By P. Marik. Globe Institute of Technology.
Seizures look like astrocytes and there are different histological are treated with anti-epileptic drugs buy nizoral 200 mg free shipping fungus gnats white vinegar. Joint swelling following an injury Symptoms may be acute due to a haemarthrosis or appear more slowly due to an effusion buy nizoral american express fungus back. Again this Joint disorders often have pain as their presenting fea- may be a mono nizoral 200mg with mastercard fungus symptoms, oligo/pauci or polyarthritis. Joint pain is described as arthralgia if there is no ac- bution of joint involvement should be elicited including companying swelling or as arthritis if the joint is swollen. The nature of the onset, duration, timing and timing and provoking and relieving factors are impor- exacerbating factors should be noted. Arthritis may involve a ated features such as joint instability should be enquired single joint (monoarticular), less than four joints (oligo about. The relationship to exercise may be important, as inamma- tory disorders are often worse after periods of inactivity Joint stiffness and relieved by rest, whereas mechanical disorders tend Joint stiffness is another presentation usually associated to be worse on exercise and relieved by rest. A full systems enquiry is necessary as are characteristic of rheumatoid arthritis but may oc- many disorders have multisystem involvement. Less than 10 minutes in sensation including tingling or numbness are often of stiffness is common in osteoarthritis compared with due to abnormalities in nerve function. Establishment of iacstiffnessisaparticularfeatureofankylosingspondyli- the distribution helps to differentiate peripheral nerve tis. Locking of a joint is a sudden inability to complete damage from nerve root damage. Loss of function is im- amovement, such as extension at the knee caused by a portant as therapy aims to both relieve pain and establish mechanical block such as a foreign body in the joint or necessary function for daily activities. Seropositivity allows prediction of severity and the need for earlier aggressive therapy and Although some of the available tests used in diagnosis increases the likelihood of extra-articular features. Combin- ing tests may allow a clinical diagnosis to be conmed Joint aspiration (see Table 8. Rheumatoid factor: These are antibodies of any class Unexplained joint swelling may require aspiration to directed against the Fc portion of immunoglobulins. The aspiration itself may be of therapeu- The routine laboratory test detects only IgM antibodies, tic value lowering the pressure and relieving pain. It is which agglutinate latex particles or red cells opsonised often coupled with intra-articular washout or instilla- with IgG. It is the presence of these IgM rheumatoid tion of steroid or antibiotic as appropriate. Examina- factor antibodies that is used to describe a patient as tion of the synovial uid may be of diagnostic value (see seropositive or seronegative. Local spread from a soft tissue infection atively birefringent, whereas the crystals of pseudogout may also occur. Previously Haemophilus inuenzae was seen in young children, Many modalities of joint imaging and direct visualisa- but it is now rare due to vaccination. Patients with tion are used to diagnose and follow the course of mus- sickle cell anaemia are prone to osteomyelitis due to culoskeletaldisordersandareoftenusedincombination. The ndings in individual conditions will be described r Direct spread from local infection may occur with later. Streptococcus, Staphylococcus, anaerobes and gram- r X-ray: Many musculoskeletal disorders have charac- negative organisms. Pathophysiology Comparison of X-ray changes over time is especially In children the long bones are most often involved; in useful in monitoring disorders that have a degenera- adults, vertebral, sternoclavicular and sacroiliac bones tive course. In- r Ulrasound is of value in examining the joint and sur- fections from a distant focus spread via the blood stream rounding soft tissue. In children the organisms usually diagnosing the cause of a painful hip not amenable to settle in the metaphysis because the growth disc (physis) palpation. Acute inammation occurs accompanied by a rise in It can demonstrate both bone and soft tissue disor- pressure leading to pain and disruption of blood ow. In children infectious conditions prior to X-ray changes, it is of the physis acts as a physical barrier to intra-articular great value in identifying malignant bone inltration spread. Bone and joint infections Clinical features Presentationrangesfromanacuteillnesswithpain,fever, swelling and acute tenderness over the affected bone, to Acute osteomyelitis an insidious onset of non-specic dull aching and vague Denition systemic illness. Complications Age r As thebonehealsandnewboneisformed,infectedtis- Normally seen in children and adults over 50 years. Aetiology Investigations Previously, chronic osteomyelitis resulted from poorly r The X-ray nding may take 23 weeks to develop. It now occurs more fre- raised periostium is an early sign that may be seen quentlyinpost-traumaticosteomyelitis. With healing there is sclerosis and seques- Pathophysiology trated bone fragments may be visible. Blood cultures are positive in the bone may remain dormant for years giving rise to 50%. Clinical features The clinical course is typically ongoing chronic pain Management r and low-grade fever following an episode of acute os- Surgical drainage should be used if there is a subpe- teomyelitis. There may be pus discharging through a si- riosteal abscess, if systemic upset is refractory to an- nus. However, if the pus is retained within the bone or tibiotic treatment or if there is suspected adjacent join the sinus becomes obstructed, rising pressure leads to an involvement. Par- enteral treatment is often required for a prolonged period (24 weeks) prior to a long course of oral an- Investigations tibiotics to ensure eradication. Theperiostiummayberaisedwithunderlying with a third-generation cephalosporin to cover for new bone formation. Management r Adequate analgesia is essential and may be improved Discharging sinuses require dressing, and if an abscess with splints to immobilise the limb (which also helps persists despite antibiotic therapy it should be incised to avoid contractures). Prolonged combined parenteral antibiotics to reduce associated muscle disuse atrophy and to are required. In early stages the joint space is preserved, but later there is narrowing and ir- Tuberculous bone infection regularity with bone erosion and calcication within adjacent soft tissue. Incidence Patients with tuberculosis have a 5% lifetime risk of Management developing bone disease. Chemotherapy with combination anti-tuberculous agents for 1218 months (see page 105). Rest and trac- tion may be useful; if the articular surfaces are damaged, Age arthrodesis or joint replacement may be required. Geography Septic arthritis Major illness in developing countries, with increasing Denition incidence in the developed world. Aetiology Tuberculous osteomyelitis is usually due to haematoge- Aetiology nous spread from a primary focus in the lungs or gas- Joint infection arises most commonly from haematoge- trointestinal tract (see pages 105 and 154). Other mechanisms include local trauma or creased the incidence of tuberculosis and tuberculous an adjacent infective focus such as osteomyelitis. The patient complains of pain and later swelling due to Pathophysiology pus collection.
Motor function /response Posture of the patient: o Quadriparesis and flaccidity: suggest pontine or medullary damage o Decorticate posturing: flexion of the elbows and the wrists with supination of the arms buy nizoral in united states online fungus gnats in grass, and extension of the legs order 200 mg nizoral overnight delivery antifungal liquid cvs, suggests severe bilateral or unilateral hemispheric or diencephalic lesion (damage above the midbrain order cheapest nizoral and nizoral antifungal nappy cream. Differential Diagnosis: Psychogenic Coma (hysteric coma): patient often has history of psychiatric illness, and non physiologic response on physical examination. Management Ideally the, care of comatose patient is started together with the initial assessment to identify the etiology. This treatment is given if hypoglycemia is even remote possibility, and thiamine is given with glucose in order to avoid eliciting Wernicke disease in malnourished o Naloxone(0. Seizure and Epilepsy Learning objectives: at the end of this lesson the student will be able to: 1. Definition: Seizure is a paroxysmal event due to abnormal excessive discharge of cerebral neurons. Depending on the distribution of the discharge, the manifestations may be: Motor Sensory Autonomic or Psychiatric manifestation. Epilepsy is a syndrome characterized by recurrent (two or more) unprovoked seizure attacks, due to a chronic, underlying process in the brain. This definition implies that a person with a single seizure, or recurrent seizures due to correctable or avoidable circumstances, does not necessarily have epilepsy. International classification of seizures: Epileptic seizures can be classified in many different ways. Commonly used classification is the one developed by International League against Epilepsy. This classification is useful in understanding underlying etiology, selecting appropriate treatment and understanding the prognosis of seizure type. Analysis of 468 epileptics seen in neurology clinics of Addis Ababa showed highest incidence in males aged 11-20 years. The commonest type of seizure was found to be grand mal seizure accounting for 60% of all cases. Etiology of seizure or risk factors: The causes of epilepsy/seizure are vary greatly in different age groups and across different regions of the world Idiopathic or cryptogenic: in which the cause is unknown, accounts for the majority. Partial Seizures: these are seizures, which arise from localized region of the brain. This seizure activity may spread over one side of the body (Jacksonian march) to involve larger body part. The patient is unable to respond appropriately to visual or verbal commands during the seizure, and has impaired recollection or awareness of ictal phase. These are usually tonic-clonic type and difficult to differentiate from primary generalized tonic-clonic seizure. Generalized seizures There are seizure disorders which arise from both cerebral hemispheres simultaneously, with without any detectable focal onset. After 10 20 seconds the tonic phase evolves to clonic phase characterized by bilateral jerking clonic movement involving the whole body. Patients gradually regain consciousness over minutes to hours, and during this transition there is typically a period of postictal confusion, headache, muscle ache and fatigue that can last for many hours. Complications Status epilepticus Accidents Hypoxic brain damage Mental retardation and impairment of intellectual function Sudden death Psychosocial (Social stigma). Diagnostic approach/Evaluation Patients history and physical examination can aid in the determination of whether or not a seizure or some other transient event was responsible for the patients symptoms History should include: - History of the event Presence of any prodromal symptoms Description of seizure by reliable observer 527 Internal Medicine Post ictal symptoms Urinary incontinence, myalgia and tongue bite or oral lacerations are clues to the proper diagnosis. Differential Diagnosis for Seizure Syncope Psychogenic seizure (hysteric conversion) Transient Ischemic attack Migraine 528 Internal Medicine Management: Goal of therapy: Complete control of seizure Prevent development of complications and socioeconomic consequences. Avoidance of precipitating factor Maintain normal sleep schedule Avoid taking excess alcohol Reduce stresses using, physical Exercise, meditation or counseling 3. General principles: An attempt is usually made to prevent subsequent seizure using a single agent, in order to limit side effects. The addition of a second drug is associated with worsening of adverse effects; hence care should be taken, before one decides to add a second drug to the original regimen. Phenytoin: is the usual prescribed as a second line drug in resource limited settings like ours mainly because of its availability and cost. It is often given for the treatment of partial seizure Dosage: a low initial dosage with gradual increase is advised. Side effects Aplastic anemia Dizziness drowsiness 531 Internal Medicine Skin rash Transient diplopia When to stop antiepileptic drugs? The more severe and long lasting a patients active epilepsy before remission, the greater the risk of relapse. When to refer patients to a neurologist or tertiary level hospital Failure to respond to treatment Recurrence of previously controlled seizure Change in clinical pattern of seizure Appearance of previously absent symptoms/sign Development of side effects of a drug 4. Surgical interventions include Temporal lobe resection Corpus callosum sectioning Status epilepticus A condition characterized by continuous or repetitive discrete seizure with impairment of consciousness during interictal period, which lasts for more than 30 minutes. Patients may have mild clonic movement of only the fingers, or fine, rapid movement of the eyes. Complications of Status epilepticus: Aspiration Hypoxia Metabolic acidosis Hypotension Hyperthermia Rhabdomyolysis and associated myoglobinuria Multiple physical injures including vertebral bone fracture Irreversible neuronal injury Management 1. Parkinsons Diseases and other movement disorders Learning objectives: at the end of this lesson the student will be able to: 1. Parkinsonism: Definition: Parkinsonism is a clinical syndrome characterized by:- Bradykineisa: slowness and paucity of movement Tremor: This occurs at rest Rigidity Snuffling gate and Flexed posture Etiologies: 1. These degenerative changes are believed to be due to accumulation of the presynaptic protein -synuclien. Bradykinesia/akinesia: It is the most disabling feature which interferes with all aspects of daily living. Patients have trouble in walking, rising from seated position, turning over in bed, dressing etc. Brief regular interruption of resistance during passive movement may give rise tocogwheels rigidity. Pharmacotherapy of motor symptoms: Therapy to control motor symptoms should be initiated as soon as the patients symptoms begin to interfere with the quality of life. This drug has minimal effect on symptoms when used as monotherapy or as an adjuvant to Carbidopa/levodopa. Advanced Therapy c) Levodopa/Carbidopa Formulation (Sinemet, Atamet) Levodopa: is converted to dopamine by presynaptic neuron and therefore increase the amount of neurotransmitter available to the post synaptic dopamine receptor. Some of the neuroprotecitve treatment trails arte Non steroidal anti-inflammatory agents Estrogens replacement therapy in post menopausal women Selegilline therapy delays the need for levodopa therapy by 9 -12 months in newly diagnosed patients. Studies demonstrated that patients who remain on Selegilline for 7 yrs experienced slower motor decline. Therapy of non motor symptoms Insomnia due to nocturnal akinesia : treated with night time supplemental dose of Carbidopa /levodopa Depression : Responds to anti depressants like Amitriptyline Psychotic patients: first remove anticholinergics and amantadine if the patient is taking.
Aetiology The cavity or syrinx is in continuity with the central Aetiology canal of the spinal cord purchase nizoral 200mg without prescription fungi septa definition. Some cases have been re- ation of the cerebellar tonsils and medulla through the ported post-vaccination 200mg nizoral fungus gnats control uk. Pathophysiology Pathophysiology The expanding cavity may destroy spinothalamic neu- Inammation may be due to vasculitis buy discount nizoral 200 mg urine antifungal, or the preceding rones in the cervical cord, anterior horn cells and lateral infection. Clinical features Mixedupper and motor neurone signs, sometimes in an odd distribution, it is usually bilateral, but may affect Clinical features one side more than the other. The patient trinsic muscles of the hand, with loss of upper limb may complain of a tight band around the chest, which reexes and spastic weakness in the legs. Upper motor neurone changes are loss of pain and temperature sensation signs are found below the lesion. C5 to T1 with preservation torneurone signs are found at the level of the lesion, due of touch. Neuropathic joints, neuropathic ulcers and to involvementofthe anterior horn cells. Other investigations are di- fth nerve nuclei causes loss of facial sensation, classi- rected at the underlying cause, e. Microscopy Disorders of muscle and Affected muscles show abnormalities of bre size, with neuromuscular junction bre necrosis, abundant internal nuclei and replacement by brofatty tissue. Muscular dystrophies Complications Myotonic dystrophy Patients show neurobrillary tangles of Alzheimers dis- ease in the brain with ageing. Infants born to mothers Denition withmyotonicdystrophymayhaveprofoundhypotonia, Inherited disease of adults causing progressive muscle feeding and respiratory difculties, clubfeet and devel- weakness. Sex M = F Prognosis The condition is gradually progressive with a variable Aetiology/pathophysiology prognosis. Each generation has increased numbers of repeats resulting in an earlier onset and more severe dis- Denition ease. Thegenecodesforaproteinkinase,whichispresent Acquired disorder of the neuromuscular junction in many tissues, the mechanism by which this causes the characterised by muscle fatiguability, ptosis & dys- observed clinical features is unknown. Clinical features Incidence Patients develop ptosis, weakness and thinning of the 4in100,000. The thymus appears to be in- r Nervestimulation shows characteristic decrement in volved in the pathogenesis, with 25% of cases having evoked muscle action potentials following repetitive athymoma and a further 70% have thymic hyperplasia. Management r Myasthenic syndromes can be caused by d- Oral anticholinesterases such as pyridostigmine treat the Penicillamine, lithium and propranolol. Care ference with and later destruction of the acetylcholine should be taken when prescribing other medications as receptor. Thymectomy in older patients ercise increases the degree of muscle weakness, and rest with hyperplasia alone is more controversial, tumours allows recovery of power. This can cause difculty with swal- r Plasmapheresis and intravenous immunoglobulin are lowing and eating the chin may need support whilst usually reserved for severe acute exacerbations. The respiratory muscles may be affected in Severity uctuates but most have a protracted course, amyasthenic crisis requiring ventilatory support. Ini- exacerbations are unpredictable but may be brought on tially the reexes are preserved but may be fatiguable, by infections or drugs. Aetiology/pathophysiology Investigations Antibodies directed against the presynaptic voltage- r Edrophonium (anticholinesterase) Tensilon test gated calcium channels have been detected. The ocular and smell) although this may be found in elderly patients bulbar muscles are typically spared. Test ability of each nos- gravis, weakness tends to be worst in the morning and tril to detect several common smells. The optic nerve Investigations Anatomy r Nerveconduction studies show an incremental re- The optic nerve carries information from the retina via sponse when a motor nerve is repetitively stimulated, the optic chiasm, the lateral geniculate bodies and optic in direct contrast to the ndings in myasthenia gravis radiation to the occipital lobe where the visual cortex is (where there is a decremental response). Vision Management Clinical features Treatment of the underlying tumour can lead to These depend on the location of the lesion (see Fig. Plasmapheresis and intravenous im- Field loss: munoglobulin may be used, and drugs which increase r Eye lesions include diabetic retinal vascular disease, acetylcholine release from presynaptic terminals appear glaucoma, retinitis pigmentosa. The olfactory receptors lie in the olfactory epithelium r Tunnel vision occurs in other conditions, e. The axons form bundles which pass through the Diseasesaffectingtheopticnerveandtherestoftheoptic cribiform plate (ethmoid bone) to the olfactory bulb. The olfactory bulb neurones project through the olfactory tract to the Abnormalities of the optic disc frontal cerebral hemispheres, the medial temporal lobe and the basal ganglia. Denition The optic disc is where the retinal bres meet to form Function the optic nerve. Diseases affecting the optic nerve may Smell cause the disc to look abnormal: 1 Swollen, i. Papilloedema Management This term should be reserved to describe swelling of the Directed at the underlying cause. The increased pressure causes axonal transport to become abnormal, causing swelling of the Horners syndrome nerves. The term is often used to cover all causes of a swollen disc, but this is the differential diagnosis of papilloedema (see Table 7. Optic atrophy Optic atrophy may follow any damage to the optic nerve, Clinical features particularly after ischaemia, optic neuritis and optic The condition presents with unilateral pupillary con- nerve compression. Associated features Clinical features may include a hoarse voice (due to either recurrent la- The degree of visual loss depends on the underlying ryngeal nerve palsy or lower cranial nerve involvement), cause. Optic neuritis and ischaemic neuropathy typically or signs in the neck, chest or hands pointing to the level cause early visual loss. Location of lesion Examples r Inferior ramus travels with superior ramus, but gives Sympathetic chain Carotid artery aneurysm or branches to inferior rectus and medial rectus muscles. It exits pos- wall of the cavernous sinus, then divides into: teriorly from the brainstem and winds around to the r Superior ramuswhich enters orbit via the lower part front, then passes in the lateral wall of the cavernous of superior orbital ssure within a tendinous ring. It exits from the brainstem and 1 V supplies the forehead, the upper eyelid and eyeball. Pain and temperature bres are also carried on the three divisions back to the trigeminal ganglion, but then dive Specic causes down into the medulla to the spinal nucleus of V which Particularly at risk from raised intracranial pressure or extends as far as the upper cervical cord. If touch is lost, but pain and temperature intact, Emerges as two roots (large sensory and small motor the lesion has to be in the pons or medulla. The Function motor nerve cell bodies are in the facial nerve nucleus in The motor components supply the muscles of mastica- the pons. Here the sensory nerve Management cellbodies cause a swelling called the geniculate ganglion If the patient is unable to close their eye completely, ar- and give off the nerve to stapedius and chorda tympani ticial tears should be used and the eye taped shut at (taste and lacrimation) before exiting the skull through night to prevent corneal ulceration. In cases that do not resolve tars- (frontalis) receives some innervation from each hemi- orrhaphy (suturing of upper to lower lid, laterally) may sphere, so that unilateral upper motor neurone lesions be necessary. Cosmetic surgery and/or reinnervation us- cause sparing of the forehead, whereas unilateral lower ing a lingual nerve transfer for example, can be used for motor neurone lesions cause forehead involvement. Function Prognosis Muscles of facial expression and taste of the anterior two A signicant proportion do not completely resolve and third of the tongue. The auditory bres arise from the cochlea and pass to the pontine auditory nucleus.
While voluntary contractions of the anal sphincter can occur during sexual arousal and are sometimes used by women to facilitate or enhance arousal buy discount nizoral line fungus gnats cannabis yield, involuntary contractions occur only during orgasm (2 purchase 200 mg nizoral otc fungus gnats larvae picture, p discount nizoral 200mg mastercard fungus gnats worms. Such contractions are more frequently observed during masturbation than during coitus. As with uterine contractions, few studies on anal sphincter contractions during orgasm have been published (9). A number of questionnaire studies have reported that orgasm through stimulation of the so-called G-spot (named after Ernst Grafenberg, who report- edly rst described the phenomenon) causes a substantial number of women to expel uid from their urethra (11). However, there has been no scientic evidence to support the assertion that women ejaculate a uid distinguishable from urine at the time of orgasm. Moreover, there has not been consistent evidence for any anatomical structure or spot on the anterior vaginal wall apart from the known paraurethral glands and spongiosal tissue around the urethra, which could cause sexually pleasurable sensations when stimulated (12). Physiological changes noted to occur after orgasm (retrospective) include areolae (the pigmented skin area around the nipple of the breasts) decongestion, enhanced vaginal pulse amplitude (measured by photoplethysmography), and raised prolactin levels. During sexual arousal, the primary areolae swell up, likely due to both vasocongestion and smooth muscle contraction. The volume expansion can become so marked that the swollen areolae hide a large part of the base of the erect nipples making it look as though they have lost their erection. At orgasm, the loss of volume is so rapid that the areolae become corrugated before becoming atter. In the absence of orgasm, the areolae detumescence is much slower and the corrugation does not develop. Changes in the blood supply to vaginal tissue before, during, and after orgasm were recorded by photoplethysmography in seven young women by Geer and Quartararo (13). Immediately after the end of orgasm, however, vaginal pulse amplitude was actually signicantly greater than before orgasm in ve of the seven women (71%) and was not signicantly less in the other two. The postorgasmic period of maximum amplitude lasts for $1030 s and then slowly returns to its resting level. Studies by Exton and colleagues (14) have reported that prolactin secretion (a peptide hormone secreted by the lactotrophic cells of the anterior pituitary gland) is not activated by sexual arousal per se but is specically activated and doubled in plasma concentration with orgasm. Orgasms can be induced via erotic stimulation of a variety of genital and nonge- nital sites. The clitoris and vagina (especially the anterior wall including Halbans fascia and urethra) are the most usual sites of stimulation, but stimu- lation of the periurethral glands (15), breast/nipple or mons (2, pp. Orgasms have been noted to occur during sleep (1,18,19), hence consciousness is not an absolute requirement. Cases of spontaneous orgasm have occasionally been described in the psychiatric literature where no obvious sexual stimulus can be ascertained (20). The precise mechanism that triggers orgasm has been a topic of debate for many years but, as of yet, no denitive mechanisms have been identied. Only very recently have investigators examined the brain areas activated during orgasm in women (21). Some of these areas may be more involved in the perception of sexual stimuli than with the actual triggering of orgasm. Further studies that compare brain imaging during sexual arousal without orgasm with brain imaging at orgasm are needed to determine whether there are any areas of the brain specically involved in generating orgasm. Masters and Johnson (2) claimed that all orgasms in women were physiologically identical regardless of the source of stimulation. However, they did not have the instrumentation to obtain detailed muscular recordings for possible differences between clitoral- and vaginal- induced orgasms. There is now some limited physiological laboratory evidence to suggest that different patterns of uterine (smooth muscle) and striated pelvic muscular activity may occur with vaginal anterior wall stimulation as opposed to clitoral stimulation (15). Several other physiological differences between male and female orgasms have been proposed. First, unlike men, women can have repeated (multiple) orgasms separated by very short intervals, and women can have extended orgasms that last for long periods of time (2). Secondly, men have a divided rhythmic pattern of muscular contractions that has not been noted in women (9). Thirdly, in men, once orgasm is initiated its further expression is automatic even if sexual stimulation is stopped. In contrast, if stimulation is stopped in the middle of either clitoral-induced or vaginal-induced orgasm, orgasm is halted in women (26). In terms of gender differences in the psychological experience of orgasm, written descriptions of orgasms by men and women with any obvious gender clues removed could not be differentiated by sex, when read by other males and females (27). It is generally accepted that female orgasms are not essential for reproduction, and any benet that they may have for female biology is, as yet, unclear. Early theorists believed that orgasm via intercourse activated ovulation and closed off the womb to air, thus facilitating conception (28). When it was later shown that the human female was a spontaneous ovulator at mid-cycle, and that this was unconnected to coitus, the discourse re-focused on the role of uterine suction created by orgasmic contractions in moving ejaculated spermatozoa through the cervix into the uterus and then fallopian tubes. However, there is now good evidence that the fastest transport of spermatozoa into the human uterus is actually in the sexually unstimulated condition (29). An essential feature of sexual arousal of the female genitalia is to create the expansion of the vagina (vaginal tenting) and elevation of the uterocervix from the posterior vaginal wall. By dissipating arousal and initiating the resolution of the tenting, orgasm may allow the earlier entry of the spermatozoa into the cervical canal and their subsequent rapid transport to the fallopian tubes. It has been suggested that women may use orgasm, initiated either from coitus or masturbation, as a way to manipulate the ejaculate in the vagina (30,31). This highly contentious concept is based on the amount of owback (semen/uid) lost from the vagina. The claim is that the amount of owback con- taining spermatozoa varies with the precise timing of the womans orgasm in relation to the time of deposition of the ejaculate into the vagina. Low sperm retention is thought to be associated with female orgasms that occur less than 1 min before vaginal deposition while maximum retention is thought to occur with orgasms occurring shortly after deposition. If orgasm occurs earlier than 1 min before the ejaculate, deposition sperm retention is the same as when there is no orgasm. According to Baker and Bellis (31) the effect of orgasm on sperm retention lasts only for the period of 1 min before semen deposition and up to 45 min later. An additional function of womens orgasm, which may play a role in the reproductive process, is that if the woman attains orgasm during coitus, the associated contractions of the vagina can facilitate male ejaculation. If prolactin in plasma is able to enter into the vaginal, cervical or uterine uids, it may inu- ence the entry of calcium into the sperm and this action could play a role in the activation of spermatozoa in the female tract (32). There have been a number of other explanations offered for why women have orgasms. To the extent that orgasm is an intensely pleasurable sensation, it serves as a reward for the accep- tance of the danger of coitus with its possibility of pregnancy and of possible death in childbirth. Orgasm serves as a means for resolving pelvic vasoconges- tion and vaginal tenting, and for inducing lassitude to keep the female horizontal and thereby reducing seminal owback.