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Hippocrates’ works (370 BC) Hippocrates’ works (370 BC)

Hippocrates’ works (370 BC) - PowerPoint Presentation

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Hippocrates’ works (370 BC) - PPT Presentation

The blood of females is subject to intermittent agitations and as a result the agitated blood makes its way from the head to the uterus whence it is expelled3 four landmark stages parallel ID: 204609

pms symptoms pmdd therapy symptoms pms therapy pmdd treatments cycles respect pharmacological premenstrual symptom menstrual women menses days recurrence

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Slide1
Slide2

Hippocrates’ works (370 BC)

The blood of females is subject to intermittent

‘agitations’ and as a result the ‘agitated blood’

makes its way from the head to the uterus whence

it is expelled.3Slide3

four landmark stages parallel

our understanding of the premenstrual disorders.

From the ‘agitations’ of Hippocrates (370 BC) to

premenstrual tension (PMT);1 recognition and description of symptoms

From PMT to PMS;2 in this period, the link between

the ovarian hormone cycles and symptoms was

recognized.

recognition and description of symptoms

attempt to define and

quantify premenstrual disorders and the theory of

progesterone deficiency was explored and refuted.

From PMDD to the present day; in this period there

has been the realization that women are sensitive to

normal levels of

ovulatory

progesterone, that this

possibly has a

neuroendocrine

explanation, and that

therapy can be achieved by altering

neuroendocrine

status with psychotropic drugs (notably selective

serotonin reuptake inhibitors [SSRIs]) or by elimination

of ovulation.Slide4

The diagnosis of PMS/PMDD – the current

debateSlide5

Current diagnostic criteria for PMS/PMDD

ICD-10

ACOG

DSM-IVSlide6

ACOG

Occur 5 days before menses

Remit within 4 days of onset of before menses

No recurrence at least until

day 13 of cycleSlide7

PMS can be diagnosed after the patient prospectively

documents at least one of the affective or somatic

symptoms during the 5 days prior to menses for three

menstrual cycles. Symptoms should be of such severity

as to impact social or economic performance. There

should be no concomitant pharmacological therapy,

hormone ingestion, or drug or alcohol abuse.

Other

psychiatric and medical disorders must have been

excluded as a potential cause of the symptomsSlide8
Slide9

DSM-IV

Occur during the last week

Remit within few days after

No recurrence at least until onset of follicular phaseSlide10

At least five symptoms, with at

least one of: depression,

anxiety, or tension, anger or

irritability, and monthly swings

Other qualifying symptoms are:

decreased interest, difficulty

concentrating, lack of energy,

changed sleep, overwhelmed,

out of control, change in

appetiteSlide11
Slide12

Other physical symptoms such

as breast tenderness, bloating

headaches, pain

Markedly interferes with work,

social activities, relationships

Most menstrual cycles during

past year

At least two consecutive cycles

Not merely an exacerbation of

another disorder

Not associated with

pharmacological, hormone,

alcohol or drug use or abuseSlide13

UNSOLVED ISSUES WITH CURRENT

DIAGNOSTIC CRITERIA

lack of universal agreement on the nature of the

PMS as well as lack of universal acceptance of the criteria

per se.

definition of PMDD as

a diagnostic entity, independent of PMS.Slide14

Any mood, behavioral or physical symptom(s), or

cluster(s) of symptoms that occur recurrently and cyclically

during the

luteal

phase of the menstrual cycle.

● The symptom(s) remit(s) shortly following the

beginning of menses and consistently do not exist

for at least 1 week of the follicular phase of most

menstrual cycles.

● The symptom(s) cause emotional or physical distress

and/or suffering and/or impairment in daily

functioning, and/or impairment in relationships.

● The recurrence,

cyclicity

, and timing of the cycle,

and severity of the symptoms as well as existence of

a

menstrually

related symptom-free period are documented

by daily monitoring and/or reports.Slide15
Slide16
Slide17

Proposed or researched PMS treatments

Non-pharmacological treatments:

● Counseling

● Relaxation therapy

● Psychotherapy

● Cognitive behavioral therapy (CBT)

● Stress management

● Homeopathy

Intravaginal

electrical stimulation

● Rest

● Isolation

● Yoga

● Aromatherapy

● Exercise

● Music therapy

● Hypnosis

● Dietary manipulation

● Salt restriction

● Self-help groups

Agnus

castus

● Irradiation of ovariesSlide18

Non-hormonal pharmacological treatments:

● Tranquilizers

● Antidepressants

● Lithium

● SSRIs initial studies

● Vitamin B6

● Beta-blockers

● Evening primrose oil

● Diuretics,

spironolactone

● Magnesium, zinc, and calciumSlide19

Hormonal treatments:

● Progesterone (

pessaries

, injections, vaginal gel)

Progestogens

(

norethisterone

,

dydrogesterone

,

medroxyprogesterone

acetate, Depo-Provera)

● COC pill: cyclical/continuous

● Testosterone

Bromocriptine

Mifepristone

, RU-486

Cyproterone

acetate

Tibolone

Danazol

,

gestrinone

Estradiol

(oral, patch, implant)

GnRH

agonist analogs

● Non-steroidal anti-inflammatory drugsSlide20

Surgical treatments:

● Hysterectomy

● Hysterectomy and bilateral

oophorectomy

● Endometrial ablation techniquesSlide21
Slide22

SHOULD PMS BE REGARDED AN

ENDOCRINE CONDITION OR AS

A BRAIN DISORDER?Slide23

women with premenstrual

complaints differ from controls

not with respect

to ovarian function, but with respect to how responsive

the target organs are to the influence of

gonadal

steroids.

One important target organ for sex steroids is the

central nervous system.

Receptors

in

many brain regions including the

amygdala

and the hypothalamus.Slide24

IS PMS DUE TO SEROTONERGIC

DYSFUNCTION?Slide25

many

studies however do lend support to the notion that

women with PMS/PMDD differ from controls with

respect to various indices of

serotonergic

activity, indicating

that serotonin in fact may play a significant part

in the

pathophysiology

of this conditionSlide26

recent pilot studies suggesting that symptomatic women differ from non-symptomatic controls with respect to uptake of a serotonin precursor and density of

serotonergic

5HT1A receptors, respectively.

Eriksson O, Wall A,

Marteinsdottir

I et al. Psychiatry Res 2006; 146:107–16.

Jovanovic

H,

Cerin

Å,

Karlsson

P et al.

Psychiatry Res 2006; 148:185–93.Slide27