dementia
following
head
injury.
I
Neurol
NeurosurgPsychiatrv
1956;19:163-85.
21
British
Medical Association's
Board
of
Science
and
Education
Working
Party
on
Boxing.
Report.
London:
BMA,
1984.
22
Lesin
HS,
Lippold
SC,
Goldman
A,
et
al.
Neurobehasioral functioning
and
MN1R
imaging
findings
in
young boxers.
.YNeurosurg
1987;67:657-67.
23 Whiteson AL. Injuries
in
professional boxing.
Their
prevention
and
treat-
ment.
Practitioner
1981;225:1053-7.
24
Atha
J,
Yeadon
MR,
Sandover J,
Parsons
KC. The
damaging
punch.
BrMedJ
1985;291:
1756-7.
25
Oates JC.
On
boxing.
London:
Bloomsburs-,
1987.
26 Wills
G.
Blood
sport.
Ness
Y'ork
Review
of
Books
1988;2:5-7.
27
Anonymous.
Brain
damage
in
sport
[Editorial].
Lancet
1976;i:401-2.
28
Anonvmous.
Boxing
[Editorial].
Lancet
1959;i:
1185-6.
29
Anonymous.
Boxing brains
[Editorial].
Lancet
1973;i:1064-5.
30
Anonvymous.
Boxing
and the
brain
[Editorial].
BrMedJ
1973;ii:439-40.
31
American
M\edical
Association.
Report
on
scientific
affairs:
brain
injury
in
boxing.
JAMA
1983;249:254-7.
32
Lundberg GD.
Boxing
should be banned
in
cisilised
countries-round 2.
standpoint.
BrMedj
1957;i:357-66.
JAMA
1984;251:2696-7.
33
Lundberg
GD.
Boxing
should
be banned
in
civilised countries-round
3.
7AMA
1986;255:2482.
34
Lundberg
GD.
Brain
injury
in
boxing.
Am J
Forensic
Med
Pathol
1985;6:
192-8.
35
Jordan
BD.
Medical
and
safety
reforms
in
boxing.
J
Natl Med
Assoc
1988;80:407-12.
36
Ludwig
R.
Making
boxing
safer: the Swedish model.
JAMA
1986;255:2482.
37
Hughes
R.
The
samurai
deep
ill
the
soul
of
McGuigan.
Sunday
Times
1988
April
17:A21.
38
Hughes
R.
The
cagcd
lion whose mind
is
his
own
kingdom.
Sundayv
Times 1987
June
28:14.
ANY
QUESTIONS
Is
there
any
risk
in
administering
the measles, mumps,
and
rubella
(MMR)
vaccine
to
children
who
have
already
been
immunised
against measles?
1
Stetler
HC,
Gens
RD, Seastrom
GR.
Severe local
reactions
to
live measles
virus
vaccine
following
an
immunisation
programme.
Amn7
Public
Health
1983;73:899-900.
2
Stetler
HC,
Orensten
WA,
Bernier
RH,
et
al.
Impact
of
revaccinating
children who
initially
received measles
vaccine
before
10
months
of
age.
Pediatnrcs
1986;77:471-6.
3
Christenson
B,
Bottinger M,
Heller L.
Mass
vaccination
programme aimed
at
eradicating
measles,
mumps,
and rubella
in
Sweden: first
experience.
BrMedj
1983;287:389-91.
As far
as
I
know
there
is no
research
that
has
specifically
looked
at this
question,
but
there
are
studies
that
throw some light
on it.
Severe
local
reactions
were
reported in nine recipients of
live
measles
vaccine.'
Six of
them
had
previously
received
killed
measles
vaccine,
and this was
found
to
be
a
significant
association. Killed
measles
vaccine
has
not
been used
in
the
United
States,
from where
these
cases
were
reported,
since
1967
and
no
child
in
the United
Kingdom presenting
for
MMR vaccine will
have
received
it. Many
studies
have
looked
at
the
effect
on
antibody
levels
of
reimmunising
children who
first received
live measles
virus
vaccine
when
under
1
year
old.
Most make
little
or
no
mention of
adverse reactions,
the
assumption being
that
they
were
not
a
particular
problem. One study
did
look
at
this
and
found
that
children
being reimmunised
were
less
likely
to
develop
a
fever
and
more
likely
to
have
a
rash
than
children receiving
vaccine
for the first
time.2
The latter
difference
did not reach
statistical
significance.
Sweden,
Finland,
and
Norway
have
a
policy
of
giving
MMR
vaccine
twice
in
childhood.
In
none
of these
countries
has
the
programme
been
going long enough
for any studies
on
revaccination
to
have been
performed,
but
reactions
to MMR
vaccine
in
12
year
old
children were
found
to
be less
common
than those
in
18
month
olds.'
A
substantial
number of
the
12
year
olds
would
have
received measles
immunisation,
so
this lack
of
adverse reactions
is
reassuring.
There
is
a
small
incidence
of vaccine failure after
measles
immunisation,
and
a
second
dose,
given
as
MMR
vaccine,
may
produce
immunity
in
some
children
not
otherwise
protected.
The
administrative
problems of storing
and
administering
a
separate
mumps
and
rubella
vaccine
would
be
considerable
and there would be
little,
if any, saving
in
vaccine
costs.
All
the
evidence
so
far points
to
the
safety
of
giving
MMR
vaccine after
previous vaccination
with live
measles virus
vaccine
as
currently
used.
-
DAVID
A
C
ELLIMAN,
lecturer
in
community
child
health,
London
What is
the significance
of
a
positive Venereal Disease
Research Laboratory
(VDRL)
test
in an
elderly
confused patient,
and
how
should
the
test
be
interpreted
before
starting treatment
for
neurosyphilis?
Neurosyphilis
in an
elderly patient may cause
a
confusional
state
as
a
result
of
meningovascular
lesions
or
the dementia
or
psychosis
of
"general
paralysis."
The
diagnosis
depends
on
identifying
the
presence of
one
of
two
types
of antibodies:
either
non-specific (reagin)
antibody-for
example,
the
VDRL
slide
test-or specific treponemal
antibodies,
which
are
mostly
commonly identified
by
fluorescent
treponomal
antibody
absorption
or
Treponema
pallidum
immobilisation
tests.
The
latter
are
positive in
practically
every
instance of neurosyphilis,
and
if
there
is
doubt
one
of
these
tests should
be
performed.
The
VDRL
test is
less
specific
when
blood
is
tested,
but if
cerebrospinal fluid
shows
a
positive result
it
is
virtually diagnostic.
Active
infection
in
the cerebrospinal fluid is usually
shown
by
pleocytosis
and raised
concentrations
of
proteins.
For
practical purposes
a
positive result
of
VDRL
testing
of
cerebro-
spinal
fluid
is
diagnostic
of neurosyphilis
as
are positive results of
fluorescent
treponomal
antibody
or
Treponema
pallidum
immobilisation
tests
on
blood
or
cerebrospinal
fluid. Current treatment
is
aqueous
benzylpenicillin
12-24
million units given
intravenously
once a
day
for
10-14 days or
aqueous
procaine
penicillin
2-4
million units given
intra-
muscularly
daily
accompanied
by
oral probenecid 500 mg
four
times a
day
for
14
days.
Follow
up
examinations of
the
cerebrospinal
fluid
should be
done
at
three
months,
six
months,
one
year,
and
two
years.
-J M S
PEARCE,
consultant
neurologist,
Hull
BMJ
VOLUME
298
14
JANUARY
1989
109

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