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Year : 2007  |  Volume : 10  |  Issue : 1  |  Page : 3-11

My tryst with women in neurology

Department of Neurology, Vivekananda Institute of Medical Sciences, Kolkata, India

Correspondence Address:
Ambar Chakravarty
Department of Neurology, Vivekananda Institute of Medical Sciences, Kolkata
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How to cite this article:
Chakravarty A. My tryst with women in neurology. Ann Indian Acad Neurol 2007;10:3-11

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Chakravarty A. My tryst with women in neurology. Ann Indian Acad Neurol [serial online] 2007 [cited 2022 Aug 17];10:3-11. Available from:

The president's job is indeed a challenging one, but perhaps the most difficult one is delivering the Presidential Oration which I believe need to be based on one's own contribution. I have never been a great research worker in my life and it was therefore quite a job for me to choose the topic of my oration. I discovered at the end, that the only through research I had ever done in my life really concerns women in their various facets and roles. I have always been stimulated in every possible way by their presence - psychic and intellectual - the result had been a love and interest in the medical problems of women. When I was young and at the medical school, I wanted to be a gynecologist but soon discovered that I could not be contended with a subject with limited scope for diversification. And I turned towards my teenage love neurology but could never get out of my interest in the affairs of the women race. The result is the title of this oration. However, as I have been rather akathisic, shifting my interest from one topic to another in my life, my oration would really be a collection of short stories rather than a fiction.

It is always wise to follow the foot steps of illustrious predecessors and I wish to do this by following the tradition set by great men in the past by paying tributes to my subjects, the fairer sex in this context, quoting a few interesting but utterly true quotes that I could put my hands on. But firstly let us consider wherefrom this interesting race women, really originate from as I quote from the Old Testament:

And the Lord God caused a deep sleep to fall upon Adam and he slept and he took one of his ribs and closed up the flesh instead thereof and the rib, which the Lord God had taken from man. Made He a woman

Old Testament, Genesis

It would also be of interest to note how the medical fraternity looked at this wonderful race and indeed a great organization like the Royal College of Physicians, London paid due credit to Alice Leevers by licensing her to practice medicine in 1586 and she was indeed a demented old wife! (College commentary, Royal College of Physicians, London, January 2006).

Now the following quotes would certainly pay 'rich tributes' to my subjects:

'In this book I propose with God's help, to consider diseases peculiar to women. And since women are. for the most part, poisonous creatures, I shall then proceed to treat of the bites of venomous beasts'

Arnold of Vallinova 1235-1311

Commentaries Book III

'Women, in whom the nervous system is generally more movable than in men, are more subject to nervous complaints and have them in higher degree'.

Roert Whytt 1764

Observation on .. Disorder

Commonly Called Nervous

'There are no worse occupations in this world than feeling a woman's pulse.'

Laurence Sterne 1713-1768

A Sentimental Journey

'Not Tonight; I have a Headache'

Napolean Bonaparte's wife

And this would bring me to discuss our studies in primary headaches in women.

   Initial Studies in Migraine in India (VIMS studies 1990-95) Top

A number of studies on the phenomenology of migraine in Indian patients (mostly women) were carried out at our Department between 1990-95[1] and the results are summarized in [Table - 1].

   Migraine Pain Location Top

In recent years, some of these features are being studied in greater detail. One aspect which has been studied in detail is migraine pain location at onset and during established headaches in 800 migraine patients (M: F = 1: 4.56)[2] The migraine diagnoses had been based according to the International Headache Society Classification (ICHD II) of 2004[3] and included: ICHD 1.1-668 subjects (83.5%); ICHD 1.2.1 - 18 subjects (2.25%) and ICHD 1.6.1 -114 subjects (14.25%).

The sites of migraine pain at onset and during established headaches are shown in [Table - 2],[Table - 3].

Two important observations are worth mentioning: In Indian patients with migraine, strictly unilateral headache occurred in only 40.5% patients and true hemicranial headache (oculo-fronto-temporoparietal or fronto-temporoparietal) occurred in only 1/5 th of all subjects on most (>50%) occasions of migraine attacks. These figures are in sharp contrast to overall experience in the west specially in the recently published report by Kelman[4] (hemicranial headache in 71.2% of subjects with episodic migraine and in over 60% of those with chronic migraine). In this context, the inclusion of unilaterality of migraine headaches in the diagnostic criteria (ICHD-2), perhaps needs careful re-consideration. Around 31% of subjects with unilateral onset of migraine pain had been side-locked.

Secondly, location of migraine pain at onset in the cervico-occipital region (noted in over a quarter of subjects in the in the present series) is worth noting and specially the occurrence of predominantly cervical onset pain in over 10% of subjects. This had not been addressed to adequately in the western literature. It is true of course, that most subjects in the present study with cervico-occipital location of pain at onset, subsequently experienced either holocranial or hemicranial headaches. But a little less than 10% of all subjects with migraine only experienced cervico-occipital pain on most (>50%) occasions of established migraine. Overlapping clinical aspects between common migraine and cervicogenic headaches had been commented upon earlier by Sjaastad et al[5] Ethnic variation in disease phenomenology is worth recording and may provide insights into pathophysiology.

As similar study had been carried out in 200 cases of pediatric migraine[6] (M:F =1:0.69; ICHD - 1.1-197 (98.5%); ICHD 1.2.1 -3 (1.5%) and the differences from adult patients are shown in [Table - 4].

   Chronic Daily Headaches in Women Top

Studies in primary chronic daily headaches (CDH) had been carried out in adults[7] and children.[8] Between 1998-1999, a total of 849 adult patients with primary chronic daily headaches were encountered and chronic migraine constituted the vast majority (699 out 849 patients); of these 205 subjects (M:F 34:71) who could be followed up for more than 1 year were studied in detail and reported. Chronic migraine constituted 169 out of the 205 patients and the salient clinical aspects are depicted in [Table - 5]. Their mean age was 39 years and male:female ratio was 1: 4.7.

From the results of this study we concluded that (1) CDH in India is not uncommon, (2) analgesic / ergot overuse need to be recognized early and (3) the average dose of analgesic implicated in CDH seems much less compared to that reported from the west. A study of CDH in children was carried out at a later date.[8] Compared to adults, CDH in children is uncommon. Only 22 cases where encountered over a 2 years period. The salient clinical differences between pediatric and adult CDH are depicted in [Table - 6].

   Women and Cluster Headache in India Top

Cluster Headache (CH) in relatively uncommon in Indian patients with hedache.[9] Between 1985-2002, 41 patients with episodic cluster headache (CH) and 7 patients and chronic cluster headache were encountered by the author's group and their clinical profile to depicted in Tables.

Not a single female patient was encountered in the series. Is this related to difference in life style? In India, at least judging from the present observation, CH seems to be a disease exclusively affecting the male sex.[9] Only 10% of affected patients in an Italian series were women.[10] The sex bias noted in Indian patients is worth mentioning. During an observation period of more than 30 years, Ekbom et al[11] noted a trend towards a decreasing male preponderance; the male: female ratio was significantly higher among patients with onset before rather than after 1970. The sex bias noted in the present study may be related to environmental factors related to lifestyle pattern differences between Indian women and their western counterparts. The importance of lifestyle pattern in the epidemiology of CH has been mentioned by Finkel[12] A decreasing male: female ratio has been noted,[11] perhaps attributable to lifestyle trends adopted by more women that were previously associated with men, such as tobacco use, alcohol consumption and working outside the home.

The present study was conducted in an institution which caters mostly for the middle-class Bengalee population of Calcutta and its neighbourhood. Tobacco use and alcohol consumption are still very uncommon amongst women in the Indian middle class population. This factor combined with the overall rarity of CH in the population itself probably accounts for the striking sex bias noted in the present study. Ethnic and racial difference may be involved but difficult to comment upon in a hospital-based study. Referral bias seems unlikely to explain the sex difference noted in the present study, as in our hospital migraine population the sex difference noted is very similar to western figures.

   Primary Headaches in Women Associated with Sexual Activity Top

The International Headache society (IHS) in its recent (2004) classification and diagnostic criteria of headache disorders[3] recognizes primary headache associated with sexual activity as a distinct form of primary headache disorder and prefers this terminology to previously used ones such as sex headache, coital cephalgia, benign vascular sexual headache and sexual headache. The association of headache with 'immoderate venery' (excessive sexual activity) has of course been known since the time of Hippocrates. In modern times, the first clear description of benign sexual headache (BSH) was made by Kriz[13] in 1970 and was soon followed by two brief reports by Martin[14] and Lance.[15] It was of course Lance[16] who published an editorial on the subject in the British Medical Journal.[17] Lance[16] and Paulson[18] recognized three different forms of BSH: Type 1 (a muscle contraction type of headache in the preorgasmic phase), Type 2 (a bursting vascular type of headache at height of orgasm) and Type 3 (a post-orgasmic postural headache due to CSF leak from dural tear). The IHS in 2004 made some modification to this classification system. Type 1 BSH has been designated as preorgasmic headache (4.4.1) and Type 2 as orgasmic headache (4.4.2.). Thunderclap headache is coded separately (4.6) but its association with sexual activity is clearly indicated when it should be coded as 4.4.2.

Sexual headache (precipitated by coitus or even masturbation) undoubtedly remains under-diagnosed and under-reported because of the reluctance on the part if sufferers to volunteer such information. This is all the more important in Indian society where significant social taboo prevents scientific studies on sexuality and medical disorders related to sexual activity.

Between 1985 ad 2004, a total of 24 (M:F 18:6) patients with primary headaches associated with sexual activity were seen at the author's clinic[19] their clinical / diagnostic aspects are given in [Table - 7]. The timing of headache was preorgasmic in men (14/18 vs none) orgasmic in women (1/18 vs 4/6) or masturbatory 3/18 vs 1/6). The single female patient presenting with a thunderclap headache posed diagnostic confusion and is described herein:

This 35-year-old lady, married for more than 10 years, presented one evening with acute onset of severe explosive headache with one bout of vomiting which developed in the same afternoon while taking a shower. Though found normotensive and having no meningeal sings, she was admitted with a provisional diagnosis of subarachnoid hemorrhage. CT scan and CSF study done within 24 hours were negative and the headache settled down with analgesic and tranquilizers in about 12 hours. Digital subtraction cerebral angiography (DSA) to exclude an unruptured aneurysm a week later was also negative. She was diagnosed to have had a 'thunderclap headache' but the cause was not apparent. Later on, on closer questioning, she admitted having had a 'particularly passionate' sexual act with her husband in the shower and developed the sudden explosive headache at the height of the orgasm.

The pathogenesis of primary headache associated with sexual activity remains largely unexplored. Years ago, Lance[16] raised the possibility of muscle contraction (selectively in neck and cranial muscles) in the genesis of pre-orgasmic cephalgia (Type 1 BSH) and some subjects with Type 1 BSH were prone to tension-type headache also. Patients at times can reduce the intensity of pre-orgasmic headache by adopting relaxation methods while continuing sexual activity. Also, some may experience similar headache even while playing only a passive role but feeling tension building up in the forehead, jaw and neck muscle. While the analogy with tension-type headache may appear simple, not all tension-type headaches are associated with increased contraction of pericranial muscles and this has not been documented to occur, either, in patients with pre-orgasmic cephalalgia of the dull pressing type.

It is tempting to hypothesize that cephalalgia (BSH Type 2) of vascular (throbbing/bursting) nature is related to the hemodynamic alterations which occur at the height of orgasm. The systolic BP may go up by 40-100 mmHg and the diastolic by 20-40 mmHg, accompanied by a significant rise in heart rate. This simple explanation also appears incomplete. A significant rise of BP and heart rate occurs in many individuals during several forms of activity in daily life, but they rarely produce headaches. Some individuals who develop benign exertional headache (which has been closely linked to BSH) usually experience these at times of performing strenuous work involving an increase in intrathoracic pressure. In some others, however, the headache may be related to a transient rise of BP and heart rate. Based on transcranial doppler studies, such headaches may result from impaired autoregulation of cerebrovascular smooth muscle. This dysregulation in susceptible individuals may render resistance vessels unable to respond adequately to increased blood pressure during exercise, resulting in abnormal vasodilation, vessel wall edema or increased blood volume.[20] A similar phenomenon may occur in subjects prone to benign orgasmic cephalalgia. The coexistence of exertional headache and orgasmic cephalalgia is well documented and such headaches may occur close to each other, suggesting a 'priming of vessels' by one type of headache for the other. On the other hand, although an increase in BP is universal during sexual activity, a recent study has shown that patients with sexual headache experience a significantly greater increase of BP during standardized physical exercise compared with healthy subjects and migraine patients.[21] This observation raises the question of altered central autonomic control of BP in these individuals.

Must All Patients with BSH Fulfill ICHD-2 Criteria?

Two cases (both women) recently described by the author needs attention.[22]

Case 1

A 32 year old lady married for over 8 years, never suffered from any significant headaches till the very first night of marriage when she had her first sexual experience. She developed dull band like holocranial headache of moderate severity unaccompanied by any nausea which began from the start of the foreplay and lasted till the end of the sexual act. Such headaches recurred every time whenever she had sex with her husband. Although she could achieve orgasm on most occasions, there had been no significant change in the intensity or nature of the ongoing headache with sexual excitement. Neurological evaluation was normal. Detailed interview revealed that she was a university graduate whereas her husband had school level education only, though he was quite well off and very caring. It was during sexual activity only and at no other times, the patient thought of this difference in their respective educational status and developed the headaches. However that thought and the accompanying headache immediately ceased, the moment the sexual act was completed. She volunteered that the thought never came to her mind at any other times and they were happily married. She underwent detailed psychological testing which failed to detect any evidence of an anxiety disorder or major depression. A number of counselling sessions with a psychologist however failed neither to solve her headache problem nor the intrusion of the aforementioned unusual thought only while having sex.

Case 2

A 30 year old lady, married for eight years, presented with recent onset (about one year) of moderately severe non-pulsatile, dull, holocranial tightening headaches occurring immediately after completion of sexual intercourse on almost all occasions. These headaches lasted for almost an hour. These were associated with some degree of 'inner irritability'. Neurological evaluation was normal. Closer questioning revealed severe frustration in the post-coital period out of failure to achieve satisfying orgasm inspite of 'all her efforts' while having sex and development of tension-type headaches. Such headaches never occurred at any other times. Detailed psychological testing was not done in this case.

Questions can be raised whether such headaches conform to the diagnostic criteria laid in the ICHD-2[3] and diagnosed as variant forms of primary headaches associated with sexual activity (code 4.4). Strictly speaking the answer would be in the negative. In Case 1, there had not been any increase in the intensity of the headache with mounting 'sexual excitement' - an essential component in the diagnostic criteria for both the preorgasmic and orgasmic forms. Also, some unusual psychic factor appeared to have been implicated in the genesis of the headaches in this case and involvement of psychic factors is not highlighted in the ICHD-2 diagnostic criteria.[3] In Case 2 also, tension-type headaches developed on many occasions immediately after having sex and some degree of anxiety and/or depression appeared to have been involved as well (frustration out of failure to achieve a satisfying orgasm). The ICHD-2 diagnostic criteria in essence takes into account of headaches occurring during the actual sexual act but do not clearly make any comment about headaches developing in the immediate post-coital period. A comment made by Cutrer and Boes[23] in a recent review my be relevant in this connection. "Sexual headaches my arise during the build up toward, at the moment of or during the minutes or hours after sexual orgasm resulting from intercourse or masturbation".

It is worth noting, that the term used in ICHD-2 is primary headache 'associated' with sexual activity and not 'by' or 'during' sexual activity. In this sense, the headaches experienced by the two women reported by the author, were indeed always 'associated' with sexual activity (though post-coital in one case).

   Women and Epilepsy Top

Perhaps the most fascinating aspect of neurology of women is the problem of women with epilepsy.

   Historical Aspect Top

Of all the great people with epilepsy, there stands the name of one women and she was Joan of Arc. She was born round the year 1410 in a hamlet of ancient Lorraine. At an early age she was distinguished by her passion for contemplation, her melancholy and her love of devotions. From the age of 13 she experienced frequent visual and auditory hallucinations, unknown voices resounding in her ears when she believed herself to be in prefect solitude. When older she thought herself visited by the Archangel Michel, by the Angel Gabriel, by Saint Catherine and Saint Margaret.

France was at war with the combined forces of England and Burgundy and her visions ordered her in the name of God to deliver the city of Orleans. As an example of her experiences, she said: 'I heard this voice to my right towards the church; rarely do I hear it without its being accompanied also by light. The light comes from the same side as the voice'

She was eventually captured and imprisoned by the Burgundians and subject to humiliation. She was arraigned by a court on charges of witchcraft and heresy, but still insisted that the saints appeared to her and spoke to her. There were not the outpourings of an overactive imagination. She insisted these were true heavenly voices. She was burned at the stake in Rouen when less than 20 yeas of age. It was noted that her heart failed to burn. One explanation of this was that she had tuberculosis. Thus, cerebral tuberculoma would explain the temporal lobe seizure disorder and a tuberculous pericarditis the robustness of her heart.[24] It has been suggested that Joan of Arc may have suffered from musicogenic epilepsy, her seizures being provoked by the sound of church bells.

Juvenile Myoclonic Epilepsy (JME) in Bengalee Women One of our recent works had been in relation to clinical and electroencephalographic aspects of JME amongst ethnic Bengalees and we tried to provide follow up data of 200 patients (males 68), who were followed up for a minimum period of 5 years.[25] All had myoclonus, while GTCS was present in 94.5% and absence in 6.5%. Seizures were precipitated by awakening (57.5%), sleep deprivation (69%), sound (9.5%), watching TV (3.5%), menstruation (7.5%) or stress of examination (2.5%).

The study population was dominated by women. Their interictal EEG was abnormal in 82% cases and showed generalized polyspikes or spike and waves (51%), generalized single spike (14%), generalized high amplitude slow waves (15%) or photoconvulsive response (2%). On treatment seizures remitted (76%) or reduced less than 90% for 8%, between 50-90% for 10% and less than 50% for 6% patients. When AEDs were withdrawn at three years (n=130) seizures relapsed (myoclonic jerks -66% and GTCS 34%). The 100% seizure recurrence noted in our population is obviously discouraging and somewhat higher than reports from western countries. No such long term follow up data is available from Indian workers in the field.

Does valproate produce polycystic ovarian disease (PCOD) in women with epilepsy?

The complex relationship between Valproate use and development of PCOD in women with epilepsy have been recently discussed by the present author elsewhere.[26] Without going into the debate about any cause - effect relationship, our experience with the problem needs highlighting.

The results of an earlier preliminary abdominal ultrasonographic study in a small number of women on Valproate monotherapy for a period of over two years[27] showed that six had normal ovaries, three had 6-8 cysts in both ovaries, two had smaller cysts in the ovaries with menstrual irregularities and three had normal sized ovaries with cysts less than 4 mm size.

More recently, in our study of JME patients[25] out of 132 female patients 16 developed frank features of PCOD at 2 years follow up characterized by obesity, hirsutism, amenorrhoea / oligomnorrhoea, positive pelvic UGS, increased level of leutinising hormone (LH) or altered LH: FSH (Follicle stimulating hormone) and raised level of plasma testosterone. Attempt was made to switch therapy from Valprote (SV) to Clobazam(Clbz) in 16 of them with variable results (nor relapse of seizures (9), seizure recurrence requiring return to SV (7). Menstruation regularized and PCOD regressed on ultrasonogram in nine patients, six had decreased hirsutism and obesity.

The success rate had been over 50% and this had been gratifying. The problem of dealing with menstrual irregularities in women on Valproate is common and indeed a tricky one. The risk benefit ratio of seizure recurrence in one hand and normalizing menstrual cycle on the other demands well judged decision and action.

   Epilepsy and Pregnancy Top

This indeed is a multifaceted problem and no doubt a complex one. Only pregnancy outcome in women with epilepsy would be presented. In the course on my practice over the post 20 years, I had encountered a large number of women with epilepsy at various stages of pregnancy who had been mostly referred by obstetric colleagues for checking on their antiepleptic drug (AED) regime. Most could not be followed up for long to record the outcomes of their pregnancies. However, between 1985-2005, 60 women attending our clinic regularly had 68 pregnancies, the outcomes of which could be recorded adequately. Molar pregnancy and tubal pregnancy one each, spontaneous abortion (4, including one of cervical incompetence), term delivery (62). The babies Apgar score was >7 for 59 one each (on valproate) had tricuspid atresia, However, out of 22 children who were re-evaluated after the age of 1 year, two revealed presence of congenital heart diseases. No case of neural tube defect has yet been encountered by the author in women on valprote or any other anticonvulsant. The present author shares the majority view of avoiding use of valproate during pregnancy but this is not always practicable. Basic guidelines of pre-pregnancy counselling, monotherapy schedule, use of lowest possible dosage of AED and folic acid supplementation need to be stressed. Also babies born to mothers taking AED, need careful follow up.

   Psychogenic Seizures in Women Top

An ongoing study is looking at various aspects of psychogenic seizures in women. Betts and Boden[28] described five different clinical types of psychogenic seizures: swoon or cutoff behavior; tantrum; abreactive; deliberate stimulation ad pseudo-status epilepticus.

In absence of a good video-EEG system, we have evolved a modified diagnostic criteria for evaluation that includes (1) clinical features favouring diagnosis of psychogenic seizure (2) normal interictal record (3) normal ictal (spontaneous) record (when possible to record) (4) seizure induction by suggestion and normal ictal record. The preliminary data on 128 patients (3 men 125 women, aged 7 - 56) seen over 8 months (2005-2006) is showed the psychogenic seizures could be classified as swoon (101), tantrum (10, includes all three men), abreactive (17). The likely seizure precipitating factors were disturbed interpersonal relationship, bereavement, educational stress, sexual dissatisfaction, sexual abuse or fear of sexual abuse.

The question remains why do psychogenic seizures most commonly occur in women? Briefly speaking this could be due to the difference in expression of rage and resentment between men and women. Psychogenic seizure in women express rage, fear and helplessness and the communication of these effects more often than sexual conflicts and sexual symbolism. Perhaps in grown women psychogenic seizures are similar to the temper tantrums of young child, a type of behavior that express rage and aggression of those without physical power. Childhood sexual abuse is a relatively uncommon historical event in Indian women with psychogenic seizures. While secondary gain often plays a major role, suppressed aggression towards the opposite gender could be detected in about a third.

   Neurology of Eclampsia Top

Some years back, we performed clinical neurologic and neuroimaging studies in a group of patients with eclmpsia.[29] Between 1996-1999, a total of 19 patients with eclampsia were admitted in the Institute out of which 8 subjects had full neurological evaluation. Seizures were prepartum (5) or postpartum (3). All had generalized tonic clonic seizures. Headache (6), visual impairment (5) were the other symptoms. A CT scan of brain within 48 hours (n=7) showed symmetrical hypodensity in occipital lobes (7) more in white matter than grey matter with extension in to parieto temporal region (5). MRI confirmed these features in three patients. Follow up CT/MR showed that lesions completely resolved in all except in one where a small hypointense lesion persisted in the pons.

Neurological effects of pre-eclampsia can be antepartum or post-partum, the latter being more common. These are due to irregularities in the auto regulation of cerebral circulation. Disruption of the blood-brain barrier occurs due to both the hypertension-induced capillary damage and the immune-mediated endothelial dysfunction. This leads to extravasation of red cells and plasma into perivascular space causing cerebral edema. Cerebral vasospasm, produced by a combination of reaction to hypertension, prostaglandin deficiency, defects in the X-NOS gene (coding for nitric oxide systhase) and endothelial damage, play an important role, producing ischemia and infarction in the brain tissue.[29] The impaired blood coagulation system and the abnormalities and deficiency of platelets predispose to intra-cranial bleeds. Thus, a varied picture of cerebral pathology, showing evidence of cerebral edema, micro-infarcts, cortical petechie and pericapillary hemorrhage are observed in the brains of patients with pre-eclampsia or eclampsia, which clinically manifest as headache, visual disturbances, confusion and seizures.

Neurological disorders not encountered in women

I do not wish to discuss genetic / chromosomal disorders which do not generally occur in females for obvious reasons. I would like to mention about two conditions which I have almost never encountered in any female patient in India.

Why women do not get micturition syncope?

Micturition syncope is a common clinical problem which needs differentiation form other causes of syncope and epilepsy. The diagnosis is essentially clinical, based on circumstantial and situational evidences. Many diverse mechanisms seen to operate in the genesis of micturation syncope. Usually the problem occurs when a man stands to micturate after leaving a warm bed. There is vasodilatation and therefore peripheral vascular resistance is low. As he stands motionless, the muscle pump mechanism in the leg does not operate and the dependent capacitance vessels distend leading to a sharp decrease in venous return. He may have an enlarged prostate and may have to perform a valsava type of strain - increasing the intra-thoracic pressure, further diminishing the venous retrun to the heart acutely. Relief to baldder distension may also result in reflex vasodilataition as the result of a reduced stimulus from bladder stretch receptors. The fundamental physiology seems to be one of parasympthetic overactivity. The problem appears to be limited only to the male sex and the author doubts very much if any one had ever encountered a young healthy female subject with micturition syncope in this country. The sex bias is apparently related to the difference in the posture adopted during the act of micturation.[30] While most men would stand, women often squat (in India) or use a commode seat. A common advice given to men who had suffered a micturition syncope, is that they should micturate sitting on a commode seat or in the squatting position. The idea is simple. If one squats, the chance of a major injury from a fall as a result of a black-out would be less. But does squatting offer any additional benefit?

In an earlier communication[31] we reported that in a group of 67 healthy individuals (age 24-49 years; M:F 46:21), squatting produced a small but very significant rise of systolic BP(SBP) in the order of 8.09 4.04 ( P <0.001 ANOVA) but not so much in diastolic BP(DBP). In a subsequent study[32],[33] in 104 treated hypertensive subjects (age 26-60 years; M:F 67:37) we noted a much greater rise in SBP(14.4611.63; P <0.001 ANOVA compared to controls) and DBP(9.109.19; P <0.001 ANOVA compared to controls) on squatting. This rise in BP on squatting had been explained by the increase in adrenergic drive induced by the sustained fall in venous return resulting from mechanical hindrance to venous flow while maintaining the squatting posture (flexion of hip and knee) and the rise in intra-abdominal pressure produced by the pressure of the thighs on the anterior abdominal wall. Sustained lower limb muscle contraction during squatting also contributes to increased adrenergic drive. The author hypothesizes that this increased adrenergic drive would counteract any parasympathetic over-activity during mictuition in the squatting posture.[30]

Most women in India seem to 'immune' themselves from this common malady by their inherent posturing attitude (squatting) during the act of micturition. Squatting induced rise of blood pressure may not be desirable for all.[32],[33] But it seems there is a brighter side of the coin too!

Women who influenced neurological practice

My last topic for discussion is a little delve in to history of neurology to cite some examples of women who seemed to influence neurological practice through their illnesses. It is often noted that behind every successful man there is a female and neurologists / epileptologists are no exception. Hughlings Jackson married his cousin Elizabeth Dade Jackson when he was 30 years old. They had known each other from childhood and had been engaged for seven years. Although so little is known about Hughlings Jackson's personal life, it is recorded that his wife developed cerebral thrombosis and as a consequence of this illness she developed localized seizures. Hughlings Jackson thus witnessed these first hand and it is suggested that this experience must have inspired and coloured his lifelong interest in epilepsy and his descriptions of focal seizures. His wife died at the age of 31 and thereafter Hughlings Jackson seems to have become somewhat of a social recluse, took little interest in hospital politics and traveled as little as possible.

The other epileptologist whose work may have been inspired by a woman was William Lennox. He wanted to be a missionary in China, but was persuaded to obtain medical training. After this, he went to China with his wife and three children. Two of his daughters developed whooping cough and one of them had frequent nocturnal convulsions. She was 5 years of age at the time (1921) and the attacks continued for two years. On return to the USA a pediatric neurologist diagnosed epilepsy and suggested that the child should go to an institution. Lennox, whose preferred line of therapy was prayer and physical fitness (there were no substantive treatments for epilepsy at the time), was horrified and his lifelong devotion to the understanding and management of epilepsy was born.

   References Top

1.Ravishankar K, Chakravarty A. Primary headaches - the Indian experience. Ann Indian Acad Neurol 2002;5:107-12.  Back to cited text no. 1    
2.Chakravarty A, Mukherjee A, Roy D. Migraine pain location at onset and during established headaches: A clinic based study from Eastern India. Paper presented at the 16th Migraine Trust Symposium: London; 2006. (Abstracted in Cephalalgia. November 2006).  Back to cited text no. 2    
3.Headache classification committee of the International Headache Society. The International Classification of Headache Disorders. 2nd ed. Cephalalgia 2004;24:8-160.  Back to cited text no. 3    
4.Kelman L. Migraine pain location: A tertiary care study of 1283 migraineurs. Headache 2005;45:1038-47.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Sjaastad O, Fredriksen TA, Sand T. The localization of the initial pain of attack. A comparison between classic migraine and cervicogenic headache. Funct Neurol 1989;4:73-8.  Back to cited text no. 5    
6.Chakravarty A, Mukherjee A, Roy D. Migraine pain location at onset and during established headaches in children and adolescents: A clinic based study from Eastern India. Cephalalgia 2006/2007 (accepted for publication).  Back to cited text no. 6    
7.Chakravarty A. Chronic daily headaches: Clinical profile in Indian patients. Cephalalgia 2003;23:348-53.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Chakravarty A. Chronic daily headaches in children and adolescents: A clinic based study from India. Cephalalgia 2005;25:795-800.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Kriz K. Coitus as a factor in the pathogenesis of neurological complication. Cesk Neurol Neurochir 1970;33:162-7.  Back to cited text no. 9  [PUBMED]  
10.Martin EA. Headache during sexual intercourse (coital cephalalgia). A report on six cases. Ir J Med Sci 1974;143:342-5.  Back to cited text no. 10    
11.Lance JW. Headache occurring during sexual intercourse. Proc Aust Assoc Neurol 1974;11:57-60.  Back to cited text no. 11  [PUBMED]  
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[Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6], [Table - 7]


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