Indian national calendar and other Indian calenders

Every major state in India has its own calendar And new year.

The Indian national calendar (sometimes called Saka calendar) is the official civil calendar in use in India. It is used, alongside the Gregorian calendar, by The Gazette of India, news broadcasts by All India Radio, and calendars and communications issued by the Government of India.
The term may also ambiguously refer to the Hindu calendar, and the Saka era is commonly used by different calendars as well.

The Shalivahana era, also known as the Saka era, is used with Hindu calendars, the Indian national calendar, and the Cambodian Buddhist calendar. Its year zero begins near the vernal equinox of the year 78.To determine leap years, add 78 to the Saka year - if the result is a leap year in the Gregorian calendar, then the Saka year is a leap year as well. Its structure is like the Persian calendar.

In leap years, Chaitra has 31 days and starts on March 21 instead. The months in the first half of the year all have 31 days, to take into account the slower movement of the sun across the ecliptic at this time.
The names of the months are derived from older, Hindu lunisolar calendars, so variations in spelling exist


Western Kshatrapas (35–405 BC) were Saka rulers of the western part of India (Saurashtra and Malwa: modern Gujarat, Southern Sindh, Maharashtra, Rajasthan). They were successors to the Indo-Scythians who invaded the area of Ujjain and established the Saka era (with Saka calendar), marking the beginning of the long-lived Saka Western Satraps kingdom.


The era was also used by Javanese courts from Old Javanese times until 1633, when it was replaced by Anno Javanico, a hybrid Javanese-Islamic system.

It is also this particular era which aided historians in dating the Laguna Copperplate Inscription, the earliest written document found in the Philippines.


The calendar was introduced by the Calendar Reform Committee in 1957, as part of the Indian Ephemeris and Nautical Almanac, which also contained other astronomical data, as well as timings and formulae for preparing Hindu religious calendars, in an attempt to harmonise this practice. Despite this effort, local variations based on older sources such as the Surya Siddhanta may still exist.


Vikram Samvat (Bikram Sambat, Vikram Samvat Vikram Samwat or Vikram's Era, is the calendar established by Indian emperor Vikramaditya. It is a popularly used calendar in India and the official calendar of Nepal.
The Vikrama Samvat was founded by the emperor Vikramaditya of Ujjain following his victory over the Sakas in 56 BCE, although it is popularly (and incorrectly) associated with the subsequent king Chandragupta Vikramaditya. It is a lunar calendar based on ancient Hindu tradition (see Hindu calendar and Vedic time keeping). The Vikram Samvat calendar is 56.7 years ahead (in count) of the solar Gregorian calendar. For example, the year 2056 BS began in CE 1999 and ended in CE 2000. In Northern India the calendar starts with the first day after the new moon in the month Chaitra, which usually falls in March/April in the Gregorian calendar. Again in Western India the same era begins with the first day after the new moon in the month of Kartika which usually falls in October and November in the Gregorian calendar. In Nepal, it begins in mid-April and marks the start of the solar new year.
In India, Saka Calendar is officially used but interestingly in the Hindi version of Preamble of The Constitution of India, the date of adoption of constitution 26 Nov 1949 is presented in Vikram Samvat (Margsheersh Shukla Saptami Samvat 2006 ). A confusion and ignorance there as well . . .

In Nepal, this is the calender in use.

This calendar derives its name from the original king Vikramaditya of Ujjain. After the rise of the Rana oligarchs in Nepal, Vikram Sambat came into unofficial use along with the official Shaka Sambat for quite some time. They discontinued Shaka Sambat in its 1823rd year and replaced it with Vikram Samwat for official use since then to date. Vikram Sambat came into official use in its 1958th year. The calendar is widely in use in western India, where it is known as the Vikram Samvat.
The date is supposed to mark the victory of king Vikramaditya over the Sakas, who had invaded Ujjain. To the new era was established to commemorate this event. Alternatively, it has been thought by some scholars to correspond to the Azes era, of the Indo-Scythian king Azes I, but this seems to be now thoroughly discredited by Falk and Bennett who place the inception of the Azes era in 47/6 BC.


In addition to these two major calenders, we have Tamil, Bengali and Malayali calenders. Karnataka, Andhra Pradesh, Assam and Orissa also have their own New years.

Bhrigu

Maharishi Bhrigu was a sage during the Vedic period, Treta yuga.
It was said that Maharṣi Bhṛgu insulted Lord Viṣṇu while trying to determine who amongst the Trinity of Brahma, Viṣṇu and Śiva is the greatest, but apologised immediately of his mistake and Lord Viṣṇu instead apologised to him. Upon seeing Lord Viṣṇu's humility Maharṣi Bhṛgu declared him to be the greatest.
But Lakṣmī (the goddess symbolising prosperity), wife of Lord Vishnu perceived it as an insult of her husband. She gave a curse to Maharishi Bhṛgu, that he and his community (Brahmins) to which he represents will be parted away from wealth.
After apologising from Goddess too, she suggested him to write Bhṛgu Saṃhitā which contains predictions. In this way, Brahmins can earn their living by telling past,present and future of people.
The Ashram of Maharishi was in present day Ballia (U.P.), India. Major part of Bhṛgu Saṃhitā was destroyed during Muslim Invasions at that time.
Maharishi Bhrigu was the first compiler of predictive astrology. He compiled about 500,000 horoscopes and recorded the life details and events of various persons. This formed a database for further research and study. This study culminated in the birth of the science (Śāstra) of determining the quality of time (Horā) and is the Bṛhat Parāśara Horā Śāstra.
After that, Maharishi Bhṛgu gave his predictions on different types of horoscopes compiled by him with the help of Lord Gaṇeśa in a brief and concise manner. The total permutations/possible horoscope charts that can be drawn with this is about 45 million. Maharishi taught this art of predictions to his son (Śukra) and other pupils. It is said that it was compiled by the Sage out of compassion for humanity so that humanity could cope with the pressures of its existence and move towards a more spiritual nature.

Idiopathic intracranial hypertension

Idiopathic intracranial hypertension (IIH), sometimes called by the older names benign intracranial hypertension (BIH) or pseudotumor cerebri (PTC), is a neurological disorder that is characterized by increased intracranial pressure in the absence of a tumor or other diseases (unknown etiology). The main symptoms are headache, nausea and vomiting, as well as pulsatile tinnitus (buzzing in the ears synchronous with the pulse), double vision and other visual symptoms. If untreated, it may lead to swelling of the optic disc in the eye, which can progress to vision loss which is the most serious complication of untreated disease.

IIH is diagnosed with a brain scan (to rule out other causes) and a lumbar puncture; lumbar puncture may also provide temporary and sometimes permanent relief from the symptoms. Some respond to medication (with the drug acetazolamide), but others require surgery to relieve the pressure. The condition may occur in all age groups, but is most common in young women, especially those with obesity.

Signs and symptoms

The most common symptom of IIH is headache, which occurs in almost all (92–94%) cases. It is characteristically worse in the morning, generalized in character and throbbing in nature. It may be associated with nausea and vomiting. The headache can be made worse by any activity that further increases the intracranial pressure, such as coughing and sneezing. The pain may also be experienced in the neck and shoulders. Many have pulsatile tinnitus, a whooshing sensation in one or both ears (64–87%); this sound is synchronous with the pulse. Various other symptoms, such as numbness of the extremities, generalized weakness, loss of smell, and incoordination, are reported more rarely; none are specific for IIH. In children, numerous nonspecific signs and symptoms may be present.

The increased pressure leads to compression and traction of the cranial nerves. Most commonly, the abducens nerve (sixth nerve) is involved. This nerve supplies the muscle that pulls the eye outward. Those with sixth nerve palsy therefore experience horizontal double vision which is worse when looking towards the affected side. More rarely, the oculomotor nerve and trochlear nerve (third and fourth nerve palsy, respectively) are affected; both play a role in eye movements. The facial nerve (seventh cranial nerve) is affected occasionally –- the result is total or partial weakness of the muscles of facial expression on one or both sides of the face.

The increased pressure leads to papilledema, which is swelling of the optic disc, the spot where the optic nerve enters the eyeball. This occurs in practically all cases of IIH, but not everyone experiences symptoms from this. Those who do experience symptoms typically report "transient visual obscurations", episodes of difficulty seeing that occur in both eyes but not necessarily at the same time. Long-term untreated papilledema leads to visual loss, initially in the periphery but progressively towards the center of vision.

Physical examination of the nervous system is typically normal apart from the presence of papilledema, which is seen on examination of the eye with a small device called an ophthalmoscope or in more detail with a fundus camera. If there are cranial nerve abnormalities, these may be noticed on eye examination in the form of a squint (third, fourth, or sixth nerve palsy) or as facial nerve palsy. If the papilledema has been longstanding, visual fields may be constricted and visual acuity may be decreased. Visual field testing by automated (Humphrey) perimetry is recommended as other methods of testing may be less accurate. Longstanding papilledema leads to optic atrophy, in which the disc looks pale and visual loss tends to be advanced.

Sadly most of the time neurological/ neurosurgical consultation is sought only after severe visual loss.

Causes

"Idiopathic" means "of unknown etiology". Therefore, IIH can only be diagnosed if there is no alternative explanation for the symptoms. Intracranial pressure may be increased due to medications such as high-dose vitamin A derivatives (e.g. isotretinoin for acne), long-term tetracycline antibiotics (for a variety of skin conditions) and hormonal contraceptives. There are numerous other diseases, mostly rare conditions, that may lead to intracranial hypertension. If there is an underlying cause, the condition is termed "secondary intracranial hypertension". Common causes of secondary intracranial hypertension include obstructive sleep apnea (a sleep-related breathing disorder), systemic lupus erythematosis (SLE), chronic kidney disease, and Behçet's disease.

Mechanism

The cause of IIH is not known. The Monro-Kellie rule states that the intracranial pressure (literally: pressure inside the skull) is determined by the amount of brain tissue, cerebrospinal fluid (CSF) and blood inside the bony cranial vault. Three theories therefore exist as to why the pressure might be raised in IIH: an excess of CSF production, increased volume of blood or brain tissue, or obstruction of the veins that drain blood from the brain.

The first theory that of increased production of cerebrospinal fluid, was proposed in early descriptions of the disease. However, there is no experimental data that supports a role for this process in IIH.

The second theory posits that either increased blood flow to the brain or increase in the brain tissue itself may result in the raised pressure. Little evidence has accumulated to support the suggestion that increased blood flow plays a role, but both biopsy samples and various types of brain scans have shown an increased water content of the brain tissue. It remains unclear why this might be the case.

The third theory suggests that blood flow from the brain may be impaired or congested. Only in a small proportion of patients has underlying narrowing of the cerebral sinuses or veins been demonstrated. Congestion of venous blood may result from a generally increased venous pressure, which has been linked to obesity.

Diagnosis

The diagnosis may be suspected on the basis of the history and examination. To confirm the diagnosis, as well as excluding alternative causes, several investigations are required; more investigations may be performed if the history is not typical or the patient is more likely to have an alternative problem: children, men, the elderly, or women who are not overweight.

Investigations

Neuroimaging, usually with computed tomography (CT/CAT) or magnetic resonance imaging (MRI), is used to detect any mass lesions. In IIH these scans may be normal, although small or slit-like ventricles and "empty sella sign" (flattening of the pituitary gland due to increased pressure) may be seen. An MR venogram is also performed in most cases (or according to some experts, only in atypical cases) to exclude the possibility of venous obstruction or cerebral venous sinus thrombosis.

Lumbar puncture is performed to measure the opening pressure, as well as to obtain cerebrospinal fluid (CSF) to exclude alternative diagnoses. If the opening pressure is increased, CSF may be removed for relief (see below). The CSF is examined for abnormal cells, infections, antibody levels, the glucose level, and protein levels. In idiopathic intracranial hypertension, by definition all of these are within their normal limits. Occasionally, the pressure measurement may be normal despite very suggestive symptoms. This may be attributable to the fact that CSF pressure may fluctuate over the course of the normal day. If the suspicion of problems remains high, it may be necessary to perform more long-term monitoring of the ICP by a pressure catheter.

Classification

The original criteria for IIH were described by Dandy in 1937.

Dandy criteria

1 Signs & symptoms of increased ICP – CSF pressure >25 cmH2O

2 No localizing signs with the exception of abducens nerve palsy

3 Normal CSF composition

4 Normal to small (slit) ventricles on imaging with no intracranial mass

They were modified by Smith in 1985 to become the "modified Dandy criteria". Smith included the use of more advanced imaging: Dandy had required ventriculography, but Smith replaced this with computed tomography. In a 2001 paper, Digre and Corbett amended Dandy's criteria further. They added the requirement that the patient is awake and alert, as coma precludes adequate neurological assessment, and require exclusion of venous sinus thrombosis as an underlying cause. Furthermore, they add the requirement that no other cause for the raised ICP is found.

Modified Dandy criteria

1 Symptoms of raised intracranial pressure (headache, nausea, vomiting, transient visual obscurations, or papilledema)

2 No localizing signs with the exception of abducens (sixth) nerve palsy

3 The patient is awake and alert

4 Normal CT/MRI findings without evidence of thrombosis

5 LP opening pressure of >25 cmH2O and normal biochemical and cytological composition of CSF

6 No other explanation for the raised intracranial pressure

In a 2002 review, Friedman and Jacobson propose an alternative set of criteria, derived from Smith's. These require the absence of symptoms that could not be explained by a diagnosis of IIH, but do not require the actual presence of any symptoms (such as headache) attributable to IIH. These criteria also require that the lumbar puncture is performed with patient lying sideways, as a lumbar puncture performed in the upright sitting position can lead to artificially high pressure measurements. Friedman and Jacobson also do not insist on MR venography for every patient; rather, this is only required in atypical cases (see "diagnosis" above).

Treatment

The primary goal in treatment of IIH is the prevention of visual loss and blindness, as well as symptom control. IIH is treated mainly through the reduction of CSF pressure and, where applicable, weight loss. IIH may resolve after initial treatment, may go into spontaneous remission (although it can still relapse at a later stage), or may continue chronically.

Lumbar puncture

A lumbar puncture in progress. A large area on the back has been washed with an iodine-based disinfectant leaving brown colouration. In this image the patient is seated upright, which can make the procedure easier to perform but makes any measurement of the opening pressure unreliable.

The first step in symptom control is drainage of cerebrospinal fluid by lumbar puncture. If necessary, this may be performed at the same time as a diagnostic LP (such as on in search of a CSF infection). In some cases, this is sufficient to control the symptoms, and no further treatment is needed.

The procedure can be repeated if necessary, but this is generally taken as a clue that additional treatments may be required to control the symptoms and preserve vision. Repeated lumbar punctures are regarded as unpleasant by patients, and they present a danger of introducing spinal infections if done too often. Repeated lumbar punctures are sometimes needed to control the ICP urgently if the patient's vision deteriorates rapidly.

Medication

The best-studied medical treatment for intracranial hypertension is acetazolamide (Diamox), which acts by inhibiting the enzyme carbonic anhydrase, and it reduces CSF production by six to 57 percent. It can cause the symptoms of hypokalemia (low blood potassium levels), which include muscle weakness and tingling in the fingers. Acetazolamide cannot be used in pregnancy, since it has shown to cause embryonic abnormalities in animal studies. Also, in human beings it has been shown to cause metabolic acidosis as well as disruptions in the blood electrolyte levels newborn babies. The diuretic furosemide is sometimes used for a treatment if acetazolamide is not well-tolerated, but this drug sometimes has little effect on the ICP.

Various analgesics (painkillers) may be used in controlling the headaches of intracranial hypertension. In addition to conventional agents such as paracetamol, a low dose of the antidepressant amitriptyline or the anticonvulsant topiramate have shown some additional benefit for pain relief.

The use of steroids in the attempt to reduce the ICP is controversial. These may be used in severe papilledema, but otherwise their use is discouraged.

Surgery

Two main surgical procedures exist in the treatment of IIH:

optic nerve sheath decompression and fenestration and shunting. Surgery would normally only be offered if medical therapy is either unsuccessful or not tolerated. The choice between these two procedures depends on the predominant problem in IIH. Neither procedure is perfect: both may cause significant complications, and both may eventually fail in controlling the symptoms. There are no randomized controlled trials to guide the decision as to which procedure is best.

Optic nerve sheath fenestration is an ophthalmological operation that involves the making of an incision in the connective tissue lining of the optic nerve in its portion behind the eye. It is not entirely clear how it protects the eye from the raised pressure, but it may be the result of either diversion of the CSF into the orbit or the creation of an area of scar tissue that lowers the pressure. The effects on the intracranial pressure itself are more modest. Moreover, the procedure may lead to significant complications, including blindness in 1–2%. The procedure is therefore recommended mainly in those who have limited headache symptoms but significant papilledema or threatened vision, or in those who have undergone unsuccessful treatment with a shunt or have a contraindication for shunt surgery.

Shunt surgery, usually performed by neurosurgeons, involves the creation of a conduit by which CSF can be drained into another body cavity. The initial procedure is usually a lumboperitoneal (LP) shunt, which connects the subarachnoid space in the lumbar spine with the peritoneal cavity. Generally, a pressure valve is included in the circuit to avoid excessive drainage when the patient is erect and therefore has a relatively high ICP. LP shunting provides long-term relief in about half the cases; others require revision of the shunt, often on more than one occasion—usually due to shunt obstruction. If the lumboperitoneal shunt needs repeated revisions, a ventriculoatrial or ventriculoperitoneal shunt may be considered. These shunts are inserted in one of the lateral ventricles of the brain, usually by stereotactic surgery, and then connected either to the right atrium of the heart or the peritoneal cavity, respectively. Given the reduced need for revisions in ventricular shunts, it is possible that this procedure will become the first-line type of shunt treatment.

In cases of severe obesity, gastric bypass surgery has been shown to lead to a marked improvement in symptoms.

Prognosis

It is not known what percentage of people with IIH will remit spontaneously, and what percentage will develop chronic disease.

IIH does not normally affect life expectancy. The major complications from IIH arise from untreated or treatment-resistant papilledema. In various case series, the long-term risk of ones vision being significantly affected by IIH is reported to lie anywhere between 10 and 25%.

Epidemiology

The incidence of IIH is strongly determined by sex and body weight. The figures in females are in women between 20 and 45 years old.

On average, IIH occurs in about one per 100,000 people, and can occur in children and adults. The median age at diagnosis is 30. IIH occurs predominantly in women, especially in the ages 20 to 45, who are four to eight times more likely than men to be affected. Overweight and obesity strongly predispose a person to IIH: women who are more than ten percent over their ideal body weight are thirteen times more likely to develop IIH, and this figure goes up to nineteen times in women who are more than twenty percent over their ideal body weight. In men this relationship also exists, but the increase is only five-fold in those over 20 percent above their ideal body weight.

Despite several reports of IIH in families, there is no known genetic cause for IIH. People from all ethnicities may develop IIH. In children, there is no difference in incidence between males and females.

From national hospital admission databases it appears that the need for neurosurgical intervention for IIH has increased markedly over the period between 1988 and 2002. This has been attributed at least in part to the rising prevalence of obesity, although some of this increase may be explained by the increased popularity of shunting over optic nerve sheath fenestration.

History

The first report of IIH was by the German physician Heinrich Quincke, who described it in 1893 under the name serous meningitis. The term "pseudotumor cerebri" was introduced in 1904 by his compatriot Max Nonne. Numerous other cases appeared in the literature subsequently; in many cases, the raised intracranial pressure may actually have resulted from underlying conditions. For instance, the otitic hydrocephalus reported by London neurologist Sir Charles Symonds may have resulted from venous sinus thrombosis caused by middle ear infection. Diagnostic criteria for IIH were developed in 1937 by the Baltimore neurosurgeon Walter Dandy; Dandy also introduced subtemporal decompressive surgery in the treatment of the condition.

The terms "benign" and "pseudotumor" derive from the fact that increased intracranial pressure may be associated with brain tumors. Those patients in whom no tumour was found were therefore diagnosed with "pseudotumor cerebri" (a disease mimicking a brain tumor). The disease was renamed "benign intracranial hypertension" in 1955 to distinguish it from intracranial hypertension due to life-threatening diseases (such as cancer); however, this was also felt to be misleading because any disease that can blind someone should not be thought of as benign, and the name was therefore revised in 1989 to "idiopathic (of no identifiable cause) intracranial hypertension".

Shunt surgery was introduced in 1949; initially, ventriculoperitoneal shunts were used. In 1971, good results were reported with lumboperitoneal shunting. Negative reports on shunting in the 1980s led to a brief period (1988–1993) during which optic nerve fenestration (which had initially been described in an unrelated condition in 1871) was more popular. Since then, shunting is recommended predominantly, with occasional exceptions.

Absence seizure (petit mal seizure)

Petit is a French adjective meaning “small” or "little illness", a term dating from the late eighteenth century. Absence seizure also known petit mal seizure is named so because of its apparently less difficult to manage seizures in comparison to the grandmal (Generalised tonic clonic) seizures ( which may not be so actually if we see the nature of the underlying disease as a whole).

Absence seizure involves a brief (usually less than 20 seconds), sudden lapse of consciousness (generalised epileptic seizures). Absence seizures are more common in children than adults. Someone having an absence seizure may look like he or she is staring into space for a few seconds.

Compared with other types of epileptic seizures, absence seizures appear mild. But they can be dangerous. Children with a history of absence seizure must be supervised carefully while swimming or bathing because of the danger of drowning. Teens and adults may be restricted from driving and other potentially hazardous activities.

Some children who have absence seizures also have grand mal seizures. Many children outgrow absence seizures in their teen years.

Symptoms and Signs of absence seizures include:

Impairment of consciousness is the essential ictal element and may be the only clinical symptom, but this is often combined with other manifestations. The hallmark of the absence seizures is abrupt and sudden onset impairment of consciousness, interruption of ongoing activities, a blank stare, possibly a brief upward rotation of the eyes. If the patient is speaking, speech is slowed or interrupted, if walking, he or she stands transfixed; if eating, the food will stop on his way to the mouth. Usually the patient will be unresponsive when spoken to. In some, attacks are aborted when the patient is spoken to. The attack lasts from a few seconds to half a minute and evaporates as rapidly as it commenced.

1.     Absence with impairment of consciousness only as per the above description

2.     Absence with mild clonic components. Here the onset of the attack is indistinguishable from the above, but clonic components may occur in the eyelids, at the corner of the mouth, or in other muscle groups which may vary in severity from almost imperceptible movements to generalised myoclonic jerks. Objects held in the hand may be dropped.

3.     Absence with atonic components. Here there may be a diminution in tone of muscles subserving posture as well as in the limbs leading to drooping of the head, occasionally slumping of the trunk, dropping of the arms, and relaxation of the grip. Rarely tone is sufficiently diminished to cause this person to fall.

4.     Absence with tonic components. Here during the attack tonic muscular contraction may occur, leading to increase in muscle tone which may affect the extensor muscles or the flexor muscles symmetrically or asymmetrically. If the patient is standing the head may be drawn backward and the trunk may arch. This may lead to retropulsion. The head may tonically draw to one or another side.

5.     Absence with automatisms. Purposeful or quasipurposeful movements occurring in the absence of awareness during an absence attack are frequent and may range from lip licking and swallowing to clothes fumbling or aimless walking. If spoken to the patient may grunt or to the spoken voice and when touched or tickled may rub the site. Automatisms are quite elaborate and may consist of combinations of the above described movements or may be so simple as to be missed by causal observation.

6.     Absence with autonomic components. These may be pallor and less frequently flushing, sweating, dilatation of pupils and incontinence of urine.

Mixed forms of absence frequently occur. These seizures can happen a few times a day or in some cases hundreds of times a day, to the point that the person cannot concentrate in school or other situations requiring sustained, concentrated attention.

·         Vacant stare

·         Absence of motion without falling

·         Lip smacking

·         Eyelid flutters

·         Chewing motions

·         Hand movements

·         Small movements of both arms

Absence seizures last only a few seconds. Full recovery is almost instantaneous. Afterward, there's no confusion, but also no memory of the incident. Some people experience dozens of these episodes each day, which interferes with their performance at school or work.

Children who are walking or doing other complex tasks during a seizure probably won't fall, though they'll be unaware.

Absence seizures in a child may occur for some time before an adult notices them, because they're so brief. A noticeable decline in a child's learning ability may be the first sign of this disorder. Teachers may comment about a child's inability to pay attention.

Absences seizures have two essential components:

·         Clinically the impairment of consciousness (absence)

·         EEG generalized spike-and-slow wave discharges.

Absence seizures are broadly divided in typical and atypical absence seizures. Typical absence seizures usually occur in the context of idiopathic generalised epilepsies and EEG shows fast >2.5 Hz generalised spike-wave discharges. The prefix “typical” is to differentiate them from atypical absences rather than to characterise them as "classical" or characteristic of any particular syndrome.

Atypical absence seizures:

·         Occur only in the context of mainly severe symptomatic or cryptogenic epilepsies of children with learning difficulties who also suffer from frequent seizures of other types such as atonic, tonic and myoclonic.

·         onset and termination is not so abrupt and changes in tone are more pronounced

·         Ictal EEG is of slow less than 2.5 Hz spike and slow wave. The discharge is heterogeneous, often asymmetrical and may include irregular spike and slow wave complexes, fast and other paroxysmal activity. Background interictal EEG is usually abnormal.

When to see a doctor

·         The first time you notice a seizure

·         If you have a new type of seizure

Seek immediate medical attention:

·         If you observe prolonged automatic behaviors — activities such as eating or moving without awareness — or prolonged confusion, possible symptoms of a condition called absence status epilepticus

·         After any seizure lasting more than five minutes

Causes

Often, no underlying cause can be found for absence seizures. Many children appear to have a genetic predisposition to them. Sometimes hyperventilation can trigger an absence seizure.

Many children gradually outgrow absence seizures over months to years.

Complications

While most children outgrow absence seizures, some people may find that they are:

·         Experiencing these types of seizures throughout life

·         Eventually experiencing full convulsions (grand mal or generalized tonic-clonic seizures)

Other complications can include:

·         Learning difficulties

·         Absence status epilepticus, a condition in which seizure behavior lasts longer than a few minutes

Precipitating factors

Typical absences are easily induced by hyperventilation in more than 90% of the patients. This is a reliable test for the diagnosis of absence seizures: a patient suspected of typical absences should be asked to overbreathe for 3 min, counting his or her breaths. Intermittent photic stimulation may precipitate or facilitate absence seizures; eyelid myoclonia is a common clinical accompaniment.

These types of seizures are also known to occur to patients suffering with Porphyria, and can be triggered by stress or other Porphrin - inducing factors.

Syndromes of idiopathic generalised epilepsies with absence seizures

These are childhood absence epilepsy, juvenile absence epilepsy, epilepsy with myoclonic absences and juvenile myoclonic epilepsy. Other proposes syndromes are Jeavons syndrome (eyelid myoclonia with absences) and idiopathic generalised epilepsy with phantom absences

Tests and diagnosis

Some children experience episodes that resemble absence seizures, but aren't seizures. Such episodes usually can be interrupted by calling the child's name or by touching his or her shoulder. True absence seizures, on the other hand, can't be interrupted by voice or touch. Absence seizures may occur in the middle of a child's conversation or physical activity.

Absences seizures have two essential components:

·         Clinically the impairment of consciousness (absence)

·         EEG generalized spike-and-slow wave discharges.

 

A detailed description of the seizures and blood tests can help rule out other potential causes of seizures, such as a chemical imbalance or the presence of toxic substances. Other tests may include:

·         Electroencephalography (EEG)

·         Brain scans Tests such as magnetic resonance imaging (MRI) can produce detailed images of the brain, which can help rule out other types of problems, such as a stroke or a brain tumor.

Absence seizures are broadly divided in typical and atypical absence seizures. Typical absence seizures usually occur in the context of idiopathic generalised epilepsies and EEG shows fast >2.5 Hz generalised spike-wave discharges. The prefix “typical” is to differentiate them from atypical absences rather than to characterise them as "classical" or characteristic of any particular syndrome.

Atypical absence seizures:

·         occur only in the context of mainly severe symptomatic or cryptogenic epilepsies of children with learning difficulties who also suffer from frequent seizures of other types such as atonic, tonic and myoclonic.

·         onset and termination is not so abrupt and changes in tone are more pronounced

·         ictal EEG is of slow less than 2.5 Hz spike and slow wave. The discharge is heterogeneous, often asymmetrical and may include irregular spike and slow wave complexes, fast and other paroxysmal activity. Background interictal EEG is usually abnormal.

 Treatments and drugs

Finding the right medication and dosage can be challenging, requiring a period of trial and error.

Taking the medications on a regular schedule is crucial to maintaining proper drug levels in the blood.

Often, the first drug prescribed for absence seizures is ethosuximide.

 However, other medications, such as valproic acid and lamotrigine, also are effective at controlling seizures. the lowest dose possible to start with and increase the dosage as needed to control the seizures is the norm. Most children can discontinue anti-seizure medications, under a doctor's supervision, after they've been seizure-free for two years.

The drug Lamictal has been linked to an increased risk of aseptic meningitis.

Women who need treatment for absence seizures are advised against using valproic acid while trying to conceive or during pregnancy. Women who can't achieve seizure control on any other medication need to discuss potential risks with their doctors.

Contraindicated drugs

The treatment of idiopathic generalized epilepsy is demanding because many antiepileptic drugs are either ineffective or exaggerate absences and myoclonic jerks. An antiepileptic drug is contraindicated not only when it exaggerates seizures but also when it is ineffective in controlling the seizures that it is supposed to treat. It may cause unnecessary adverse reactions and deprives the patient of the therapeutic effect that could be provided by another antiepileptic drug. Carbamazepine, vigabatrin, and tiagabine are contraindicated in the treatment of absence seizures, irrespective of cause and severity. GABA agonists vigabatrin and tiagabine are used to induce, not to treat, absence seizures and absence status epilepticus. Similarly, phenytoin, phenobarbital, gabapentin, and pregabalin should not be used in the treatment of absence seizures.

Limitations and research directions

In the treatment of absence seizures there is often insufficient evidence for which of the available medications has the best combination of safety and efficacy for a particular patient. Nor is it easily known how long a medication must be continued before an off-medication trial should be conducted to determine whether the individual has outgrown the absence seizures, as is often the case in children. To date there have been no published results of any large, double-blind, placebo-controlled studies comparing the efficacy and safety of these or any other medications for absence seizures. The studies that exist have been small and not produced clear conclusions.

Lifestyle and home remedies

A person with absence seizures may elect to wear a medical bracelet for identification for emergency medical reasons. The bracelet should state whom to contact in an emergency and what medications you use. It's also a good idea to let teachers, coaches and child care workers know about the seizures and tell them what to do in an emergency.

Even after they've been controlled with medication, seizures may affect areas of life, such as attention span and learning, will require close supervision for activities such as swimming. He or she will have to be seizure-free for reasonable lengths of time (intervals vary from state to state) before being able to drive.

Pathophysiology

The current understanding of the pathogenesis of absence seizures is based on animal models that generate generalised spike-and-wave discharges on EEG.

A reverberating circuit between the thalamus and cortex is the basis for this model, with the hypothesis being that

aberrant

rhythmic

oscillations

are generated in the circuit,

analogous to a mechanism that generates normal sleep spindles.

The reticulothalamic nucleus of the thalamus has been particularly implicated and contains a predominance of inhibitory GABA-containing interneurons.

 In this case, GABA-mediated activity may trigger absence seizures by inducing prolonged hyperpolarisation and activating low-threshold Ca^2+ currents.

 The concept of 't-type' or 'low-threshold' calcium channels playing a role in absence seizures is supported by the responsiveness of typical absence seizures to medicines such as ethosuximide, which is known to block these channels.

Multiple studies have been done in the attempt to identify a single gene locus for childhood absence epilepsy (CAE), juvenile myoclonic epilepsy (JME), or even the idiopathic generalised epilepsies (IGE) in general. Most identified genes associated with IGE involving absence seizures are for different types of ion channels (channelopathies). A gene for a component of GABA^A receptor has been implicated in a large family of JME with autosomal dominant inheritance. To date, CAE has been associated with defects in gamma-aminobutyric acid (GABA)^A receptor gamma2 subunit and voltage-gated Ca^2+ channel alpha-1A subunit (CACNA1A) among others.

 Mutations in a gene that encodes voltage-gated chloride channel CLC-2 has been associated with CAE, juvenile absence epilepsy (JAE), and JME.

There have been multiple studies demonstrating a locus that may predispose to JME on chromosome 6p as well as 15q; the latter maps to the alpha-7 subunit of the neuronal nicotinic acetylcholine receptor (CHRNA7).

 Recently, some cases of early-onset absence epilepsy have been attributed to mutations in the GLUT1 glucose transporter.

 http://www.youtube.com/watch?v=y3CHYeWj3eQ