Perimenopause Power Maisie Hill

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 To every single one of you who read Period Power and sent me
a message or left a comment asking me ‘What happens next?’ – this
book is for you and thanks to you.
And to my ovaries, for doing an outstanding job.
 HOW TO USE THIS BOOK

My clients come to me wanting help. They want strategies that will

make a difference to their symptoms and their lives, and I assume
that it’s the same for you. So, if you’ve got a particular symptom
that’s bothering you, such as hot flushes or changes to your mental
health, you can head straight to the relevant chapter(s). Get the
information you need as soon as possible.
What also helps my clients is understanding why they’re having
their particular experience because knowledge alone can have a
profound effect. Seeing my clients’ faces as it all starts to make sense
to them always brings a smile to mine, which is why I’ve explained
the science behind perimenopause and postmenopause in this book.
But I appreciate that scientific language can be confusing – that’s
why there’s a glossary at the back (see here) that you can refer to, if
and when you need it.
This is a book that you can come back to as you journey through
perimenopause and enter your postmenopausal years. Some of it will
apply now, some will become more relevant later on, but, ultimately,
having an overall sense of the menopause transition will help you to
be prepared and to have a positive experience, which is what I want
for all of us.
 Language and Inclusivity
Perimenopause is a process that happens to those born with
‘female’ reproductive organs, but I appreciate that not everyone
who reads this book will be female – some of you will be non-
binary or trans. It’s with this consideration in mind that I’ve tried
to be inclusive in my choice of language, referring to women
either because that’s the language used in the research papers I
reference, or to make a point about patriarchy.
 CONTENTS

Introduction

1 WTF is happening?
2 It’s getting hot in here
3 HRT: devil or saviour?
4 Let’s talk about sex
5 Moody bitches
6 Where’s your head at?
7 Going to waist
8 Bad to the bone
9 Whip it out
10 Hormone rehab

Epilogue

Appendix
Glossary
Resources
References
Acknowledgements
Index
 INTRODUCTION

You might wonder what a 40-year-old is doing writing a book about

menopause. I mean, that’s something that happens in your fifties,
right? Not quite.
Whilst the average age of menopause is 51, menopause itself only
lasts for one day, because it simply marks the one-year anniversary
of your last period. Perimenopause, on the other hand, refers to the
period of time in which you’ll have cycles, but start to experience
‘menopausal’ symptoms. When most of us are talking about
menopause, what we actually mean is perimenopause.
Perimenopause is most likely to start in your forties, but for some it
will begin in your thirties. It can last as little as two years or as long
as 12, and if more of us were aware of the subtleties of this
transition, we’d recognise the hallmark signs of our hormones shifting
far sooner and actually be able to do something about it.
To begin with you might notice that your periods roll around
quicker than they used to and that you need to up your game in
order to manage blood loss. Symptoms such as night sweats,
insomnia, headaches, migraines and breast tenderness may appear in
the days surrounding the start of your period. These are the early
signs that your hormonal landscape is shifting and that you’re
entering your perimenopausal years. With time, those signs will
become increasingly prevalent, and in the later stage of
perimenopause, your periods will become less frequent and other
symptoms, such as vaginal dryness, joint pain and bladder changes,
will become more likely.
 You may be someone who glides through perimenopause without
any significant issues. You might hurtle into it unexpectedly and feel
rocked to your core. You might be comfortable managing your
experience without help. You might want to do things ‘naturally’ and
feel confident that you can. You could be up for taking hormone
replacement therapy (HRT) and whatever else modern medicine has
to offer. You could also find that somewhere along the line your
thoughts and feelings about how you’ll manage ‘the change’, change.
What works well for you at first may not do the same further down
the line, and one form of treatment might work wonders for your
best mate, but not for you.
Whilst we’re on the subject, just as there are no prizes handed out
for birthing a child without pain relief, there is no prize for going
through the menopause transition without using HRT. Whatever your
thoughts on how best to navigate the menopause transition are,
you’ll find explanations and strategies that will help you in this book.
Your needs are likely to change throughout this process – and it’s
okay to change your mind about how you support your health and
wellbeing. I don’t want you to judge yourself, or anyone else, for the
choices you make. Whatever course of action you decide upon, I
want you to feel good about it. My hope is that this book will help
you to make decisions about your medical care and your life, because
indecision is exhausting. Going back and forth worrying about the
‘right’ course of action takes up mental space that quite frankly, in
this stage of life, you don’t have. Not to mention preventing and
interrupting your sleep, which you could certainly do without.
By the end of this book, you’ll have a chunky toolkit of tips and
techniques that you can use to improve your experience of
perimenopause as well as your postmenopausal years. To begin with,
the decisions you make are likely to be about managing your
symptoms, but as you’ll discover, the decisions you make now will
impact the decades that follow. Perimenopause is often described as
a window of opportunity and that’s what I’d like you to consider it as.
Perimenopausal symptoms include (but certainly aren’t limited to):
• More frequent or further-apart periods (or a thoroughly
unpredictable combination of the two) • Changes to menstrual flow –
heavier, longer, shorter, lighter • Increased PMS
• ALL THE RAGE, ALL THE TIME
• Sleep disturbances
• Fatigue
• Breast tenderness
• Headaches and migraines • Brain fog
• Poor memory
• Bloating
• Hot flushes
• Night sweats
• Dry mouth
• Joint and muscle pain • Mood changes such as anxiety and
depression • Panic attacks
• Vaginal dryness
• Pain during penetrative sex • Reduced sexual desire •
Increased sexual desire (yes, really) • Bladder changes –
leakage, urgency, needing to pee in the night • Skin changes –
acne, dry skin, oily skin, loss of plumpness and elasticity • Itchy
skin
• Hair loss, or thinning • Diarrhoea or constipation, or both.
Perimenopause is more than just physical symptoms, though. In the
Autumn phase of life, we are confronted with thoughts and feelings
that may have been supressed for years; creative and sexual desires
that suddenly emerge or disappear; a greater need for self-
expression; and a deep longing to walk away from life as we know it.
And then there’s going about your daily life feeling like a tinderbox
that’s ready to ignite, thanks to the irritability, impatience and red-hot
rage that course through your body. Perimenopause is a baptism of
fire that forces you to face yourself, your history and your future.
There is an intensity to perimenopause that we are rarely prepared
for, but desperately need to be, because rather than it be something
that happens to us, we can have a sense of agency over our
experience and find our power.
The Current State of Affairs In the last three
years there’s been a 37 per cent increase in
online searching for information about the
menopause and it’s hardly surprising given
that, according to independent Nuffield Health
group, 13 million women in the UK are
currently perimenopausal or postmenopausal,
and, because of the increase in population size
that came from the first- and second-wave
baby boomers, it’s estimated that more than
50 million women and those assigned female
at birth in the US have now reached the
average age of menopause. By 2050, this
figure is expected to quadruple. Yet the sheer
volume and range of symptoms and needs of
those who are peri- and postmenopausal is not
reflected in the research, public health
education and spending. If the tables were
turned and men were the ones who were wide
awake drenched in sweat at 1am, if their
cognitive function changed and their penises
shrivelled up, how much money do you reckon
would be coughed up to help them? There
certainly wouldn’t be a worldwide shortage of
HRT, as there currently is. After menopause we
still have a third of our lives left and the impact
of the hormone shifts during the menopause
transition echoes throughout those decades,
but there simply isn’t enough research being
done to reflect this fact.
As discussion around topics such as periods and miscarriage has
come to the fore in recent years, menopause is only just starting to
get some attention. Stars such as Michelle Obama, Ulrika Jonsson,
Meg Mathews, Louise Minchin and Michelle Heaton have opened up
about their experiences of menopause and received an outpouring of
praise and public support for doing so. Psychologist and menopause
expert Diane Danzebrink is the founder of the not-for-profit
organisation Menopause Support and the driving force behind the
#makemenopausematter campaign, which seeks to improve
menopause education among GPs, include menopause in the PSHE
curriculum for teenagers and raise awareness in the workplace. It
also recommends that employers create menopause guidelines, so
that they can support their employees. This work is needed. Those
who do speak to their GP about their symptoms (many don’t) are
often supplied with outdated advice as the majority of doctors lack
sufficient training in how to identify and manage menopausal
symptoms, with most receiving little to no training in the reproductive
health of women beyond their childbearing years. One would be
forgiven for thinking that our wombs are only worthy of attention
when they’re incubating other humans. The British Menopause
Society estimates that over one third of women will spend half their
lives as postmenopausal women, yet their needs are not being
addressed by health professionals.
All of this comes at a high cost. Marriages can rapidly deteriorate,
work performance declines and 10 per cent of women consider giving
up work altogether due to their symptoms. Health risks increase and
the risk of suicide goes up. The average age of menopause is 51 and
the Samaritans reports that the age group with the highest suicide
rate for women is 50 to 54. Menopause is not a disease, it is natural
and normal, and it is also a stage of life in which we need evidence-
based guidance and helpful support, and it’s thanks to the passion
and tireless work of women like Diane that we are finally seeing
progress.
Why Me?
Who am I to write a book about perimenopause when I haven’t gone
through it yet? It’s a question I’ve asked myself repeatedly. I
considered waiting a few years until I was on the other side of it –
and I know that there will be people who think that I should have
waited. My decision to write this book was based on the countless
comments, DMs and emails I received from people who read Period
Power and wanted to know more about what happens to our
hormones during perimenopause – so many of you asked me ‘What
happens next?’ that I even considered it as a title for this book. All
those messages had an impact, because your urgent need for more
information became my urgent need to get that information to you,
so that you can understand what’s going on and that there are lots of
things that can be done to improve your experience. I’m grateful to
all the perimenopausal and postmenopausal clients that I’ve had over
the last 15 years for putting their trust in me as their practitioner and
coach, and for allowing me to share their stories with you throughout
this book. It’s thanks to their questions and pursuit of a different
experience of perimenopause that this book is in your hands.
I’m sure that this book would be very different if I had waited, but
would it be more helpful to you? I’m not so sure. I spent 10 years
supporting hundreds of families as a birth doula before I experienced
pregnancy and birth and, in all honesty, I was a better doula before I
became a mother. Once I had my son, I tried to prevent my own
experiences from muddying the waters as I helped my clients
navigate their choices and make informed decisions, but they still
hovered around in the background, whereas the decade I spent
doula-ing before I became a parent was without the prejudice of my
own experience. My clients benefitted from that and I hope you’ll feel
the same way as you read Perimenopause Power. I’ve pulled
information from different quarters, done some hefty research so you
don’t have to, and woven it together with my clinical experience so
that you’re able to make informed decisions about your health and
hormones during the menopause transition.
 I like to be ahead of the curve, and I want to prepare myself and
my family for the next phase of my life as best I can. I remember
what it was like living with a perimenopausal mother whilst I went
through my teen years, and I want a different experience for my son
and partner. One where there is dialogue, awareness and
understanding that there are times when I need to walk out the door
and stomp my way along the coast or up the hills. I wanted to know
what options will be available to me when the time comes and writing
this book has allowed me to do that. I’ve been able to make some
decisions ahead of time, some of which have surprised me. I’m also
being confronted by the challenges of midlife. I’m learning to wield
the power of my hormones and quietly relishing the radical overhaul
that they are demanding of me.
If nothing else, I hope that this book addresses the almighty cock-
up caused by the flawed findings of the Women’s Health Initiative
study – the piece of research that’s led to 20 years of largely
unfounded and scary headlines (more on this here).
So, shall we do this?
Let’s go.
 1
WTF is happening?

Throughout our reproductive years we get used to what’s normal for

us – whatever our individual experience of our cycle has been.
Amidst any cycle-related symptoms such as pain, heavy flow, PMS,
breast tenderness and bloating, and changes to your energy, mood
and behaviour, there’s a degree of knowing what to expect. Your
cycle may have resembled the stunning highs and plummeting lows
of a hair-raising rollercoaster, but at least you had an idea of what to
expect on your particular rollercoaster.
In perimenopause the ride changes. Subtly at first and then with
full force. Instead of being on the same rollercoaster ride every cycle,
it feels like you’re always on a different one, especially once you start
oscillating between shorter and longer cycles, rarely with any kind of
predictability. Yep, it’s time to say goodbye to regular cycles – if you
ever had them, as some people experience lifelong irregularity.
Clients who come to me are often unsure whether they’re
perimenopausal. They tell me that their cycle has gone off-piste in
some way; either the length of their cycle has shifted or their period
has changed. Perhaps some new symptoms have appeared or
existing ones have gotten worse. Changes such as these are often
(but not always) due to perimenopause, but because they don’t fit
the picture we have in our minds of a menopausal woman who’s hot
and sweaty, and leaning against an open freezer, my clients don’t
necessarily identify the cause as perimenopause. The hot flushes we
all associate with menopause can come further down the line.
 Others come to me because they’re experiencing a vast array of
symptoms that indicate they’re going through perimenopause, but
they’re unaware that’s what’s going on. It’s rare for anyone to talk
about perimenopause until they’re well and truly in it, and years of
subtle, even obvious, signs and symptoms may precede the hot and
sweaty phase without being categorised as perimenopause. This, by
the way, is not something that I judge. It does enrage me that so
many of us don’t have a clue about what our hormones and
reproductive organs get up to, but I don’t blame anyone for not
knowing. Patriarchy is responsible for that.
And then there are those who absolutely know and are in need of
help.
Regardless of where you’re at (because I’m hoping that some of
you are reading this waaaaay in advance of perimenopause), I want
to kick things off with understanding what perimenopause is and
when it starts, because if you’re anything like me, you want a nice
clear-cut description; a black and white way of knowing if you’re in
the club or not.
 The Shouting Stage
According to the staging system developed by a group of scientists
from five countries and multiple disciplines at the Stages of
Reproductive Aging Workshop (STRAW) in 2001, early
perimenopause begins when the length of your cycle varies by seven
or more days in consecutive cycles. They also noted that during the
late reproductive phase of life, subtle changes to flow and length may
take place. But I’ve worked with many women who I would classify
as experiencing the hormonal shifts of perimenopause who don’t
meet these criteria.
In my professional experience, symptoms do appear before getting
to a seven-day variation in cycle length and I don’t think you need to
wait until you reach this official point to describe your experience as
perimenopause. These symptoms include a shortened cycle, changes
to menstrual flow, night sweats before and around the time of your
period, the appearance of blinding headaches and debilitating
migraines, breast swelling and tenderness that leaves you fearful of
being hugged, and rage that could fuel a country.
This is also my personal experience. In the last year, my cycle has
shortened to 24 to 25 days, with an occasional ‘normal-for-me’ length
cycle somewhere between 28 and 32 days. I started struggling to fall
asleep in the days before I started bleeding and this was
accompanied by premenstrual night sweats, which at least served as
notice that my period would be early. But the first major shift was
that my premenstrual mood changes ramped the fuck up. Sound
familiar? I know I’m not the only one. Over the years, clients have
reported similar experiences to me.
This is a life phase that the Centre for Menstrual Cycle and
Ovulation Research (CeMCOR, www.cemcor.ubc.ca) has described as
‘very early perimenopause’. CeMCOR is thankfully bucking the trend
in terms of what defines the start of perimenopause, because it
places the emphasis on our changing experiences which, better than
regular cycles, indicate changes in our hormone levels. How
refreshing. On its website, CeMCOR states that ‘if our experiences
have changed, if our hormone levels have changed – the scientific
evidence is that perimenopausal oestrogen levels are higher, more
variable and unpredictable, ovulation is less frequent and
progesterone levels are lower, then perimenopause has started, even
if our cycles are regular and normal in length’. CeMCOR has published
a series of experience changes, any three of which can be used to
define the start of perimenopause in those with regular, normal-
length menstrual cycles:

• New heavy and/or longer menstrual flow

• Shorter menstrual cycle lengths (≤ 25 days)
• New sore, swollen, and/or lumpy breasts
• New or increased menstrual cramps
• New mid-sleep wakening
• Onset of night sweats, especially around flow
• New or markedly increased migraine headaches
• New or increased premenstrual mood swings
• Notable weight gain without changes in exercise or food intake.

So many of us are starting to dance with perimenopause, but we

have no idea. We miss out on opportunities to do something about it
– time where we could be proactive and positively impact our
experience of perimenopause and life beyond menopause. This is
what I want to change.

When Will It Happen?

Most of us will experience natural menopause – when periods stop –
between the ages of 45 and 55. The average age is 51, though this
figure varies slightly depending on which country you live in. You’d be
forgiven for thinking that ‘natural’ menopause refers to going through
it without HRT, as if there will be an award for doing so. (There isn’t.)
It’s a term that defines the age at which you go through menopause
naturally versus entering menopause as a result of medical
treatments or surgical intervention, such as the use of radiation or
surgical removal of the ovaries.
 Perimenopause – where you still have a cycle, but begin to
experience ‘menopausal’ symptoms – lasts on average for four years,
but can be as long as 10 to 15 years. The first subtle sign that
change is afoot is often a shortened menstrual cycle and, along with
a varying cycle length, hormone levels fluctuate, often wildly.
Although menopause is thought of as a time of hormone deficiency,
specifically the withdrawal of oestrogen, perimenopause is more
often a time when oestrogen remains high. The peak oestrogen level
in a 20-year-old will be around 500–1,000 pmol/L, but during
perimenopause oestrogen can be as high as 5,000 pmol/L – hardly a
deficiency. (It doesn’t matter if you aren’t familiar with the unit of
measurement here, which is picamoles per litre or pmol/l, the point is
the contrast.) Eventually, oestrogen does decline, and you may switch
between cycles where oestrogen is high and cycles where it is low,
but progesterone is the hormone that takes a bow first. During the
time when oestrogen is high and progesterone is low, symptoms such
as shorter cycles, heavy and/or longer periods, period pain,
premenstrual spotting, bloating, headaches and migraines, sleep
issues, anxiety, depression, irritability AND ALL THE RAGE appear.
The gradual and erratic decrease of oestrogen secretion that’s a
feature of the late stage of perimenopause, in the run-up to
menopause itself, sees your periods becoming further apart and the
emergence of symptoms such as hot flushes, night sweats and
vaginal dryness. Once oestrogen declines, changes to your genito-
urinary system take place, and the risk of cardiovascular diseases,
diabetes and osteoporosis goes up.
 Defining Menopause
Premenopause is the years in which you experience a
menstrual cycle.

Perimenopause is the period of time in which you still have

periods, although they’re likely to be irregular, and experience
‘menopausal’ symptoms. This can be further defined as:
Very early menopause: Cycle length may be the same or slightly
shorter, new symptoms appear and/or existing ones worsen.
Oestrogen is often high in relation to progesterone.
Early perimenopause: Cycle length becomes shorter. Oestrogen
is often high in relation to progesterone.
Late perimenopause: Cycle length becomes longer, symptoms
such as hot flushes, night sweats and vaginal dryness may
emerge. Oestrogen becomes low.
Menopause itself is only one day long and marks the one-year
anniversary since your last menstrual period.

Postmenopause is when periods have stopped and hot flushes

are more likely, as are increasing symptoms such as vaginal
dryness and urinary tract infections. We spend a third of our lives
in this phase.

It’s Called ‘the Change’ for a Reason

Although there is research on the age of natural menopause and the
factors underlying it, when it comes to the timing and duration of
perimenopause, the research – like most areas of female
reproductive health – is frustratingly limited. Some people will have a
positive experience of perimenopause. It is, after all, a life event not
a disease or disorder. For others it will be confusing, overwhelming
and have a huge impact on the quality of their lives.
There is no one-size-fits-all approach to this process. Your
experience of perimenopause and the years that follow will be unique
to you. And it really is a process. Just as you get used to a particular
symptom or way of feeling, things change, and then change again,
and again. No wonder it’s referred to as ‘the change’. It’s
unpredictable and it can suck. But it’s also a window of opportunity
and that’s what I encourage you to focus on (Chapter 6 will help you
to figure out how to do so).

Will a Test Tell Me if I’m Perimenopausal?

Perimenopause is not a disease, but diagnosis is usually made based
on signs and symptoms. Blood tests for hormones aren’t a reliable
determinant of perimenopause as hormone levels can vary cycle to
cycle, tend to bounce around all over the place during
perimenopause and, in some cases, they will be in the range of
someone who’s premenopausal. That being said, if you start to
experience symptoms before the age of 45, you should have the
blood tests as you may be experiencing early menopause or
premature ovarian insufficiency (POI – see here).
But if it’s not perimenopause, then what is it?

• Pregnancy (it happens more than we realise).

• Thyroid dysfunction becomes more common as we age and it
can occur alongside perimenopause, but it can also occur on its
own and, because it mirrors some of the symptoms of
perimenopause, some people will be misdiagnosed. I’ve had
clients who experienced weight gain, depressed mood, changes
to their periods and other cycle irregularities, who were
convinced that they were perimenopausal, but their thyroid
turned out to be the problem.
• High prolactin levels can interfere with the normal production
of other hormones and ovulation. Your GP will usually test your
prolactin levels alongside other hormonal checks in order to rule
it out or identify it as the cause of irregular cycles. If prolactin is
high, you’ll need a pregnancy test to rule out the most obvious
cause, have your thyroid function checked, and be referred for a
brain scan (MRI) as a common cause of high prolactin is the
presence of a non-cancerous tumour on the pituitary gland called
a prolactinoma (these often shrink during menopause).
• Amenorrhoea (missing periods) because of undereating, over-
exercising and stress.
• Stress has a massive impact on the cycle, something everyone
is waking up to since lockdown life started in 2020. If your cycle
has become shorter or longer, stress could be the reason why
and it could be causing a whole host of other symptoms too.
 Running Out of Eggs
In the past it was assumed that menopause took place when you ran
out of eggs, the pool of ovarian follicles dwindling to the point of no
return. Changes to the relationship between two glands in your head
– the hypothalamus and pituitary – were thought to take place as a
consequence of declining ovarian function. But an increasing body of
evidence suggests that is not the case. Instead, multiple factors lead
to a gradual dampening and loss of synchronisation in the way your
hormones communicate with each other and with your reproductive
system. This takes place in addition to, and independently of, what
your ovaries are up to (or not up to, as the case may be).
The communication circuits which run between your brain, the
pituitary and the hypothalamus glands in your head and your
reproductive system go through significant changes during the
menopause transition, but before we get onto that, let’s travel back in
time to your teen years.
Unlike teenagers today, you probably didn’t have a mobile phone
as a teenager. But you were keen to talk to your mates. So keen that
you’d hang around your landline family phone, waiting for it to be
6pm when off-peak charges would start. You’d have plenty to chat
about, so did your mate, and sometimes another friend would be
trying to get through to you too. If your mum was on the phone,
then you’d search for some change to take to the phone box at the
end of your road, because you couldn’t possibly wait to communicate.
I realise that this recollection ages me like nothing else, but this is
exactly what was going on with your hormonal and reproductive
system at that point in your life too – the various components were
keen to communicate and they were highly responsive to one
another.
Let’s move onto what happened as you reached adulthood. For
most of your reproductive years, communication between your brain
and hormonal glands has been tightly orchestrated and responsive,
like when you got your first mobile phone. Back in the Nokia days, it
was easy to get hold of friends because we weren’t up to much.
Instead of using up precious minutes of your plan you’d use missed
calls to send signals and receiving a text was so novel that you
always replied immediately. But as we enter perimenopause, we
forget to make calls, even ones that are important. You might go
back and forth with calls all day with someone, but fail to catch each
other at a mutually convenient time. Or your friend might spot your
message, but not reply instantly, because, let’s be honest, they can’t
be bothered. Communication between your brain, hormones and
reproductive system is not what it used to be – messages aren’t sent
out and picked up as they ought to be or the timing is off.
It’s the significant changes to these circuits of communication that
are the hallmark of perimenopause and they appear to take place
independently of declining ovarian function. As such, perimenopause
mirrors puberty in that it is a process mediated by the hypothalamus.
Menopause doesn’t simply happen when you run out of eggs.
After menopause, your ovaries still contain some remaining follicles
– intact follicles have been found in the ovaries of 70-year-olds! But
whilst they can undergo a degree of hormonal activity, for the
majority of the time, it’s not enough to cause the changes to the
lining of your uterus which would result in an episode of bleeding.
Though at age 52, 4.5 per cent of us will have a period after a year
of having none, and whilst that may be down to what a few
remaining follicles are getting up to, you need to tell your GP about
any postmenopausal bleeding. Do not assume that postmenopausal
bleeding is down to lurking follicles trying to do their thing. Any
episode of postmenopausal bleeding should be reported as it is a red
flag for endometrial cancer (see here).
Menopause marks the permanent end of your cycling years and on
average we spend three decades in postmenopause, so now is the
time for you to consider what you want the next 30-plus years to be
like.
 Anatomical Changes During Perimenopause
It’s not just your external appearance that changes with age; your
reproductive system undergoes a progressive ageing process too.
 Vulva
When most people talk about the vagina, they’re actually talking
about the vulva. If you’re confused about what’s what, you’re in the
majority, and there’s certainly no need to feel any shame about not
knowing – we’ve been made to feel shame about our bodies for a
long time so let’s lessen that burden right now. That being said, it’s
good to know the names of your body parts because a) it’s your body
and b) it’s important that you can talk about any genito-urinary
symptoms with health professionals.
Your vulva is all of your external genitalia, including your mons
pubis (that’s the mound of fatty tissue on top of your pubic bone
that’s populated with pubic hair), labia minora (inner lips) and majora
(outer lips), your clitoris and its hood, as well as your perineum (the
area between your vulva and anus) and the external openings of your
vagina and urethra (the hole that you pee from). Your vagina is the
internal tube which connects your external genitalia – your vulva –
with your uterus and it is only the opening to the vagina that can be
seen once the labia are parted.
Your vulva thins during the menopause transition, and so does your
vagina. Yes, you can get wrinkles down there too. The labia majora
lose some of the subcutaneous fat, so you might notice that they’re
less plump than they used to be. The mons pubis can become more
obvious, either because of changes to your pubic bone (pubic
symphysis) or, and you’re going to love this, because the fat that was
originally around your lower abdomen has now descended to the
start of your vulva. And to top it all off, pubic hair becomes sparser,
thins, loses its coarseness, becomes wispier … and turns grey or
white.
The entrance to your vagina – known scientifically as the vaginal
introitus – becomes tighter, which can make tampon use (if you’re
still menstruating) and penetration painful. In postmenopause, the
vulva also experiences a reduction in blood flow and your vulval skin
can be particularly irritated by excessive washing and wiping, and
unnecessary ‘cleansers’ and creams that contain propylene glycol,
parabens and fragrances can cause further irritation.
 Vagina
Your vagina cannot be seen externally. It runs at a 45-degree angle
pointing backwards towards your bum and the front of it (the anterior
wall) is slightly shorter than the back of it (the posterior wall). Your
bladder sits in front of your vagina and uterus, and your rectum (the
last section of your large intestine) sits behind it. The chances of
having pelvic organ prolapse – where an organ’s position changes –
increase after the age of 50, when declining oestrogen levels impact
the anatomy and function of the pelvic floor.
Though we tend to think of the vagina as a hole, largely because of
how it’s depicted as being something that is there to be filled, most
of the time the walls of your vagina are in contact with each other.
When something is inside your vagina, such as a tampon, menstrual
cup, sex toy, penis or baby as it’s being born, it expands in order to
accommodate what’s inside it. The vagina is able to do this thanks to
the presence of ridges called rugae, which make it highly elastic and
capable of expanding, producing the so-called tenting effect that lifts
your cervix higher when you’re aroused and stimulated. When
oestrogen is circulating throughout your reproductive years, the lining
of your vagina is thicker and you have plenty of rugae. In the years
around the time of your last menstrual period and in postmenopause,
when oestrogen becomes deficient, the vaginal lining thins and there
are fewer folds. The consequence of this is that the vagina becomes
less elastic and accommodating.
The walls of the vagina also dry and atrophy (that’s the lovely
medical term for ‘waste away’), and become pale and more prone to
irritation. The normal vaginal secretions which help to maintain a
healthy pH reduce, leaving you feeling less lubricated and increasing
the risk of tears, bleeding and infection.
In the same way that your gut has its own unique ecosystem of
friendly bacteria called the microbiome, so does your vagina, and
when it’s out of balance you can end up with recurrent bouts of yeast
infections and bacterial vaginosis. The vagina does not need to be
cleaned or rinsed out, and using vaginal cleaning products or
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all. We thus have light discharges and severe discharges at different times, or, as the habit is
established, only the light or only the severe, the manifestation depending probably upon the number of
discharging cells and the importance of the exciting cause.
31 Traité de l'Épilepsie, etc., Paris, 1845, p. 55 et seq.

When the attacks occur in alarming frequency, as they sometimes do, the condition is known as the
status epilepticus. Leuret had a patient who had eighty in two hours, and Delasiauve reports the case of
a young man fifteen years old who had twenty-five hundred in one month. They may be so numerous as
to be apparently continuous. The patient remains in a state of coma (the status epilepticus), with very
high temperature. If he be not restored, he sinks into a deeper coma, and all the signs of collapse
manifest themselves. Bed-sores form, œdema of the lungs ensues, and the patient dies. Happily, this
condition of affairs is rare.

Delasiauve calls attention to the fact that the first two or three attacks that usher in this state do not
usually attract much attention, but the succeeding ones are so violent as to immediately suggest violent
consequences. In one of my cases the attacks, when they had once become numerous, were readily
excited by the least jarring, noise, or handling, just as we find in strychnine-poisoning or tetanus.

Irregular Forms.—There are occasional cases of psychical or masked epilepsy, the study of which is
intensely interesting. Such forms are characterized by perverted consciousness and a low degree of
volitional direction which may vary from automatism to the undoubted exercise of complex functions of
the mind, though badly co-ordinated. Mesnet's soldier, when subject to a paroxysm and apparently
unconscious, would perform a number of suggested acts in a rhythmical manner and with no
subsequent knowledge of the previous event: when started off by the word of command to march, he
would blindly go on, marking time when he met with an obstruction until stopped, or when a paper and
tobacco were placed in his hands he would proceed to roll an unlimited number of cigarettes.

Two cases of a more complex exercise of certain intellectual powers, while others were dormant, came
under my observation some time ago. One of them was a young man of twenty-three, who had had
irregular epileptic seizures for some years. He went to bed one evening as usual, arose, and
breakfasted with his family without creating any suspicion that he was at all unwell. He then went down
to his place of business, and after his arrival was sent to a distant part of the city for some tool. On his
return down town he stopped at a tobacconist's and became involved in a quarrel with one of the
persons in the shop. A policeman was called, who, more intelligent than many of his class, immediately
detected something queer about the man, arrested him, and afterward took him to Bellevue Hospital.
There he remained three days, and suddenly returned to consciousness and a knowledge of his
surroundings, but was entirely ignorant of his unfortunate experience. It is unnecessary to say his habits
were perfectly good and he was not drunk at the time of the quarrel or arrest. His last recollection was
that of going to bed the night before the day of his arrest.

Another case of unusual interest which came under my care, illustrating a phase of sensory epilepsy, is
worthy of reproduction:

C. O——, aged twenty-two, is a reporter attached to one of the New York afternoon papers, who
received a severe injury of the head when but three years old. He fell from the second story of an
unfinished building to the cellar, striking the upper and back part of his head upon a beam. He was
rendered unconscious, and remained so for a day or more. He recovered from the immediate bad effect,
but has suffered from severe general headaches, which recur every week or so, with an increase in the
amount of urine excreted. About six months ago he began to have epileptic convulsions of a violent
character almost every day, and sometimes more often. These were precipitated by excitement, and he
had a great many when worried about his wife at the time of her delivery. Upon one occasion he fell
down stairs and injured himself quite severely. The attacks were, as a rule, preceded by an epigastric
aura of long duration, and occasionally by a visual aura, and, according to the testimony of his
associates, he became strange and queer. When in such a dazed condition he would restlessly wander
about his office, and suddenly, without any cry, become convulsed. After the attack he slept soundly.
The bromides of sodium and ammonium and digitalis did little or no good, but the bromide of nickel
appeared to have some influence. During the past month he has had only two or three attacks, but
these have been of a quite irregular character. He told me that there were times when he felt like doing
himself an injury, and that he had impulses to kill some one else. His companions said he was irritable,
pugnacious, and easily thwarted, and his brother-in-law stated that upon several occasions he had
queer turns, when he would raise his hand to strike some member of the family—that he subsequently
knew nothing of his conduct, and when it was detailed to him he appeared greatly astonished.

Mr. O—— came to my office in company with a friend at ten o'clock in the morning of December 27,
1883. He had had one of his attacks at the newspaper office, of rather more severe character than
usual, at eight o'clock, with a psychical aura, during the existence of which he was very morose and
sullen. Upon recovery he was speechless, though he could communicate by signs. Upon his arrival at
my office his manner was composed and he appeared somewhat dazed. His pupils were dilated, but
contracted readily to light. I asked him one or more questions regarding his inability to speak, which he
perfectly understood, and when I gave him a pencil and a piece of paper he replied without difficulty in
writing. When told to make a great effort to speak he did so, and I thought I detected the word ‘To day,’
but he could not repeat it, though he tried and expressed great annoyance. He was unable to utter any
sound except a sort of groan, which could not in any way be taken as an element of speech. I examined
his larynx, but found nothing which could explain his impaired phonation, and I sent him to Dr. Asch,
who found absolutely no abnormal appearances to account for the speech difficulty. The patient could
not phonate, and though he made attempts to enunciate the vowel-sounds, and the vocal cords were
approximated, he made no orderly sound. Asch found a slight laryngitis of no importance.

The patient went home, and remained speechless all day, and was seen by my associate, G. de Forrest
Smith, in the evening. What occurred during and after that gentleman's visit is contained in his notes: “I
was called to see patient about 8.15 P.M. He was lying upon the bed, but had not slept; recognized me
and motioned that he could not speak, and I found that he could only say one or two words, and this
with the greatest effort, and so all my questions were put so that he could answer them by nodding or
shaking his head. He knew that he had had an attack in the morning, that he had seen Hamilton and
Asch, and recalled various incidents of the day, answering intelligently my questions in regard to them.
He indicated by motions that his inability to speak was due to a lump in his throat. When asked if he had
any trouble to think of the word he wanted, he shook his head, but shortly afterward hesitated in an
answer, and when asked if this was due to his inability to think of the word, said ‘Yes.’ Was asked if he
had any loss of power in either side, and he motioned to his right arm and leg, and said that he felt a
numbness and pricking on that side. On his grasping my hands with his, the right was perceptibly
weaker.

“At one time he seemed confused as to which was his right or left side, and put up both hands, and after
looking at first one and then the other in a puzzled manner, at last decided correctly, then smiled
apparently at his confusion.

“All this time he had been half lying on the bed. He now intimated that he was tired, put his head down
on the pillow and began to belch up wind, and as he appeared about to vomit I called for a basin; but
this was only the beginning of an attack; the muscles of the neck and right side assumed a state of tonic
spasm, the extensors predominating, so that the head was turned a little to the left and forcibly thrust
back into the pillow, and the right arm and leg were firmly extended. He remained in this position about
one minute; then, taking two or three full inspirations, put his hand to his throat and said plainly,
‘Something has fallen from there.’ On being asked ‘What?’ he replied, ‘A bone has fallen from my
throat.’ I told him it was well that the bone had fallen, as now he could speak. ‘Why,’ said he, ‘I have had
no difficulty in talking.’ On being asked why he had seen Asch, he said ‘Who is Dr. Asch? I never saw
any such person.’ Further questioning showed that all the occurrences of the day (except those which
had taken place immediately before the first attack) were an absolute blank, and he thought it still
morning. He asked the time, and I told him half-past eight o'clock in the evening. At this he seemed
much surprised and said, ‘Why, I went to work this morning; how did I come here?’ I then explained to
him that he had been ill. After further conversation he said he felt sleepy, and, after resting a few
minutes, he arose, put on his slippers, and came out into the room. He walked with difficulty, because of
the loss of power in the right side, which he said felt numb and sore, as if it had been pounded, also a
sensation of pins and needles. After the attack his mind was perfectly clear, and he could talk as well as
ever, and all that had happened before the attack in the morning he could remember perfectly well, but
the interval between the two was a complete blank. His inability to speak seemed due, not to lack of
knowledge of what he wanted to say, but rather to want of power to form the words, although there was
no paralysis of the vocal muscles. When he did manage to say a word, it was invariably the correct one,
but it was always done with the greatest effort. The day after the attacks he remained at home; the next
day he went to work, but his head felt heavy and confused. Two days after he complained of a pressure
on the left side and back part of the head; otherwise he was all right. At this visit he said that after I had
left him on the night of the attacks he intently thought, striving to recall the incidents of the day, and after
a time concluded he could remember being at Thirty-third street, but did not know how he got there. He
thought he could recall going to see Asch, but would not know him if he should see him. I then asked
him how questions were answered by him on that day; he answered he did not know, as he had not
thought of that; then, after a few moments' reflection, said he must have written the answers. He was
then shown some of the answers he had written, which he recognized, and by an effort of memory could
recall some of the incidents of writing them. He was still unable to remember anything that occurred
after his arrival home previous to the last convulsion.”

January 27, 1885: This patient subsequently suffered from several attacks in which the psychical
element predominated. His head presented a remarkable deformity, there being a prominence
posteriorly which might be compared to a caput succedaneum, only it was entirely osseous. The upper
margin was separated from the anterior parts by a deep sulcus.

Under such circumstances we find very often that acts of great violence are committed by such
epileptics for which they are entirely irresponsible. Two or three cases of the kind occur to me now. One
of them was a boy who always bit every one and everything—his family, the domestic animals, and
inanimate objects; another, a most dignified and lady-like woman, who violently struck different
members of her family; and within the past week a woman was brought to me who hurled a kerosene
lamp at a perfect stranger with whom she was quietly talking before the seizure was precipitated.
Numerous instances are related where individuals while in the masked epileptic state have wandered
for long distances and committed a variety of purposeless acts, and undoubtedly many of the
mysterious disappearances are of this order.

SENSORY EPILEPSY.—Some years ago Hammond referred to certain peculiar epileptic attacks in which
sensory manifestations were very pronounced. To this condition he gave the name thalamic epilepsy,
believing the condition to be one of the optic thalamus. Among the large number of unclassified and
irregular cases reported by various authors there are many so much resembling each other that I think
they should be relegated to a special place.32 The notable examples of Sommers, Bergmann, Tagges,
Guislain, and others belong to this category.
32 I shortly afterward, believing the term a misnomer, invented that in use: “On Cortical Sensory Discharging Lesions or Sensory
Epilepsy,” New York Med. Journal and Obstetrical Review, June, 1882; also see “A Contribution to the Study of Several Unusual
Forms of Sensory Epilepsy which are probably Dependent upon Lesions of the Occipital Cortex,” New York Med. Record, April 4,
1885.

The features of this form of epilepsy are (1) the expression of some hallucination (prodromal stage), or
hemiopia; (2) supraorbital neuralgia; (3) aphasia, formication; (4) slight loss of consciousness, and little
if any motor disturbance.

I may present two illustrative cases:

A few months ago I was consulted by a medical gentleman in regard to a patient who had for years
presented a curious train of nervous symptoms, which afterward assumed a form leading me to think
she might have sensory epilepsy. She would, in the presence of the gentleman who consulted me, who
was a personal friend of the patient and a medical man, stop short in the midst of an animated
conversation, look fixedly ahead, appearing momentarily lost, remaining abstracted for a short period,
possibly a minute, and on recovering herself go on, finishing the sentence she had commenced before
the seizure. At this time she constantly had hallucinations of a visual character, when she saw animals,
birds, figures of men and women, who approached her, as well as a variety of other objects. A common
hallucination, which had been repeated quite frequently, consisted in visions in which green leaves and
white rabbits and other objects familiar to her in childhood figured extensively. Upon one occasion, while
sitting in the drawing-room, opposite a door which communicated with the hall, she suddenly called her
companion's attention to the hand of a man which she saw clasping the baluster rail. The hand was
seemingly disconnected from the arm. She was somewhat agitated, and it was nearly half a minute
before the vision was dismissed. Sometimes she would call attention to the hallucinations before the
attack, but more often she became transfixed, apparently lost, and then recovering she described her
visions minutely. She has apparently been able to foresee the attacks and ward them off by a strong
voluntary effort. So far as can be learned, there is no hysterical element in the case, but her seizures are
more frequent at the time of menstruation. In a private note it is stated that “the family history of the
patient is very good, and she has always seemed remarkably healthy and robust, and has shown more
than usual intellectual ability. She has appeared to persons generally to be of a contented, happy
disposition.... At night, when she closed her eyes, she suffered from these hallucinations, especially
after a day of fatigue. Her pupils are usually dilated, but her color undergoes no change during the
seizure.”

The second case is one of a more complex type:

J. B——, a bright boy aged sixteen, was sent to me by F. H. Bosworth in April, 1883. He comes of
nervous stock, his mother being subject to epilepsy, and his father is an eccentric man who manifests
his mental peculiarities chiefly in a morbid restlessness and irascibility. There is a brother who is healthy.
The attention of the parents was first called to the boy's condition by his recital of a sudden attack which
occurred during the summer of 1882. While rowing upon a river he suddenly and completely lost the
visual use of the right eye, so that in looking at a number of ducks swimming near his boat he failed to
perceive those upon one side of the flock. This condition lasted for twenty minutes, and after a brief and
severe pain over the right eye he became unconscious, the unconsciousness being preceded by a
tingling and numbness of the hand, forearm, arm, and left side of the tongue. He has subsequently had
eight or ten of these attacks, of which the following is an example: Usually without any bad feelings,
physical or mental, he, while engaged in any duty or at any time, suffers a sudden unilateral blindness.
This is never gradual, and not like the form of amblyopia in which the visual field is gradually reduced.
There is some hemichromatopsia. It would seem as if the retinal anæsthesia was unequal, for while
usually the loss is complete and universal, it sometimes happens that there is only a limited loss. Upon
one occasion, while reading, he suddenly lost the printed matter of the right lower half of the page below
a diagonal line extending from the right upper corner to the left lower corner. There is never diplopia.
This deprivation lasts anywhere from ten to twenty minutes; meanwhile, a distal anæsthesia, coming
very gradually, involves at first the fingers of the opposite hand, and successively extends to the
forearm, arm, and other parts, as I have already mentioned. There seems to be analgesia as well as
anæsthesia, for a pin may be run into the muscles without producing pain, and upon one occasion the
gum was freely pricked without any discomfort to the patient. It invariably happened that the cutaneous
sensory trouble occurred upon the side opposite to the hemianopsia and neuralgia, and in the greater
number of instances the left side was that affected. The third stage of the attack consists in migrainous
headache of a very severe kind, and which sometimes lasts for an hour or more. There is a subjective
feeling as if the eye was pushed forward. This disappears with nausea and relaxation. More often he
loses consciousness when the anæsthesia reaches its limit, which seems to be the extension of the
anæsthesia to the gums. Occasionally there are slight convulsive movements upon the anæsthetic side.
While the attacks involve the left side of the body as a rule, it happens that when there is primary left
hemianopsia and right-sided anæsthesia the boy becomes very much confused in speech, and
sometimes is paraphasic, the trouble being but transitory. He is sometimes unable to speak at all,
though perfectly conscious and in possession of his faculties. No pupillary disturbance has been noticed
at any time. Upon two occasions there was a swelling of gums and tongue, which was not only
subjective, but perceived by the mother. Occasionally he sees prismatic colors and rays before the
blindness, but this has been only once or twice. During his early life he had attacks of slight numbness
of the hands and feet which were not thought much of, and he had headache as well. He has been a
somnambulist.
MORBID ANATOMY AND PATHOLOGY.—The literature of the experimental physiology of epilepsy is enriched
by the observations of a variety of careful students, among them Sir Astley Cooper, Kussmaul and
Tenner, Brown-Séquard, Nothnagel, Schroeder Van der Kolk, Pitres, Hughlings-Jackson, and the
followers of the localization school, as well as many others more or less distinguished.

The experiments of many of the early writers were directed for the purpose of ascertaining the relations
of circulatory variations to convulsive seizures, and the most notable were those of Burrows and
Kussmaul and Tenner. These latter produced compression of the carotid arteries, and instituted cerebral
anæmia by free and exhausting hemorrhages. As a consequence, the emptying of the cerebral vessels
was followed by a loss of consciousness and by epileptiform convulsions, and it was necessary to
produce the same result to compress all the great afferent vessels of the brain. The experience of
surgeons generally is, that ligation of the common carotid upon one side of the neck is sometimes very
apt to produce an alarming anæmia, with occasional convulsions, and sometimes fatal consequences.

The experiments of Hall, Landois, Hermann, and others, as well as those of the writers just mentioned,
show that carotid compression results in capilliary anæmia and venous hyperæmia, and that with
cessation of this pressure there is a sudden congestion of all vessels. The susceptibility of the brain is
greatest at its posterior part and between the optic thalami and the cord. When the bulb was subjected
to sudden changes in its nutrition—such, for instance, as followed the experiments of Hermann, who
ligated simultaneously the superior and inferior venæ cavæ of a rabbit—there were not only
convulsions, but various cardiac and other disturbances which were undoubtedly due to central
impairment of function. Kussmaul and Tenner conducted their experiments with watch-glasses luted into
the cranium—a procedure which, however, at best, is unreliable.

Brown-Séquard some years ago in part established an important pathological truth, the theory of
epileptic zones, and demonstrated in certain animals that bruising and injury of the great nerve-trunks,
especially the great sciatic, would give rise to epilepsy, and that irritation of certain tracts would
precipitate the paroxysms. He further announced that the progeny of animals in whom epilepsy had
been thus induced very frequently inherited the epilepsy of the parent. By some it was held that such
epilepsies were purely peripheral, and Brown-Séquard even believed in spinal epilepsy. His spinal
epilepsic theory has, for the most part, been explained by the anatomical researches of Hitzig and the
doctrine of interrupted spinal inhibition. In fact, many of the spinal epilepsies are examples of
exaggerated reflexes.

The epileptiginous zone theory, which, while it induced many to believe that the disease might have its
origin outside of the brain, gave rise to the false assumption that attacks with distal auræ were primarily
non-cerebral, has been discarded, and most observers have arrived at the conclusion that even in these
cases the first explosion is due to some cerebral cell-discharge.

Hughlings-Jackson's grand work has revolutionized the views held prior to his first published writings,
about twelve years ago. He believes that any part of the gray matter may, through over-excitability, give
rise to convulsive attacks.

The production of convulsions by cortical irritation is now an old story.

The experiment of Pitres and Frank33 bears upon the sensorial function of the cortex in showing that,
when the cortex is irritated, epileptiform convulsions follow, but if the exposed surface be subjected to
the ether spray the same irritation will only produce definite movements, but no convulsions.
33 Gazette des Hôpitaux, No. 38, 1883.

The investigations of Van der Kolk especially, and his followers, certainly give the medulla an important
place as the locus morbi of the malady; and it must be assumed, bearing in mind the existence of the
vaso-motor centres of Dieters and the presentation of symptoms indicative of disturbance at the floor of
the fourth ventricle, that the most important pathological changes must be looked for in this part of the
brain.
Jackson's cortical explanation is, however, fully in consonance with the medullary theory. If we study the
different stages of the attack, we shall find that there is probably a suspension of cortical inhibition—that
a derangement of the cortical cells or discharge may cause a resulting disturbance in the bulb. On the
other hand, a reflex irritation through the pneumogastric or from some distal part brings about the same
disturbance of equilibrium. There is anæmia due to irritation of the vaso-motor centre, an inhibition of the
great ganglion-cells, and a disturbance of function of the important cranial nerves. The primary anæmia
and unconsciousness are accounted for by this primary irritation of sympathetic filaments and vascular
constriction; the secondary hyperæmia is explained by the experiments of Kussmaul, which
demonstrated the succeeding congestion; or by irritation of the spinal accessory and contraction of the
muscles of the neck and compression of the large veins. The pupillary, ocular, respiratory, and other
symptoms indicate the disturbance of the nerve-nuclei in the bulb. The respiratory difficulty and the
interrupted decarbonization of the blood undoubtedly account for the secondary unconsciousness.

Van der Kolk34 in localizing the lesion in the medulla found capillary dilatations in the neighborhood of
the hypoglossal nuclei in tongue-biters. In epileptic patients who were in the habit of biting their tongues
during the fit the vessels were wider than in those who did not bite the tongue, on an average in the
course of the hypoglossus by 0.096; in the corpus olivare, which certainly here plays an important part,
by 0.098 mm.; and in the raphé by 0.055. In those who did not bite the tongue, on the contrary, the
vessels in the path of the vagus were 0.111 wider than in those in the first, Table A.35
34 “On the Minute Structure and Functions of the Spinal Cord,” by J. L. C. Schroeder Van der Kolk, New Syd. Soc. Trans.

35 TABLE.
Different Epileptics. Hypoglossus. Corpus olivare. Raphé. Vagus.
Table A—tongue biters 0.306 0.315 0.315 0.237
Table B—non biters 0.210 0.217 0.217 0.348
Difference +0.096 A. +0.098 A. +0.055 A. +0.111 B.

Nothnagel36 is of the opinion that the anæmia of the brain is not the cause of the convulsions, but that
the “excitation of the vaso-motor centre and that of the centre for the muscles are co-ordinate—that both
go on side by side, and are independent of each other.”
36 Ziemssen's Encyclopædia, vol. xiv. p. 268.

He by this theory explains the occurrence of those forms of petit mal in which there is loss of
consciousness without convulsions, and, on the other hand, twitchings before the coma.

The best argument in favor of this hypothesis is in Jacksonian epilepsy, when monospasms exist
oftentimes with a succeeding extension.

In those cases which are the outgrowth of migraine the pathological condition is probably an
exaggerated tendency to angio-spasm, the original impaired vascular tonus in the beginning giving rise
simply to pain and lesser troubles, while after repeated changes of calibre not only nutritive alterations
ensue, but hyperexcitability of the bulbar convulsion centres as well.

The labors of those who have endeavored to connect epilepsy with cerebral-tissue alterations have
been attended by nothing very definite or positive, so far as pathological explanation is concerned. The
post-mortem appearances have varied widely, and the only conclusion to be reached is that which
shows that almost any morbid gross alteration of the cerebral mass may be symptomatized by
convulsions, but such a production of paroxysmal trouble is much more likely to be the case, and in a
more definite manner, when the cortical motor-centres are subject to destructive disease or irritative
pressure. This is even not always the case, for numerous cases of injury of the paracentral lobe have
been recorded with no showing of resulting convulsions. The long list of autopsies which I will not here
consider show that an epilepsy may owe its origin to the pressure of a spicula of bone, or to the
pressure exercised by depressed fragments of the same—to tumors or adventitious products,
meningitis, cortical encephalitis, vascular degeneration, ventricular œdema, contusio-cerebri, and many
other morbid processes which result in rapid or tardy degeneration. Of course, in such cases the
genesis of the disease depends not so much upon the nature of the lesion as the location. The fruitful
collections of cases of Ogle and Jackson are full of examples of limited growth or disease involving the
cerebral cortex, while numerous cases collated by other writers show disease of the bulb or various
peripheral parts which have been closely connected with the growth and behavior of the affection.

Several able pathologists have independently and repeatedly found that sclerotic degeneration of the
hippocampal folds often existed. Delasiauve and Lébert first observed this lesion, but many modern
authorities—among them Meynert, Nothnagel, and Charcot—who have also found this appearance,
regard the change as of purely secondary, and consequently unimportant, character.

Tamburini37 reports a case of hemiplegic epilepsy with induration of the left optic thalamus and the left
cornu ammonis, in which aphasia existed. Pfleger38 and Henkes have also found the sole lesion to be
induration of the cornu ammonis. Of Pfleger's39 43 autopsies, atrophy and sclerosis of the cornu
ammonis were found twenty-five times, and it was noted that the extent of the morbid change bore
relation to the violence and frequency of the seizures.
37 Sallanzani, Modena, 1879, viii. 550-557.

38 Allg. Zeitschrift f. Psychiatrie, etc., Berlin, 1879, xxxvi. 359-365.

39 Ibid., lxxvi., and Arch. de Neurologie, No. 2, 1880, p. 299.

In many examples, especially where the disease has been found to be unilateral and associated with
more or less hemiatrophy, the autopsy disclosed a corresponding hemiatrophy of the brain. Many such
cases are reported. I have frequently found epilepsy in association with cerebral hypertrophy, and as a
symptom of cerebral tuberculosis it has long been recognized, and numerous cases are reported in
which for a long time the paroxysms were the only manifestations of the condition. In one of these
cases, reported by Luys,40 the bulb was found involved by tuberculous matter.
40 Archives gén. de Méd., 1869, ii. 641 et seq.

Convulsions have very frequently been noted in association with imperfect cerebral development, and
Echeverria laid great stress upon the hyperplastic increase in volume of certain parts of the brain.

Marie Bra41 has thus summed up her conclusions relating to the morbid anatomy of epilepsy:

“1. The mean weight of the brains of epileptics is less than the physiological mean.

“2. The cerebellum is greater than the physiological mean.

“3. There frequently exists an asymmetry between the lobes (not peculiar to epilepsy). The increase
of weight is sometimes found on the right and sometimes on the left side. Equality is the exception.

“4. In no form of mental disease (excepting perhaps general paresis, which is accompanied also by
epileptiform crises) have we met with so marked and constant a variation between the weights of
the hemispheres as exists in epilepsy.”
41 Referred to by Axenfeld.

Drasche, Green, Greenhow, Löbel, and others have detailed cases in which tuberculous deposits were
undoubtedly the causes of the disease.

Kussmaul and Tenner, Hoffman, and others have held that a stenosis of the superior part of the
vertebral canal may explain, through pressure upon the cord, the genesis of the attack, and Kroon found
asymmetry of the medulla oblongata.
The microscopical changes that have been found in brains where no gross lesion was apparent are by
no means distinctive. I have myself examined the brains of many epileptics with discouraging results.
The varying granular cell-degeneration, capillary dilatation, and exudative changes are common
enough. In several cases of cortical epilepsy I found more or less advanced degeneration of the great
cells in limited regions.

By far the most important and exact changes are those observed in the cases of sensory epilepsy. I
have elsewhere collected some continental cases. In brief, areas of occipital softening or degeneration
have been discovered in those cases with hallucination, sensory expressions, and hemiopia. In one
case attended by hallucination of smell the autopsy disclosed the following:

M. M——, was a stout Irish woman about forty years of age. She had suffered from a light form of
epilepsy dating from the tenth year, and resulting, as she stated, from a fall, when she struck her head
and was unconscious thereafter for some hours. No scar was visible, however. No satisfactory history
could be obtained regarding her early life and the first paroxysms. In the beginning these were rather
frequent, and she had as many as four or five a month. They afterward diminished in number and
severity, and for many years she had but three or four in the course of the year. They were not very
severe, and she was enabled to pursue her work as a housemaid, but did not keep her places for any
great length of time. She rarely bit her tongue, but usually frothed at the mouth and became livid and
convulsed for a short time. There was no history of one-sided spasms. As I have stated, I could gain no
accurate account of the previous attacks, except that she nearly always had an aura of a peculiar
character, which was a prominent feature of the seizure and very pronounced. She suddenly perceived
a disagreeable odor, sometimes of smoke, sometimes of a fetid character, and quite uncomplicated by
other sensory warnings; and afterward became unconscious, and remained so for two or three minutes.
She was invariably able to describe her sensations when she recovered, which she always did when I
asked her, comparing her warning to the smell of burning rags, to the smell from a match, and, as she
expressed it, it sometimes rose up in her head and choked her. She was under my observation for one
or two years, but eventually developed phthisis, and died, her attacks occurring from time to time until
her death.

Besides well-marked tuberculous lesions in the lungs, there was little of interest so far as the visceral
examination was concerned. The brain was removed and its peculiarities were carefully observed. A
great quantity of fluid was found, especially at the dependent portions of the membranes and in the
ventricles, while the dura was thickened and pearly in spots. There was a condition that might be
likened to a low grade of hemorrhagic pachymeningitis, and at the base of the brain old plastic changes
were found, there being adhesions, especially in the region of the middle lobes, but more particularly on
the right side and near the median line. The brain as a whole was small, and weighed forty-one ounces
and a fraction. The sulci were deep and gaping, and the convolutions were distinct. There was no
atrophy of the fore-brain convolutions, and no other pathological appearance was presented except that
found in the meninges, but at the lower part of the temporo-sphenoidal lobe of the right side an
appearance was found of an exceedingly interesting nature. At this point a decided shrinkage of tissue
was discovered, with depression and adhesion of the pia, the induration involving the uncinate gyrus
and parts of the adjacent convolutions, as represented in the drawing. No induration or softening of the
great motor tracts was observed, and the optic thalamus and parts adjacent were uninvolved, as was
the cord. An attempted microscopic examination, undertaken some months subsequently, was
unsatisfactory, because of the bad condition of the brain, the preserving fluid having been improperly
made. The olfactory nerves were not involved. The third frontal convolution was examined, but no
disease was found there. Consequently, it is to be inferred that no lesion of the external root of the
olfactory nerve existed.
 FIG. 27.

Lower Face of Right Hemisphere.

DIAGNOSIS.—Having spoken of epilepsy as in most instances a

symptomatic disorder, it would be proper to confine this section to
the differentiation of the simpler and more classical form of the
idiopathic disorder from certain purely eclamptic attacks or those due
to cerebral tumor or coarse degeneration. The epileptic attack itself
is to be considered from its time of happening, its duration, the
element of unconsciousness, its associations, and the antecedent
history of the individual. It may be confounded with the similar
phenomenon dependent upon cardiac weakness, uræmic poisoning,
toxic or alcoholic saturation, etc.

Of course, when we find recurring seizures with a certain amount of

what Carter-Gray calls quasi-periodicity, preferring perhaps the night,
the early morning, or only the daytime, we are almost sure of
epilepsy. This supposition is strengthened by the association with
attacks of petit mal. The duration of an attack, which may be from a
few seconds to several minutes, is also a guide, for in certain toxic
and other paroxysms the rule is for a succession of attacks to occur.

The question of consciousness is one that has drawn forth a great

deal of discussion, especially with reference to medico-legal cases. I
think the majority of clinicians are agreed that loss of consciousness
is an absolute belonging of epilepsy, yet there are cases in which the
lapse is scarcely perceptible. It is a dangerous precedent to
establish, for the convulsive symptoms in such cases are taken from
the epileptoid category. It is quite true that there are many hemi-
epilepsies in which the intellectual condition is one that may easily
be mistaken. I have seen numerous cases in which an apparent
conservation of consciousness remained throughout a slight
monospasm, but I do not feel at all sure of this; and in cases of
aborted or masked epilepsy there is a dual mental state which would
readily deceive the lay observer. The case of Mrs. S—— is an
example of this kind. After the obvious subsidence of the dramatic
and conspicuous feature of the fit she remained for hours and days
in a state of undoubted transposition, performing acts which required
something more than a high degree of automatism—going to the
table, talking about certain subjects which were suggested, with
apparent ease, but not connecting them intelligently with her
surroundings, as she would before and after the epileptoid state.
After a time she apparently resumed her normal state, but was
entirely unconscious of the happenings of her previous hours or
days, not even recollecting her simplest actions. Julian Hawthorne's
hero in Archibald Malmaison, though not drawn by a physician's pen,
suggests the state of which I speak, and it has the merit of being
based upon one of the elder Forbes Winslow's interesting cases.

When we find paroxysmal attacks occurring in individuals with

atypical heads, thick swollen lips, scarred tongues, and irregular
teeth, we may strongly suspect the patient to be epileptic. To these
we may add the appearance of the eyes, the fishy, lack-lustre
expression which betokens old epilepsy. The hands are clammy and
the skin mud-colored; the hair is dry and coarse; and the body often
has a death-like odor.

In children, certain mental peculiarities are to be inquired into.

Unnatural brightness or dulness—what may be called the clumsy
organization—is often present, and the muscular use is often
imperfect. We find that there is often but little nicety in walking, in
using the hands, in speaking, or after learning to write there is an
incapacity, with ever so much teaching, to develop a character or
style. Such children can never become ambidextrous. These little
points may seem trifling, but to the physician who carefully studies
his cases they may prove of great help. The history of the nights may
often lead to the discovery perhaps of a long-existing nocturnal
epilepsy. Incontinence of urine, blood upon the pillow, nightmares,
morning headache, and petechiæ betoken unsuspected night
attacks; and Le Grand du Saulk mentions the case of a young
Englishman who committed a purposeless crime and was
discovered to be epileptic, the diagnosis being confirmed by an
antecedent history of nocturnal seizures, and subsequent watching
resulted in the discovery of many night attacks.

As to special conditions with which the epilepsy may be confounded,

I may refer to cardiac weakness. It not rarely happens that simple
fainting attacks are confounded with those of an epileptic nature.
Such is the case more often in heat-prostration, when some rigidity
attends the loss of consciousness. The duration of such a state, the
condition of the pulse and color, however, will easily clear up any
doubts upon the part of the observer. The existence of a cause
should also be considered, and the fact that usually the epileptic
paroxysm is sudden, while a feeling of depression and feebleness
precedes the fainting attack, should be remembered. I may present
in tabular form the points of difference:

EPILEPSY. SYNCOPE.
Loss of consciousness Loss of consciousness follows
sudden. feeling of faintness.
Period of complete Unconscious throughout, no
unconsciousness usually convulsions.
short.
The existence of auræ of a The existence of preliminary vague
well-defined type. prostration, nausea, and irregular
heart action.
Often involuntary discharge Quite rare or never.
from bowels and bladder.
Patient usually falls into heavy After slight weakness patient is
sleep or is indifferent after anxious and worried, and quickly
convulsion. seeks relief.

The difficulty of diagnosis, however, is only in cases of petit mal.

There are light forms of auditory vertigo that may resemble
vertiginous epilepsy. In the former there is never loss of
consciousness, and the patient refers to the rotary character of the
vertigo. A history of antecedent attacks, tinnitus, aural disease, and a
certain constancy which is not a feature of petit mal, may be
mentioned.

There are cases, however, which are puzzling, and come under the
head of auditory epilepsy rather than auditory vertigo; and in these
there is a multiplicity of expressions, the auditory symptoms
predominating.

Of uræmic convulsions it is hardly necessary to speak. There is a

previous history of renal disease which the microscope and less
delicate tests will reveal, and clinically there is antecedent headache,
some stupidity, and not unrarely thickness of speech and
somnolence. There are some cases, however, which are obscure. I
have known patients with chronic renal disease—such as waxy
kidney, for instance—to develop a species of epilepsy, the
paroxysms recurring from time to time and behaving very much as
the idiopathic disease would; and their occurrence would mark some
imprudence in diet or exposure, and their disappearance an
improvement in the patient's general condition. The attacks were not
classical, inasmuch as there seemed to be but one stage of violent
clonic convulsion, preceded by intellectual dulness, and followed by
a semi-comatose condition which was far mere profound than the
somnolent stage of epilepsy. The movements were not accompanied
by a great degree of opisthotonos or pleurosthotonos.

Alcoholic and absinthic epilepsies are usually preceded and followed

by symptoms indicative of profound saturation.

The consideration of hysterical epilepsy may be found elsewhere,

but it may do to briefly refer to some cases which do not present the
phenomenon first described by Charcot and Bourneville. The
ordinary hysterical attack is never attended by loss of
consciousness, by any of the pupillary changes so constant in
epilepsy, by the mobility of the pupil between the attacks which is
present in a large number of true epileptic individuals. There are
never the succeeding changes of color, and the seizures are
commonly produced or attended by some emotional disturbance, or
are associated with ovarian disturbance.

Epilepsy is occasionally simulated by malingerers, and sometimes

the skill of the subject is so great as to even deceive the practised
eye. Prisoners, soldiers, and litigants may counterfeit an epilepsy,
and go through with great personal suffering to accomplish their
purpose. “Clegg, the dummy-chucker,” whose remarkable case has
figured in the medical journals, upon one occasion threw himself
from an iron platform to the stone floor of the jail, nearly twenty feet
below, to convince a suspicious physician of his honesty. The
simulator rarely bears close watching. The dilatation and contraction
of the pupil cannot be simulated, nor can the corneal or pupillary
insensibility. The fraud cannot voluntarily change his color, as is the
case in true epilepsy, and as a rule the thumbs of the impostor are
never flexed, as they should be. Suggestions for a purpose are
readily heard, and sometimes adopted, by the apparently
unconscious man. Gottardi42 lays great stress upon the use of the
ophthalmoscope as a means of detecting simulated epilepsy. He
calls attention to the frequency of retinal changes with facial
asymmetry and other evidences that suggest cerebral disease or
non-development. Gottardi has found that the pulse in true epilepsy
is always lower after an attack, but it soon reaches its normal
standard.
42 Abstract in Journal of N. and M. Dis., Oct., 1881, p. 843.

The differentiation of idiopathic epilepsy from that due to syphilis is

possible when we consider the element of pain. Besides the tibial
pains of syphilis, the epilepsy thus produced is often preceded by
intense frontal headache, while that of ordinary epilepsy follows the
attack. The syphilitic epilepsy is not attended by so great or
continued a loss of consciousness as the non-specific form, and the
movements are apt to be most violent on one side or the other. The
association of the attacks with various bodily signs, such as nodes,
old scars, alopecia, erosions, etc., and in connection with possible
cranial nerve-paralyses, will throw light upon its true character. The
paralyses referred to seem most frequently to involve the motor
ocularis, abducens, and patheticus. Syphilitic epilepsy, too, is quite
irregular in its time of manifestation, and is not unrarely followed by
aphasia; but the interparoxysmal mental state is one of extreme
dulness, memory being blunted and there being a peculiar hebetude.

PROGNOSIS.—Within the past quarter of a century the ideas of the

medical profession regarding the curability of epilepsy have certainly
undergone a change. The statistics of Bennett and others show that
since the introduction of the bromic salts the proportion of cures has
been decidedly increased. Nevertheless, the disease is a most
discouraging and troublesome one to manage, and especially is this
the case when it assumes the form of petit mal. The rapid recurrence
of light attacks is, as has already been said, very apt to lead not only
to mental enfeeblement, but is very often followed by very severe
paroxysms.

Epilepsy of a more or less constant form, in which the seizures

resemble each other, is far more incurable than that of variable type;
for example, we find that unilateral seizures are much more apt to be
associated with established cortical disease than when they are
general and simply explosive manifestations. It has been held that a
tendency to permanency is marked by a diminution in the extent of
the interval. This is by no means true. I have had cases under
observation for ten or twelve years in which attacks separated by
intervals of six months or one year marked the course of the
disease, in which frequent initial attacks were present. These cases I
regard as very bad so far as prognosis is concerned. I much prefer a
history of irregular and comparatively disorderly attacks. In female
subjects the menstrual influence is not always a bad factor. When we
are enabled to remove some production of an exciting cause in
connection with the catamenia the prognosis is more hopeful; but an
opinion must be expressed with great caution, especially in those
cases beginning at an early age and not after the establishment of
the menses. Traumatic cases are not always bad, but those in which
the element of heredity plays a part most certainly are, Herpin and
Gowers to the contrary; and though these cases for a time do well
under treatment, its good effects are not constant. Individuals with
misshapen heads, whose deformity suggests premature sutural
ossification, are not susceptible to the influence of treatment, and all
other osseous changes, such as exostosis, plaques in the dura, and
bony growths, whose existence can only be guessed at or inferred
from suggestive appearances elsewhere, give rise to a variety of
epilepsy which is beyond the reach of drugs. With symptomatic
epilepsies the case is sometimes different, for while the seizures
which arise from the irritation of a cerebral tumor are almost as
hopeless as the form I have just mentioned, we know from
experience that the epilepsy of syphilis and other allied diseases,
and those of toxic origin, with the exception sometimes of those
occasionally due to alcohol or lead, are curable. The meningeal
thickening of alcoholic origin or the encephalopathy of lead may be
the pathological bases of very intractable paroxysms.

So far as age is concerned, it may be stated that many eclamptic

seizures of young children which are due to well-recognized irritable
causes are promptly cured if there be no hydrops ventriculi or
preossification of the coronal sutures, and if the epileptic habit is not
established. The epilepsies of six or eight years' standing are not
encouraging from a therapeutic point of view, and those of advanced
life developing in aged persons are equally unfavorable.

The treatment of epilepsy due to heat-stroke is by no means

satisfactory, and, though the attacks are often separated by long
periods, they are apt to recur in spite of drugs.

Gowers has prepared several valuable tables which show the

influence of age upon recovery. He says: “The following table shows
that age has a distinct influence on prognosis. The percentage of the
unimproved cases to the whole is 30 (43:143::30:100). The
percentage of the cases commencing at each age arrested and
unimproved is stated, and between brackets is indicated the excess
of the arrested or unimproved cases at each period of life over the
proportion for the whole 30 and 70 per cent. respectively:

———Cases.——— ———Percentage.———
Unimproved. Arrested. Unimproved. Arrested.
Under 10 14 29 32.5(+2.5) 67.5
From 10-19 23 45 34 (+4) 66
20 and over 6 26 19 81 (+11)
43 100 30 70

Thus, the proportion of the cases commencing under twenty in which

arrest was obtained is considerably less than the proportion of cases
commencing over twenty, the difference amounting to about 13 per
cent. The period of the first twenty years of life at which the disease
commences has little influence, but the prognosis is little better in the
cases which commence under ten than in those which commence
between ten and twenty: arrest is more frequently obtained. The
cases which commence in women at the second climacteric period
are also obstinate, although not sufficiently numerous to be
separately given.”

He also finds, from an analysis of the same cases, the fact noted by
others, that the prognosis is favorable in inverse proportion to the
duration of the disease.

Attacks which chiefly occur in the daytime are much more amenable
to treatment than the nocturnal seizures, and especially is this the
case in the tongue-biting form. Sudden blows upon the head or falls
have been known in isolated cases to effect an amelioration in the
patient's disease, but these examples are rare.

The existence of an aura is much better than if none existed.

Death from the attack itself is rare, yet in the large pauper institution
with which I was connected for many years I have known of several
cases. More often the death results from asphyxia resulting from a
bolus of food which chokes the patient or from a fall in some
dangerous place—into the fire or elsewhere. Accidental death from
drowning is more common than any other form.

The status epileptica into which patients sometimes pass who have
had many convulsions is occasionally a fatal termination of the
malady, and is always a serious feature.

The influence of different epochs in life is worthy of consideration: of

menstruation, of marriage, of pregnancy, and of the menopause
there is much to be said. I have sufficiently spoken of the
establishment of the menstrual flow, and I would only add another
word of caution against giving a too favorable prognosis except in
those cases of very recent origin. Marriage appears to have very
little to do with changing the attacks, unless they be of an hysteroid
character. I have never known epilepsy to influence the course of a
pregnancy in any unfavorable way, and I think this has been the
observation of others. Gowers refers to cases in which the attacks
ceased during the time the mother was carrying the child.

The occasional bad influence of the pregnant state has been

illustrated by a case reported by Terrillon.43 This example was a
woman who had been the victim of epilepsy of hereditary origin since
her seventh year. At the commencement of menstruation her attacks
became periodic, and recurred every two months, and she had
several two or three days before the flow. Two pregnancies followed
several years afterward. During the periods they were increased in
number and severity, and occurred several times daily. She had
more attacks at this period than in all the time after delivery.
43 Annales de Gynécologie, June, 1881, p. 401.

I have found that the relief of uterine flexion or the establishment of

menstruation has exercised a decidedly modifying influence for the
better in several cases.

Sometimes the disease is interrupted by the menopause, but very

often in my experience it has changed in type and been followed by
mental degeneration.
The prognosis of the epileptoid mental state is serious in the
extreme, and even when in early life the attacks are aborted or
changed to perversion of the intellect or emotions existing as a
complication, the hope of cure dwindles almost to nothing.

The spontaneous cure of epilepsy is rare. Its course, however, is

more often interrupted by some intercurrent disease. Of 33 cases
observed by Delasiauve in which there was some complicating
disease, such as erysipelas, pneumonia, pleurisy, acute articular
rheumatism, burns and contusions, scarlatina, erythema, or the
condition of pregnancy, it was found that in 25 cases there was a
decided improvement (une heureuse influence), and in 8 only was
there no modification of the attacks. Axenfeld is disposed to believe
that acute and febrile disorders more decidedly influence the course
of epilepsy than those of a chronic nature. The influence of either
may be small or may diminish the number of attacks without curing
the disease.

TREATMENT.—The treatment of epilepsy depends so much upon the

form of the disease that no arbitrary rule can be laid down upon
general principles, and we must bear in mind the necessity for
removing the exciting causes if possible, the preservation of the
balance of cerebral blood-pressure and cell-equilibrium, and the
nutrition of the cerebral mass. It may be our purpose to remove
various toxæmic or cachectic states as well. As a minor division of
treatment we must consider the abortion of the attack when auræ
are detected. It has been the custom, I think among too many, to
manage the disease in an empirical manner, depending upon some
routine course of treatment, such as the indiscriminate use of the
bromides, for example. I am convinced that the intractable character
of the disease has come to be greatly exaggerated through failures
attendant upon the wholesale use of the bromic salts, without regard
to the indication in each particular case. It behooves us first to select
a reliable bromide, and then to give it with relation to the time of the
fit, its severity, and the condition of the individual. The importance of
this has impressed me very often. An equally divided daily dose will
not do a patient who has matutinal attacks the same good as will a
large dose at night, and in certain anæmic individuals the bromides
very often increase the attack. Then, too, the cases in which
seizures of petit mal predominate are not benefited to the extent that
those are in which the repetition of severe attacks is the feature. The
bromide should always be well diluted and given when the stomach
is empty or nearly so. The bromide of sodium is, to my mind, the
most serviceable salt, and when given alone or combined with the
bromide of ammonium is better than the potassic salt or the various
others. It should be carefully kept in solution or in waxed-paper
powders in a tight preserve-jar. As to its method of administration, I
much prefer the use of a solution which shall combine other
adjuvants which I will presently mention, and separate powders as
well, which may be used to reinforce the dose. The latter are to be
employed by the patient in the event of an unlooked-for series of
attacks, and are to be used to the point of producing mild bromism at
the time. In certain cases it is all-important to take into consideration
the condition of the heart. In some cases where there is manifest
and continued cerebral congestion, with full vessels and hard pulse, I
have found that the combination with chloral or aconite was
desirable. In other cases where the heart's action was irregular and
weak my experience with digitalis and nitro-glycerin or with
strychnine was most happy. In those cases that passed large
quantities of clear urine of low specific gravity the action of nitro-
glycerin and digitalis has been most prompt, and the same has been
true of epilepsies of migrainous origin.

There have been various methods of using the bromide suggested

which are more or less practical. The writers of a few years ago
suggested the prompt production of bromism—a state in which the
patient should be kept for a long time. This I strongly disapprove of,
not only because the mental and physical depression is a very
disagreeable and sometimes permanent condition, but because I
have found that the attacks are often increased after a time, though
at first they may have been suppressed. Others believe in giving the
bromides at intervals, with periods when no medicine at all is
administered.
For my own part, I am in favor of the establishment of a mild
bromism which does not extend beyond a slight anæsthesia of the
fauces or the appearance of slight acne. If I find it necessary to
increase the dose, I give cod-liver oil, iron, and bark or some of the
many preparations of the hypophosphites for a time; and they do not
diminish the specific effects of the drug to any great extent. In the
event of a series of attacks I direct the patient to take an extra dose
at such time as will anticipate the seizure.

This treatment should be kept up for at least two or three years after
the attacks have disappeared, and it may be even necessary to
continue a bromide course in a small way for an unlimited period.

If there be an hysterical element, or if ovarian excitement is

supposed to have anything to do with the attacks, the combination of
cannabis indica is strongly recommended. This suggestion holds
good in the cases where migraine is associated with the epilepsy, or
the latter is an outgrowth of the former.

Next to the bromides of potassium and sodium I have been very

successful with the nickel bromide. I find that it is retained with little
trouble, producing no gastric derangement if taken after eating. A
syrup prepared by most of the good pharmacists is preferable to any
other method of administering the salt. Quite recently Leaman44 has
reported two cases of severe epilepsy which were greatly benefited.
His conclusion is that it does most good in the form of the disease
when the attacks are separated by long intervals.
44 Med. News, Apr. 18, 1885.

The bromate of potassium, which has been used by Weir Mitchell45

and Hinsdale, may be worthy of a trial. It should never be given,
however, in larger doses than five or ten grains thrice daily. These
investigators found that thirty grains slowed the heart very
considerably, and forty grains produced watery discharges from the
bowels and drowsiness. In their hands, notwithstanding these
disagreeable effects, it controlled the seizures. The hydrobromate of
conia is a comparatively new remedy which has been