The Effects of Curcumin on Epilepsy

A 2010 study entitled 'Protective effect of curcumin against seizures and cognitive impairment in a pentylenetetrazole-kindled epileptic rat model' looked at the effects of curcumin on epilepsy. Curcumin is known to have anti-convulsant properties and neuro-protective properties as well as the well known antioxidant and anti-inflammatory properties. The study investigated curcumin's potential to ameliorate seizures, cognitive impairment and oxidative stress in rats given pentylenetetrazole (PTZ), a drug known to induce seizures in rats and primates. The rats in the study were divided into three pretreatment groups, 100, 200 and 300 mg/kg curcumin. The results indicated that "pretreatment with curcumin ameliorates seizures, oxidative stress and cognitive impairment in PTZ induced kindling in rats. These results thus suggest the potential of curcumin as an adjuvant in epilepsy both to prevent seizures as well as to protect against seizure induced memory impairment."

A research paper (2017) entitled 'The effect of curcumin on epilepsy: an experimental review' looked at the databases of Science direct, PubMed and Google Scholar between 2008 and 2016to see what the existing research had to say about the effects of curcumin on epilepsy and seizures. The research was conducted using the search terms turmeric, curcumin, Diferuloylmethane, Epilepsy, and Seizure. The conclusion to the report stated that "Curcumin- the major extract of turmeric- has found to have antiepileptic effect according to recent investigations. It has been demonstrated to be safe in animal studies in a number of species. But, it has to be mentioned that the metabolism of curcumin between human and rats is different and humans can tolerate higher doses of this medicine without significant side effects. It not only has no critical adverse effect, but also can protect patients from other antiepileptic drugs severe side effects and hopefully it makes it possible to gradually decrease the dose of antiepileptic drugs in long-term combination therapy".

The History of Epilepsy

Epilepsy is a disorder with a long history. Epilepsy is referred to in the laws of Babylon in 2080 BC, (Rogan, 1992). The name epilepsy originally came from the Greek word ‘epilambanein’ which means to seize or to attack passively, (Griffin & Wyles, 1991). One of the first people to write about epilepsy was Hippocrates (460 – 377 BC) who wrote a book called ‘The Sacred Disease’. In his book, Hippocrates argued against the prevailing belief of the time that the aetiology of epilepsy was as a result of supernatural forces. This belief was espoused because epileptic attacks were thought to be brought about by changes in the environment such as the weather etc. The environment was thought to be the product of God, epilepsy was therefore thought to be a product of God and therefore ‘The Sacred Disease’. Hippocrates argued that the belief was the result of ignorance or fraud. Hippocrates believed that epilepsy was a disorder of the brain that could be explained in terms of humorous medicine and hypothesised that epilepsy was a result of an imbalance of phlegm in the brain that may be hereditary, (Temkin 1971).

Many years later, a story in the New Testament of the Bible led people to believe that epilepsy was caused by demon possession. In the story, Christ drove out an evil spirit from a young boy who has since being a young child, been thrown to the ground where he would foam at the mouth and convulse. Although Christ did not mention epilepsy by name, the story is thought to relate to epilepsy because of the close match of the boy’s symptoms with epilepsy. Over the centuries, people with epilepsy were ostracised from society because of the belief that epilepsy was the result of demon possession, (Meinardi 1989).

In the relatively recent past, the aetiology of epilepsy being the result of demon worship was replaced by the belief that epilepsy was due to excessive masturbation and sexual activity. Although a false belief, a drug was prescribed for epileptics to cure their supposed promiscuous sexual activity. The drug that was prescribed was Bromide. By a quirk of fate, Bromide happened to be the first effective anti-convulsant for epilepsy, (OHE 1971).

Although Hippocrates argued that epilepsy was a disorder of the brain, it was not until many centuries later that his hypothesis was confirmed although not in terms of humorous medicine. In 1860, the National Hospital for the Paralysed and Epileptic was opened in London. One of the Doctors who came to work at the hospital produced one of the first accurate descriptions of epilepsy, (Scott 1969). “Epilepsy is the name for occasional, sudden, excessive, rapid and local discharges of grey matter.” (Hughlings Jackson 1873) Hughlings Jackson’s description of epilepsy was later supported by the work of Hans Berger who in 1929 published a paper on the human Electroencephalograph. Electroencephalography measures the electrical activity of the brain that can be described in Jackson’s terms as being “local discharges of grey matter”.

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Causes of Epilepsy

The cause of epilepsy, like the classifications and types of epilepsy are broad and complex. In the past, the causes of epilepsy were divided into two areas which were idiopathic (primary) and symptomatic (secondary). Idiopathic epilepsy is epilepsy where no reason for the epilepsy can be found by investigating the sufferer’s history or through medical examination. Symptomatic epilepsy is epilepsy that has an underlying cause such as an injury to the brain. Symptomatic epilepsies can have many different causes including insults, neurovascular disease etc. In recent years it has been argued that the aetiology of epilepsy is more complex than the simple dichotomy of idiopathic and symptomatic causes. It has been argued that the appearance of epilepsy can be influenced by many factors that include genetics, the environment and normal physiological factors, (Griffin & Wyles, 1991).

The French League Against Epilepsy, Aircardi et al (1969), have argued that the genetic influence of epilepsy should be viewed in terms of an increased predisposition to convulse. The predisposition to convulse may not necessarily result in the appearance of a seizure because the individual may never come into contact with the environmental triggers that may precipitate a seizure. The avoidance of such triggers would therefore mitigate the expression of seizures. Brown (1976) has argued that the child of one epileptic parent has a two to three percent chance of developing epilepsy. However, the chance of developing epilepsy if both parents have epilepsy rises dramatically to twenty five percent.

Epilepsy is not always a discrete illness, that is to say epilepsy occurs in many individuals as a bi-product of an overall disorder or illness. An example would be that of a metabolic disorder such as hypoglycaemia which results in low blood glucose levels and resulting epileptic seizures. Although the individual does not have epilepsy, low blood glucose levels can precipitate an epileptic seizure. Low calcium levels and drugs, especially alcohol, can precipitate epileptic seizures.


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Classification of Epilepsy

Epilepsy can be defined in a number of ways. Firstly, an epileptic seizure can be described as either a generalised seizure, that encompasses all of the brain or a partial seizure that involves only part of the brain that is known as a focus. Generalised seizures fall within two categories that are primary generalised seizures and secondary generalised seizures. Primary generalised seizures are sudden onset seizures that involve both hemispheres of the brain. Secondary generalised seizures start with a focus as in a partial seizure and the seizure activity spreads across and to both hemispheres of the brain, (Rogan 1992).

An example of a generalised seizure is that of a tonic clonic seizure whereby the sufferer falls to the ground and exhibits tonus which is stiffening of the muscles and clonus which is twitching of the muscles. Tonus and clonus are usually then followed by a state of confusion before the sufferer proceeds into a deep sleep. Other examples of generalised seizures are absence seizures, myoclonic seizures and atonic seizures, (Rogan 1992).

Partial seizures are confined to one part of the brain. Partial seizures have also been divided into two categories that are simple partial seizures and complex partial seizures. Simple partial seizures can be further subdivided into two categories which are focal motor and focal sensory. A typical focal motor seizure would produce twitching of the muscles or bodily movements that are relative to the area of the brain that is experiencing abnormal electrical discharges. Focal sensory seizures are similar to focal motor seizures except the disturbances occur in perception and sensation such as visual or auditory distortions. Focal sensory seizures can occur in the temporal lobe which can produce feelings of deja’vu, (Rogan 1992).

Complex partial seizures involve an impairment of consciousness and can display behaviours that are inconsistent with the sufferer’s normal behaviour. The person may smack his/her lips, move objects and undertake activities without no obvious reasons for doing so. Complex Partial Seizures include seizure behaviour that used to be classified under Temporal Lobe Epilepsy and Psychomotor Epilepsy. Both simple and complex partial seizures can become secondary generalised seizures, (Rogan 1992).

There has been some controversy regarding the classifications of epilepsy. The findings of The Commission on Classification on Terminology of the International League Against Epilepsy (1981) differed markedly to the previous findings of the First International Classification of Seizures (Gastaut 1970; Gastaut 1973) which was used widely between 1969 and 1981. The revised system argues that the evolution of seizures should be described. The revised system argues that a seizure such as an absence which then proceeds to a tonic clonic seizure, would be described as a convulsive generalised seizure under the earlier classification system with no acknowledgement of the evolution of the seizure. Under the revised classification system, the aforementioned seizure would be designated as a non convulsive to convulsive seizure. Furthermore, the revised system argued that partial seizures should not be divided into categories dependent on clinical manifestations. Firstly a partial seizure that occurs without any conscious impairment is designated as a simple partial seizure. A partial seizure that involves conscious impairment is designated as a complex partial seizure. Under the original classification system, a complex partial seizure was defined as any partial seizure leading to complicated clinical manifestations with or without amnesia. This has led to considerable confusion with regard to what terms such as generalised seizure and complex partial seizure mean when being used without reference to the classification system being used.

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Electrical Activity in the Brain

The brain can be divided into three separate areas that are the Cerebrum, the Cerebellum and the Brain Stem, (Pinel 1997). It is the electrical activity of the rich nerve fibres that are found in the Cerebrum that are recorded by Electroencephalograph. The Electroencephalograph does not record the activity of single neurones but records the gross electrical activity between two electrodes placed on the scalp of a participant, (Binnie, 1982). Neurones, which are also known as nerve cells differ widely but all share some basic characteristics. All neurones contain a cell body, a nucleus and an axon, (Binnie 1982). Contained inside the neurone are high levels of positively charged potassium ions (K+). Outside of the neurone, positively charged potassium ion (K+) levels are low. The opposite is true of positively charged sodium ions (Na+). There are low levels of positively charged sodium ions (Na+) inside the neurone and high levels outside. The membrane of the neurone is permeable and positively charged potassium ions are able to leak out of the neurone and similarly positively charged sodium ions are able to leak into the neurone. The membrane of the neurone is selectively more permeable to the positively charged potassium ions than the positively charged sodium ions, that is to say it is easier for the positively charged potassium ions to leave the neurone than it is for the positively charged sodium ions to enter the neurone. This activity results in an eventual loss of positive charge within the neurone. Once the inside of the neurone reaches –70 mV, the permeability of the neurone membrane changes and no longer allows the escape of positively charged potassium ions. It is at this stage that there is a level of equilibrium is found and this is known as the neurone’s resting potential, (Binnie 1982).

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It is the gross differences between action potentials and resting potentials that allow the Electroencephalograph to measure electrical activity in the brain. The Electroencephalograph is able to do this by amplifying the small electrical fields that are found on the scalp with the aid of small electrodes. The Electroencephalograph is aided by the amplification of the signals on the scalp that have to pass through three layers of meninges, cerebral spinal fluid and a thick layer of skull.

The Electroencephalograph machine measures electrical activity in the brain in two ways. Firstly it measures the amplitude of the signals. Secondly the Electroencephalograph records frequency of signals emanating from the brain. The Electroencephalograph records the frequency in Hz, which are cycles per second. The frequencies are found using the Electroencephalograph have been classified into frequency bands. The first band, which is the delta frequency, is activity that is below 4Hz. Theta is 4 – 7 Hz, Alpha is 8 – 13 Hz and Beta is all frequencies above 13 Hz, (Binnie 1981).

In his 1929 paper, Berger described a low amplitude rhythmic waveform with a 10 Hertz frequency in the occipital areas of the brain when his participant was resting with eyes closed. Berger named the activity the alpha rhythm. Clinically, the alpha rhythm is considered to be the most important aspect of an Electroencephalograph recording, (Binnie 1982). The alpha rhythm is responsive to changes in visual attention. The alpha rhythm is usually found in a normal subject who has his/her eyes closed. Opening of the eyes and concentrating on a cognitively demanding task will cause alpha to disappear. This is known as alpha blocking. A person can produce alpha in the awake state by staring into space or daydreaming. Alpha varies considerably between adults and children and also between individuals. As a diagnostic tool, the Electroencephalograph looks for symmetry and balance. Differences in those factors could be predictive of disorder or disease.

An example would be that of finding a 50% difference in amplitude between the cerebral hemispheres. This difference is found in less than 6% of the population and would therefore be viewed with suspicion by the Electroencephalograph technician. Furthermore, in a normal Electroencephalograph, right-handed people tend to present slightly higher amplitude in the right hemisphere. Therefore higher left hemispheric amplitude in a right handed person or asymmetry greater than 50% would raise suspicions of the Electroencephalograph technician who would investigate further.

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The Abnormal EEG Reading

Berger (1929) was the first person to recognise spike wave activity during epileptic seizures using the electroencephalograph. However, since this major discovery it has been argued that paroxysmal, abnormal neuronal discharges do not always produce clinical manifestations of seizures, (Binnie 1991). Because of the lack of any clinical manifestations, such discharges were described as ‘sub-clinical’, ‘larval’ or ‘inter-ictal’, (Binnie 1991). Schwab (1939) investigated ‘sub-clinical activity’ in petit mal epilepsy (absence seizures) by conducting an experiment using an electroencephalograph and a simple reaction time task. Schwab found that spike and wave activity recorded on the electroencephalograph that was not associated with clinical manifestations of absence seizure behaviour did however correlate with reaction time. That is to say, spike and wave activity appeared to increase reaction time and also the failure to respond. Since Schwab’s study, over forty other experiments have supported Schwab’s findings.

Aarts et al. (1980) defined the impairment in cognitive ability during spike and wave activity as ‘transitory cognitive impairment’ because the cognitive impairment is not permanent but appears from time to time. Furthermore, Binnie (1991) has argued that inter-ictal epileptiform activity is a more appropriate term to use rather than sub-clinical activity because it can be argued that transitory cognitive impairment is a type of clinical manifestation. Binnie has also argued that the term Inter-ictal epileptiform activity should be used because it describes epileptiform activity between ictal phases (seizures).

In their study, Tizard & Margerison (1963) found that participants were able to respond to most stimuli during spike and wave activity and even during overt absence seizures. Prechtl et al (1961) conducted experiments to see if there was relationship between paroxysmal EEG patterns and changes in the behaviour of participants. Prechtl et al (1961) designed a test for use with a group of ‘normal’ participants and a group of participants with clinical symptoms of epilepsy. A test of performance was used that would engage the participant in continuous activity but would not allow the participant to automate the activity. The test consisted of five small lamps with five buttons. One button corresponding to each of the lamps. In the test, only one lamp lit up at a time and the pushing of the corresponding button would extinguish the lamp. The lamps lit up in a random order and the participants were requested to extinguish the lamps as quickly as possible. During the test, each individual participant was connected to an EEG machine. Correct and incorrect button pushes were recorded on the EEG by the way of markers. The test lasted three minutes followed by a short break and then the participant was asked to take a further test of three minutes.

The results from the study indicated that epileptiform activity and EEG recordings did not show simple temporal correlations. One of the participants in the study managed to complete the experiment without any errors whilst displaying ten seconds of generalised spike and wave activity. Focal spike and wave activity also appeared to have little affect on the performance of the test. However, Prechtl et al found that changes in test performance correlated with an undifferentiated flattening of the EEG, which is known as suppression. Overall, the results indicated that spike and wave activity did not show any significant correlation with changes in test performance as opposed to suppression which did. Prechtl et al have argued that suppression is usually followed by an epileptic discharge and is not seen in non-epileptic patients. It was also noted that the frequency of epileptic discharges in the epileptic patient was reduced during periods of concentrated attention opposed to relaxed periods when the participant displayed alpha rhythms. It could therefore be argued that alpha blocking might have a relationship with the reduction of epileptic discharge.

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Davidoff et al (1963) conducted a study that involved the participation of people with epilepsy who had met a number of criteria prior to entering the study. To enter the study, the participants needed to have a referring diagnosis of idiopathic epilepsy, absences of neurological disorders including disease and an EEG recording that had shown abnormal paroxysmal, bilaterally synchronous bursts of activity that appeared abruptly. The EEG readings must also have shown normal electrical activity prior to the paroxysmal burst and normal electrical activity following the paroxysmal burst.

The participants in the study, which was undertaken at an army medical research centre, were referred with differing diagnoses of epilepsy. Of the thirty-six participants that were referred, nineteen were diagnosed as suffering from Grand Mal epilepsy, eighteen were diagnosed with Petit Mal epilepsy and Nine others were diagnosed as having miscellaneous types of epilepsy. In the study, the participants were requested to undertake four tasks, which were tapping with the right index finger rhythmically, repeating digits, serial subtraction of seven from one hundred and counting backwards. The participants undertook the tasks whilst exposed to intermittent photic stimulation. Prior to the tasks been undertaken using photic stimulation the participants undertook the tests without photic stimulation so that they could act as their own controls.

After the experiment, EEG paroxysms were classified into four categories which were petit mal type (PMT), atypical spike and slow wave (ASW), multiple spike bursts (MSB) and slow wave burst (SWB). The EEG paroxysms were also classified as either clinical or subclinical depending on the observations of the participant made by the experimenters during the test. Behaviour such as blinking, head movements or reports by the participant of feelings of strange sensations by the participant during paroxysmal discharges was classified as clinical discharges. If no movements or the participant did not report any unusual sensations during paroxysmal discharges, the discharges were classified as subclinical discharges. After the completion of the experiment, the duration of paroxysmal discharges were measured and classified in terms of whether or not they were induced by photic stimulation or spontaneous. The participants were also divided into two groups dependent on whether or not they showed breaks in functioning with regard to the tests. That is to say, if the participant paused during a particular test such as the finger-tapping test, it would be classed as a break if both experimenters agreed that it was. Breaks in the finger tapping experiment included pauses and irregularities in finger tapping rhythm. It was noted that the halting of finger tapping behaviour completely was unusual. It was also noted that participants who stopped finger tapping at the beginning of a paroxysmal burst usually restarted the finger tapping and continued to do so despite the continuation of the discharge. The results from the study displayed a wide variability between individual participants and bursts of activity. The results indicated that participants with clinical bursts of paroxysmal activity were more likely to have breaks in functioning during the tests than the participants with subclinical bursts of activity. Fifty four percent of the clinical paroxysmal bursts were associated with breaks in activity as opposed to twenty six percent of subclinical bursts that were associated with breaks in activity.The results also showed that there was a significant difference in the mean number of paroxysmal bursts between the twenty-four participants in the break group and the thirty-six participants in the no break group. Participants in the break group had significantly longer bursts of paroxysmal activity with greater variability of duration.The results also indicated that fifty seven percent of discharges from the break group were photically stimulated as opposed to twenty six percent in the no break group. It was therefore argued that breaks in functioning were more likely to be associated with photically induced paroxysmal bursts than spontaneous paroxysmal bursts of activity.

The subtraction test was most effected by paroxysmal discharges. Eighty percent of participants who had an error on the test showed paroxysmal discharges as opposed to thirty four percent of errors correlating with paroxysmal discharges in the digit repetition test. Overall the results from Davidoff et al indicate that Clinical paroxysmal bursts are more likely to cause breaks during tests, the length of paroxysmal bursts are likely to increase the chance of a break in performance, photically stimulated paroxysmal bursts are more likely than spontaneous paroxysmal bursts to cause a break in performance and breaks in performance are more likely to be caused by clinical paroxysmal activity as opposed to subclinical activity.

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The Normal EEG Reading

Before considering abnormal EEG behaviour and any possible correlation with transitory cognitive impairment, the normal EEG should first be considered. Binnie (1981) has argued that the normal EEG is often spikey by nature and adolescents and children will exhibit positive spikes when drowsy. This phenomenon does not however have an diagnostic significance in relation to epilepsy. Binnie has also noted that a phenomenon known as ‘spike wave phantom’ which exhibits low amplitude, six Hz and is also of no diagnostic significance with regard to epilepsy. Benign Epileptiform Transients of Sleep produces short sharp spikes over temporal regions during sleep with slow waves and is found in forty percent of normal participants, (White et al 1977). In further research relating to Benign Epileptiform Transients of Sleep, Westmoreland et al (1979) noted that in participants with partial epilepsy and Benign Epileptiform Transients of Sleep, they were unrelated in terms of an epileptic focus.

Mid temporal Rhythmic Discharge is a phenomenon that exhibits a six Hz frequency over the temporal regions and appears for minutes at a time and shows no relationship with arousal or sleep. Lipman & Hughes (1969) have argued that although this phenomenon is rare, its occurrence is increased in a number of groups including those suffering from epilepsy. Gibbs & Gibbs (1952) have argued that the presence of Mid Temporal Rhythmic Discharge is not reliable in terms of the diagnosis of epilepsy. A typical finding in a normal EEG is what is known as a Mu rhythm. The Mu rhythm usually exhibits an eight to thirteen Hz frequency (in the alpha range) and is identifiable by its shape that resembles a fence like waveform. The Mu rhythm can be blocked by intent to move (contralaterally) a part of the upper body such as the arm or the hand, (Binnie, 1982).

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