Introduction: In 1896, in his work The Man of Genius, Lombroso presented a daring concept about key role of epilepsy in genesis of human genius. Aim of paper: The aim of this paper is to present the history of lives of some outstanding men and women afflicted by epilepsy and controversies associated with this diagnosis. Discussion: Mahomet most probably suffered partial seizures since his 4th decade and his visions were subsequently denoted by his followers. Some authors believe, that the heroic Jeanne d’Arc had epileptic seizures caused by an intracranial tuberculoma. A brain tumor might have been a cause of Julius Caesar’s epilepsy. Dostoyevsky had secondarily generalized seizures with ecstatic aura and used his epilepsy-associated experiences in his literary works. Personages of his books The Brothers Karamazov and The Idiot also suffered epilepsy. Based on an analysis of Dostoyevsky case, Freud suggested a neurotic background for his condition. Retrospective attempts at determining the nature of van Gogh’s illness include a dozen or so different diagnoses, of which epilepsy seems the most probable. Descriptions of partial complex seizures may be found in many letters by van Gogh to his brother Theo and are also reported by the artist’s doctor. Antiepileptic drugs available then and implemented by van Gogh (potassium bromide and digitalis) might have had an impact on his artistic output. Digitalis side-effects leading to visual disturbances are illustrated by his works Starry Night and Night Café. Flaubert, who suffered three types of epileptic seizures (partial simple, partial complex and secondary generalized), was considered by Sartre a hysteric. Flaubert’s epilepsy was probably caused by a congenital vascular malformation in the occipital lobe, which probably caused his death too.
Status epilepticus (SE) is a life-threatening emergency in which continuous or recurrent seizures, lasting more than 30 minutes without full recovery of consciousness between seizures occur. Seizures activity lasts more than 60 minutes and fails to respond to appropriate first-line drug treatment in refractory SE. SE is divided into convulsive and non-convulsive. It may occur in the patients with epilepsy (with low antiepileptic drug serum level), or it may be a symptom of acute (organic or metabolic) lesion of CNS. Management in SE should provide: regular functioning of the respiratory and cardiovascular systems, suppressing seizure activity, compensating metabolic disturbance and then diagnosis and casual treatment. The benzodiazepines followed by phenytoin are the first-line drug. Next, other drugs and finally general anesthesia with using barbiturate or unbarbiturate anesthetic agents. EEG performs an important part in diagnosis and monitoring of SE, especially in refractory SE, where medications are administered to achieve a burst suppression pattern on EEG. Every epileptic seizure, lasting more than 10 minutes, should be considered as a potential status epilepticus.
The 18-yer-old woman was transferred to the Department of Neurology from a psychiatric ward. She had 16-yer history of epilepsy with complex partial seizures with secondary generalisation. Cause of epilepsy – unknown. There had been several hospitalisations because of drug resistance and two episodes of status epilepticus partial seizures secondarily generalised. In October 2003 her seizures increased in frequency and were accompanied by behavioural abnormalities. A change of antiepileptic drug /AED/ therapy did not improve seizure control. He patient was hospitalised in the neurological and psychiatric wards and was then admitted to the Department of Neurology where she was developed status epilepticus. Neurological examination revealed asymmetry of the tendon reflex L>R. Brain CT scan was normal. The treatment used to resolve status epilepticus included maximum recommended doses of diazepam, clonazepam, valproate solium, phenytoin, phenobarbital, lidocaine, midazolam and 2-days thiopental-inducted coma. The patient was fed through a tube and the formerly used AEDs: TGB, VPA, TPH were continued. Despite this therapy the patient experienced up to 50 seizures daily with an upward rolling of the eyes, blinking, salivation, bradycardia, mouth movements, shoulder jerks and head bend. EEG revealed generalised seizure pathology and CSF analysis showed increased protein levels. Administration of propofol intravenously and levetiracetam through the tube resulted in seizure termination within an hour and improved EEG recording. The propofol therapy caused decreases in arterial blood pressure, witch required a 4-day administration of presser amines. On treatment day 14, the patient was extubated. Her neurological status was good, with no intellectual regression. The patient remained seizure – free for 4 weeks.
Many examples of experimental epilepsy show that epileptic seizures occur due to release of stimulatory neurotransmitters into intracellular spaces. In CNS adenosine suppresses exocytosis of glutamate and asparginate but guanosine increases the reverse uptake of glutamate by astrocytes and thus lowers it concentration outside the cell. In this process both nucleosides participate in suppressing the epileptic seizures. By decreasing concentration of ectoadenosine and ectoguanosine outside the cell, that compounds can protect neurons from cellular degeneration. It was shown in many animal models for experimental epilepsy that adenosine A 1 and A 2A receptors were involved in the process of stopping the seizures. Moreover, some of the conventional anti-epileptic drugs reveal enhance their therapeutic abilities by interactions with the adenosine receptors, being either agonists or antagonists. These interactions modulate the activity of receptors and consequently regulate the neuroprotection processes. Some agonists of adenosine receptors increase the epileptic episodes reaction to those compounds. Anti-episode action of adenosine and guanosine as well as agonists and antagonists of nucleoside receptors indicate the possibility of applying the knowledge about these processes towards production of new anti-epileptic medication. Successful anti-epileptic medication may be based on compounds that have the ability to increase the concentration of ectoadenosine i.e; adenosine deaminase inhibitors, adenosine kinase inhibitors or compounds with ability to suppress reverse uptake of nucleosides. Another method to increase the concentration of extracellular adenosine is to increase the activity of 5’-nucleotidase. That in effect will increase the amount of ectoadenosine by degradation of ectoAMP. There are very promising results revealed that oral administration of guanosine and GMP as well as guanosine by itself given intraperitoneally and intraventricularly what halted epileptic seizures caused by quinolinic acid which is a glutamate agonist.
Since the eighties of the 20th century, studies have been carried out on the health state of children of epileptic mothers. These studies indicated quite high percentage of children with mental retardation and inborn defects. They are thought to be associated with less effective treatment in pregnancy, application of antiepileptic drugs of marked teratogenic properties (phenobarbital, phenytoin) and also with polytherapy as the principle of antiepileptic management. Then, the groups of pregnant women with epilepsy were not subjected to specialistic care of a neurologist and obstetrician. Current studies evaluating neuropsychological state of offspring of epileptic mothers point to the occurrence of psychomotor retardation, increased risk of manifestation of central nervous system significant and insignificant dysfunction, epilepsy as well as lower than on the average global intellectual ability and insignificant neurological dysfunction. Psychomotor retardation concerns mainly visual and auditory coordination, speech and social contacts. The latest prospective studies of epileptic mothers’ offspring indicate that epilepsy is significantly more frequently manifested among them (7% till the end of the first decade) than it was reported in earlier retrospective studies. In this period, generalized epilepsy (different syndromes) is more often revealed in offspring of mothers with early manifestation of epilepsy with attacks of unconsciousness. Polytherapy and monotherapy with walproine acid is a very important factor of the risk of decreased intelligence quotient and less beneficial results of learning. The importance of other risk factors including environmental has not been recognized sufficiently. Low socioeconomic level and the child’s male gender modify distinctly unbeneficially the effect of antiepileptic drugs administered in pregnancy. However, the so far carried out studies have not comprised sufficiently numerous groups of offspring of epileptic mothers and the methods of assessment applied by particular authors differ significantly. Furthermore, majority of mechanisms of the way different genetic and environmental factors affect the development of cognitive functions in offspring of epileptic patients are not known.
Status epilepticus or continuous seizures occur as a result of many hard disorders and complications in epilepsy which appear in brain on different backgrounds. Most often these cases may become serious danger for the patient’s life, so they demand immediate intervention and appropriate treatment. Particularly it concerns convulsion epilepsy seizure, appearing with metabolic disorders, which lead to acidosis and brain oedema. The aim of pharmacological treatment of status epilepticus is to stop its clinical symptoms (seizures and its other forms) as quickly as possible and to normalize its bioelectric exponent EEG. Giving the classic drugs (benzodiazepines, phenytoin, phenobarbital – phenobarbiturates, sodium valproate) not always helps to take control over this state. In case of the lack of results of this treatment one may try to use the drugs of new generation. Last days there have appeared some information concerning the efficiency of topiramate treatment in status epilepticus unresponsive to traditional pharmacological therapies. The authors present a case of a 26-year-old patient with partial epileptic attack with secondary generalization, in whom there occurred status epilepticus resistant to treatment with commonly applied drugs. Only the administration of topiramate did allow to control the status epilepticus.
Epilepsy in the elderly differs from that in younger people. It is an important and increasingly common clinical problem. Old age is the most common time to develop seizures and around 25% of new cases of epilepsy occur in elderly people. In people of 70 years and above, the prevalence of epilepsy has been estimated two times more to compered with the general population. The epidemiological studies showed that the value of incidence and prevalence in elderly epilepsy are similar in many countries. About one-half of cases of epilepsy in elderly cannot be linked to an identifitable cause, in the rest – 33% cerebrovascular disturbances, 12% dementia. In the elderly partial epilepsy dominated on tonic-clonic seizures. In connection to elongation of average age of population in Poland the number of the elderly epilepsy will be increase. Especially of the number of ischemic stroke in connection with epilepsy is typical in this age. To realize of scale of this problem the author according to the generally accepted the value of prevalence and incidence of epilepsy estimates suitable accounts with reference to our country.
Neuropathic pain, beside the nociceptive one, is clinically difficult in terms of a diagnosis as well as the treatment process. The variety of mechanism engaged in its pathogenesis is basics to apply the medicine about different mechanisms of operations. Neuropathic pain result from the damage caused to the pain track above the nociceptors in the peripheral and central nervous systems. Difficulties in neuropathic pain treatment emerge from the process of structural rebuilding within damaged fibres and neighbouring healthy ones. Early interrupt of the pain prevent the structural rebuilding. Antiepileptic drugs, in addition to antidepressants and opioids, are fundamental and often applied group of medications in neuropathic pain treatment of various aetiology. Their efficacy has been well known for a very long time. The medications of older generation as well as the newest ones are equally applied. Carbamazepine is generally used in treatment of neuropathic pain and the best efficacy and recommendations of this medicine is for trigeminal neuralgia. The medications of newer generation, such as gabapentine and pregabaline, appeared to be most effective in neuropathic pain treatment and diabetic neuropathy as well as after herpes zoster. Most antiepileptic drugs, particularly of the newest generation, exert significant efficiency in neuropathic pain treatment. There is lamotrigine, oxcarbazepine and topiramate among them, evaluated in a number of medical reports as helpful in its treatment.
Polyunsaturated fatty acids (PUFA), omega-3 are essential for normal development and function of the central nervous system. They are an essential structural component of neuronal cell membranes and are a source of biologically active substances, which perform complex functions, and participate in signal transmission within cells. Disorders of lipid metabolism and FFA are observed in the course of many disorders and mental illness, i.e. schizophrenia, bipolar disorder, attention-deficit/hyperactivity disorder, autism. Those disturbances are genetically based and contribute along with other abnormalities to increased vulnerability to particular disorder’s symptoms development. In addition, the diet of most residents of European countries does not provide enough omega-3 PUFAs, are exogenous substances, i.e. not synthesized in sufficient quantities in the human body. Moreover, in the course of many mental disorders an excessive loss of long-chain PUFA through excitotoxicity processes and oxidative stress is observed, which further contributes to depletion of the available pool of PUFAs. In the case of schizophrenia, numerous experimental and clinical studies have led researchers to formulate hypotheses explaining the development of this disease based on the presence of lipid metabolism dysfunctions. The paper presents a review of recent literature and results of the original research conducted by the authors dealing with PUFAs metabolism disturbances in patients with mental disorders listed above.