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9
April
1966
Correspondence
MEDICALJOURNAL
923
accident,
which
had
led
to
his
admission
with
dysphasia
(to
the
local
general
hospital
ini-
tially,
where
his
hypertension
and
associated
symptomatic
epilepsy
had
previously
been
under
surveillance),
enables
a
comparison
to
be
made
of
morbid
anatomical
and
E.E.G.
findings.
The
latter
(16
June
1961)
revealed
bursts
of
high
voltage
1-2
cycles/second
activity
clearly
localized
over
the
left
fronto-temporal
region,
suggestive
of
a
space-occupying
lesion
deep
in
the
hemisphere.
The
brain,
on
the
other
hand
(Fig.),
showed
a
large
ragged-walled
brownish
cyst
in
the
left
cerebral
hemisphere,
above
and
lateral
to
the
ventricle
and
extending
from
anterior
to
posterior
horn.
It
was
maximal
in
cross-section
at
the
middle
cut
illustrated,
which
was
taken
down
the
central
sulcus
I
NCHES
I
2
3
4
5
1
23
4
5 6 7
8
9
10
II
12
13
CENTI
METRES
(leaving
the
temporal
lobe
intact).
Super-
imposed
on
these
long-standing
changes,
recent
haemorrhage
had
occurred
into
the
cyst
and
ventricle
posteriorly,
and
upwards
into
surrounding
tissues
anteriorly
as
far
as
the
superior
cerebral
cortex.
Macroscopically
no
major
artery
was
thrombosed,
and
both
left
temporal
lobe
and
whole
right
cerebral
hemisphere
appeared
normal.
I
am
indebted
to
Mr.
H.
A.
Milne
for
the
photograph.
-I
am,
etc.,
Dartford,
Kent.
J.
P.
CRAWFORD.
REFERENCES
1
Crawford,
J.
P.,
Lancet,
1962,
2,
888.
2
Brain,
Lord,
Speech
Disorders,
1965.
London.
s
Crawford,
J.
P.,
Psychiat.
Quart.,
1964,
38,
512.
4-
Ibid.,
1965.
39, 729.
Infections
of
the
Hand
SIR,-I
have
recently
read
the
observations
of
Dr.
H.
R.
Shepherd
(25
December,
p.
1550)
on
the
treatment
of
paronychia.
I
think
there
are
two
points
to
be
made.
If
the
standard
teaching
of
the
late
Dr.
Alan
B.
Kanavel
is
in
question,
his
name
should
have
been
spelt
correctly.
I
think
he
would
have
agreed
with
the
method
Dr.
Shepherd
is
advocating
as
entirely
adequate
for
infections
confined
to
the
nail-
fold.
Unhappily,
some
infections
have
al-
ready
progressed
beyond
this
limit,
and
pus
is
present
under
the
nail
and
sometimes
even
in
the
pulp
space.
Standard
teaching
for
these
infections
has
continued
to
insist
on
removal
of
the
nail
base
and
drainage
of
the
pulp
in
cases
which
demand
it.-I
am,
etc.,
The
Infirmary
HAROLD
BOLTON.
Stockport.
Prevention
of
Heart
Disease
SIR,-I
would
like
to
associate
myself
with
Dr.
A.
R.
Southwood's
letter
(29
January,
p.
296)
stating
that
little
has
been
said
about
the
prevention
of
ischaemic
heart
disease.
The
lack
of
interest
in
this
aspect
of
the
subject
is
shown
in
the
aim
of
the
Cardiovascular
Research
Unit
recently
set
up
by
the
Medical
Research
Council.
"Parti-
cular
emphasis
will
be
on
research
into
the
care
of
patients
after
coronary
thrombosis
and
into
methods
for
improving
diagnosis
and
treatment"
(29
January,
p.
305).
No
mention,
however,
is
made
of
prevention.
My
interest
in
this
problem
was
stimulated
by
a
special
study
of
the
climacteric.
On
several
occasions
I
expressed
the
view1
2
that
the
menopause
is
not
only
the
phase
of
a
woman's
life
when
menstruation
ceases
but
the
time
when
the
ageing
processes
develop
and
so
lead
to
the
degenerative
diseases
of
old
age.
One
of
these
is
coronary
heart
disease.
P.
D.
White,3
the
American
cardiologist,
labels
arteriosclerosis
an
epidemic
disease.
The
most
effective
results
in
the
field
of
epidemic
diseases
were
achieved
not
by
treat-
ment
but
by
prevention.
Some
cardiologists
suggest
that
the
failure
in
the
prevention
of
coronary
heart
disease
is
the
result
of
a
lack
of
knowledge
about
the
aetiology
of
arterio-
sclerosis.
Some
progress
has
been
made
in
that
field
of
research,
three
aspects
of
which
are:
(1)
the
study
of
the
serum
cholesterol
and
other
lipids
;
(2)
the
capillary
fragility
of
the
vasa
vasorum;
(3)
the
role
of
oestrogens.
Although
no
proof
exists
that
cholesterol
plays
a
role
in
the
causation
of
arterio-
sclerosis,
one
cannot
overlook
the
fact
that
the
cholesterol
content
of
the
blood
in
people
with
ischaemic
heart
disease
is
actually
raised.
It
has
also
been
shown
that
lipids
reduce
the
fibrinolytic
enzyme
normally
present
in
blood,
thus
contributing
to
coronary
thrombosis.4
It
has
been
suggested
that
fragility
and
resulting
haemorrhage
of
the
coronary
capil-
laries
(vasa
vasorum)
play
an
important
role
in
the
causation
of
coronary
thrombosis,
and
that
atheromatous
plaques
are
the
product
of
the
degeneration
of
the
extravasated
blood.5-9
There
is
evidence
that
cessation
of
ovarian
activity
leads
to
an
increase
in
the
incidence
and
severity
of
ischaemic
heart
disease,
and
to
an
increase
of
cholesterol
and
lipid
levels
in
the
blood.'0
Women
who
have
had
bilateral
oophorectomies
in
early
life
have
a
four
times
higher
incidence
of
coronary
heart
disease."
Significantly
fewer
cases
of
coronary
arteriosclerosis
are
found
in
men
who
have
received
oestrogen
for
treatment
of
cancer
of
the
prostate
compared
with
similar
untreated
patients."
The
incidence
of
abnormal
electrocardiographic
tracings
were
lower
in
hormone-treated
castrates
than
in
untreated
women."
Recent
controlled
studies
suggested
that
the
lives
of
men
and
women
with
previous
coronary
thrombosis
might
be
lengthened
by
oestrogen
administra-
tion
compared
with
those
who
received
only
placebos.""
1
There
is
also
some
evidence
that
oestrogen
deficiency
is
responsible
for
capillary
fragility
causing
unexplained
bruis-
ing
and
bleeding.'6'8
Apart
from
some
preventive
measures
suggested
by
Oliver
and
Stuart-Harris,"9
replacement
of
sex
hormones
by
implants
of
oestrogen
and
testosterone
in
women
and
men
during
the
climacteric
may
be
an
impor-
tant
factor
in
the
prevention
of
coronary
heart
diseases.
London
W.
1.
E.
SCHLEYER-SAUNDERS.
REFERENCES
Schleyer-Saunders,
E.,
Med.
Press,
1960,
244,
337.
2
-
Brit.
med.
7.,
1960,
1,
1274.
3
White,
P.
D.,
Ther.
Nts,
1964,
No.
44.
4
Astrup,
T.,
Blood,
1956,
11,
781.
6
Duguid,
J.
B.,
and
Robertson,
W.
B.,
Lancet,
1957,
1,
1205.
6
Patterson,
J.
C.,
Arch.
Path.,
1938,
25,
474.
7
Winternitz,
M.
C.,
Thomas,
R.
M.,
and
Le
Compte,
P.
M.,
The
Biology
of
Arterio-
sclerosis,
1938.
Springfield.
8
Wartman,
W.
B.,
Amer.
Heart
7.,
1938,
15,
459.
9
Morgan,
A.
D.,
Pathogenesis
of
Coronary
Occlusion,
1957.
Oxford.
10
Sznaiderman,
M.,
and
Oliver,
M.
F.,
Lancet,
1963,
1,
962.
l
Robinson,
R.
W.,
Higano,
N.,
and
Cohen,
W.
D.,
Arch.
intern.
Med.,
1959,
104,
908.
12
Rivin,
A.
U.,
and
Dimitroff,
S.
P.,
Circulation,
1954,
9,
533.
13
Davies,
E.
M.,
Jones,
R.
J.,
and
Jarolim,
C.,
Amer.
7.
Obstet.
Gynec.,
1961,
82,
1003.
14
Marmorston,
J.,
Magdison,
O.,
Kuzma,
O.,
and
Moore,
F.
J.,
7.
Amer.
med.
Ass.,
1960,
174,
241.
13
Stamler,
J.,
et
al.,
ibid.,
1963,
183,
632.
16
Poliwoda,
H.,
Nature
(Lond.),
1961,
191,
400.
17
Clementson,
C.
A.
B.,
and
Blair,
L.
M.,
Amer.
7.
Obstet.
Gynec.,
1962,
83,
1269.
18
Heikinheimo,
R.,
and
Kalliomaki,
J.
L.,
Curr.
ther.
Res.,
1963,
5,
135.
19
Oliver,
M.
F.,
and
Stuart-Harris,
C.
H.,
Brit.
med.
7.,
1965,
2,
1203.
Bradykinin
SIR,-The
following
sentence,
".
. .
this
leads
to
the
activation
of
the
enzymes
kalli-
krein
and
bradykinin,"
in
your
leading
article
(18
December
1965,
p.
1448)
is
incorrect.
Kallikrein
is
an
enzyme
which
is
present
in
an
inactive
form
of
blood,
pancreas,
and
small
intestine
and
in
an
active
form
in
saliva
and
urine.
The
substrate
for
kallikrein,
which
is
an
a2-globulin,
is
present
in
blood,
lymph,
and
colostrum.
Kallikrein
releases
kallidin-9
(or
bradykinin)
from
this
substrate.
Kallidin-
9
(or
bradykinin)
is
not
an
enzyme;
it
is
a
polypeptide
(nonapeptide)
which
accounts
for
almost
all
the
pharmacological
activity
of
kallikrein.-I
am,
etc.,
K.
D.
BHOOLA.
Department
of
Pharmacology,
Middlesex
Hospital
Medical
School,
London
W.
1.