Evolution of concepts in epilepsy surgery.

At the time of the first meeting of the International League Against Epilepsy (ILAE) in 1909, surgical treatment for epilepsy had been accepted as an alternative therapy for over two decades, but was rarely practiced, considered a last resort for carefully selected patients. Localization was based on ictal semiology and identification of a structural lesion. Very few papers on epilepsy surgery were presented at ILAE meetings or published in Epilepsia during the first half of the 20th century. A modest explosion in interest in epilepsy surgery at mid-century resulted from recognition that "invisible" epileptogenic lesions could be identified by EEG, especially for temporal lobe epilepsy. Epilepsy surgery received a second boost in popularity toward the end of the 20th century with the advent of structural and functional neuroimaging, and the number of epilepsy centers worldwide doubled between the first Palm Desert conference in 1986 and the second Palm Desert conference in 1992. Neuroimaging also helped to increase application of surgical treatment to infants and young children with severe epilepsies. Epilepsy surgery was accepted as standard of care for drug-resistant focal epilepsy and was well-represented at international ILAE congresses and in Epilepsia. Advances continue into the 21st century with the introduction of laser ablation, and palliative neuromodulation approaches, which have greatly increased the population of patients who can benefit from surgery. Modern presurgical evaluation techniques have also made surgical treatment possible in many countries with limited resources. Three randomized control trials now have definitively proved the safety and efficacy of epilepsy surgery, however, this alternative therapy remains under-utilized even in the industrialized world, where less than 1% of potential candidates are being referred to epilepsy centers. Furthermore, those who are referred receive surgery an average of 20 years after onset of epilepsy, often too late to avoid irreversible disability. The major challenges in realizing the full potential of epilepsy surgery, therefore, are not as much in the continued improvement of the treatment itself, as they are in addressing the treatment gap that is preventing appropriate patients from being referred to full-service epilepsy centers.

A neurosurgeon`s view: Laser interstitial thermal therapy of mesial temporal lobe structures.

Stereotactic laser ablation of mesial temporal structures is a promising new surgical intervention for patients with mesial temporal lobe epilepsy (MTLE). Since this procedure was first used to treat MTLE in 2010, the literature contains reports of 37 patients that underwent MR-guided stereotactic laser amygdalohippocampotomy (SLAH) using Laser Interstitial Thermal Therapy (LITT) with at least 1year of follow-up. This early body of data suggests that SLAH is a safe and effective treatment for MTLE in properly selected patients. Moreover, SLAH is substantially less invasive when compared with open surgical procedures including standard anterior temporal lobectomy and its more selective variants, results in immediate destruction of tissue in contrast to radiosurgical treatments for MTLE, and can more readily ablate larger volumes of tissue than is possible with techniques employing radiofrequency ablation. Finally, evidence is accruing that SLAH is associated with lower overall risk of neuropsychological deficits compared to open surgery. Thus, LITT constitutes a novel minimally invasive tool in the neurosurgeon's armamentarium for managing medically refractory seizures that may draw eligible patients to consider surgical interventions to manage their seizures.

Familial temporal lobe epilepsy in the 19th century.

PURPOSE: To draw attention to a publication showing that familial temporal lobe epilepsy had been described in 1895, considerably earlier than 1994, usually thought to be the date of the original account of the disorder METHODS: Examination of the contents of Sir James Crichton-Browne's Cavendish lecture on 'Dreamy mental states' that was published in the Lancet in mid-1895 RESULTS: At a time when the clinical phenomena that later became associated with the idea of temporal lobe epilepsy were beginning to become known, Creighton-Browne described the presence of this disorder in members of four consecutive generations of a British family throughout the course of the 19th Century CONCLUSIONS: There is evidence that the genetic abnormality responsible for familial temporal epilepsy had probably appeared considerably earlier than hitherto thought.

Scott Fitzgerald: famous writer, alcoholism and probable epilepsy.

Scott Fitzgerald, a world-renowned American writer, suffered from various health problems, particularly alcohol dependence, and died suddenly at the age of 44. According to descriptions in A Moveable Feast, by Ernest Hemingway, Fitzgerald had episodes resembling complex partial seizures, raising the possibility of temporal lobe epilepsy.

Scott Fitzgerald: famous writer, alcoholism and probable epilepsy / Scott Fitzgerald: famoso escritor, alcoolismo e provável epilepsia

ABSTRACT Scott Fitzgerald, a world-renowned American writer, suffered from various health problems, particularly alcohol dependence, and died suddenly at the age of 44. According to descriptions in A Moveable Feast, by Ernest Hemingway, Fitzgerald had episodes resembling complex partial seizures, raising the possibility of temporal lobe epilepsy.

RESUMO Scott Fitzgerald, reconhecido escritor americano, mundialmente famoso, apresentou vários problemas de saúde, particularmente a sua dependência ao álcool, tendo morte súbita aos 44 anos de idade. Relatos publicados no livro de Ernest Hemingway “Paris é uma festa” dão conta de que Scott Fitzgerald apresenta prováveis crises parciais complexas, sugerindo a hipótese de epilepsia do lobo temporal.

H.M. never again! An analysis of H.M.'s epilepsy and treatment.

On August 25, 1953, the patient H.M., aged 27, underwent a bilateral surgical destruction of the inner aspect of his temporal lobes performed by William Beecher Scoville with the aim to control H.M.'s drug refractory epileptic seizures and alleviate their impact on his quality of life. Postoperatively, H.M. presented for 55 years a "striking and totally unexpected grave loss of recent memories". This paper reports what we know about H.M.'s epilepsy before and after surgery and puts forward arguments supporting the syndromic classification of his epilepsy. We attempted to elucidate what could have been the rationale, in 1953, of Scoville's decision to carry out a bilateral ablation of H.M.'s medial temporal lobe structures, and we examined whether there was any convincing argument published before 1953 suggesting that bilateral hippocampal ablation could result in a permanent and severe amnesia. Our a posteriori analysis of H.M.'s medical history suggested that he was most probably suffering from idiopathic generalized epilepsy with absences and generalized convulsive seizures worsened by high dosage phenytoin treatment, or less probably from cryptogenic frontal lobe epilepsy. Importantly, he did not have temporal lobe epilepsy. Scoville based his proposal of bilateral mesial temporal lobe ablation on his experience as a psychosurgeon and on the assumption that the threshold of generalized epileptic activity could be lowered by some kind of hippocampal dysfunction potentially epileptic in nature. Given the scanty information on the link between amnesia and medial temporal lobe lesions that was available in humans in 1953, one can understand why Scoville was so surprised by the "striking and totally unexpected" memory loss he observed in H.M. after the bilateral ablation of his mesial temporal lobe structures.

Frédéric Chopin and his neuropsychiatric problems.

Few musicians who suffered from any kind of serious neuropsychiatric problems were able to create works that are still admired today. This new research will show that Frédéric Chopin, who reinvented piano music in the first half of the nineteenth century, was one of those few. He died in Paris aged only 39. While the somatic illness that killed him continues to generate speculation, his recurrent depressive mood swings have remained largely unexamined. A few neuropsychiatric publications make a simplistic effort to assign his emotional condition to a modern diagnostic category, e.g., temporal lobe epilepsy. Because it is impossible to prove such hypotheses, these studies are nothing more than erudite speculation. This chapter will instead incorporate the cultural and medical context of the first half of the nineteenth century in order to explore new possibilities for medical biographies of musicians.

[Norman Geschwind: career and works].

Norman Geschwind was an outstanding American neurologist. He first majored in psychology and then medicine at Harvard University. After graduation, he received neurological training at Beth Israel Hospital, the National Hospital at Queen Square in London, and Boston City Hospital, under the guidance of Denny-Brown, Charles Symonds, and Fred Quadfasel. He later moved to the Boston Veterans Administration Hospital, and established the Boston University Aphasia Research Center with Edith Kaplan. This center played a cardinal role in aphasia research in the United States. In 1969, Geschwind became a Professor at Harvard Medical School. Disconnection syndromes, which made Geschwind's name famous worldwide in the field of neurology, are reviewed here in regard to pure alexia, conduction aphasia, pure word deafness, isolation of the speech area, and apraxia, with reference to the Wernicke-Geschwind model. Other contributions by Geschwind are also described, such as behavioral changes in temporal lobe epilepsy (Geschwind syndrome) and cerebral lateralization, including the Geschwind-Galaburda hypothesis.

A retrospective diagnosis of epilepsy in three historical figures: St Paul, Joan of Arc and Socrates.

It has been suggested that undiagnosed epilepsy profoundly influenced the lives of several key figures in history. Historical sources recounting strange voices and visions may in fact have been describing manifestations of epileptic seizures rather than more supernatural phenomena. Well-documented accounts of such experiences exist for three individuals in particular: Socrates, St Paul and Joan of Arc. The great philosopher Socrates described a 'daimonion' that would visit him throughout his life. This daimonion may have represented recurrent simple partial seizures, while the peculiar periods of motionlessness for which Socrates was well known may have been the result of co-existing complex partial seizures. St Paul's religious conversion on the Road to Damascus may have followed a temporal lobe seizure which would account for the lights, voices, blindness and even the religious ecstasy he described. Finally, Joan of Arc gave a detailed narrative on the voices she heard from childhood during her Trial of Condemnation. Her auditory hallucinations appear to follow sudden acoustic stimuli in a way reminiscent of idiopathic partial epilepsy with auditory features. By analysing passages from historical texts, it is possible to argue that Socrates, St Paul and Joan of Arc each had epilepsy.

Temporal lobe epilepsy.

In the last two decades our understanding of MTLE and its pathophysiology has grown remarkably. Perhaps the most important recognition is that it is not a single entity with a uniform pathology. Rather, it is associated with significant variations in pathology that, in turn, are likely associated with different causes, functional anatomies, physiologies, and outcomes to treatment (medi-cal and surgical). There are numerous changes in the expression of channels and receptors that contribute to the development of epilepsy and, perhaps, drug resistance. This progress in our understanding has also been aided immeasurably by the development of animal models with many parallels to the human condition.These models have allowed us to look at changes in anatomy and physiology and to dissect the circuits in ways that have not been possible in humans. The animal models have also allowed us to create hypotheses about the pathophysiology of the disorder that we have started to exam-ine with the new imaging tools. At present, it is best to summarize our understanding of MTLE by saying there are multiple changes in multiple sites that contribute to the development of the chronic condition. For this reason alone, we should consider MTLE to be a systems disorder.

Frederic Gibbs and his contributions to epilepsy surgery and electroencephalography.

Frederic Gibbs' (1903-1992) long research career was devoted to the understanding and treatment of epileptic phenomena and closely associated with the development of electroencephalography (EEG). After medical school, he joined the Harvard Neurological Unit at Boston City Hospital directed by Stanley Cobb. In the early 1930s, Gibbs developed a thermoelectric blood flow probe and, with William Lennox, proved in animals and humans that a seizure increases cerebral blood flow. By 1934, Gibbs became a pioneer in the field of EEG while working at Harvard with Hallowell Davis and Lennox, and was the first to convincingly record and report EEG findings in epilepsy and states of altered consciousness. Several years later, Gibbs and Lennox were the first to recommend cerebral excisions in several patients with uncontrolled epilepsy based on EEG. Moving to the University of Illinois at Chicago in 1944, Gibbs founded a consultation clinic for epilepsy, performed the first EEG depth recordings using pneumoencephalography-guided stereotaxy, and noted that sleep EEGs in patients with psychomotor seizures frequently disclosed temporal epileptic patterns. Gibbs convinced Percival Bailey to collaborate on patients with refractory temporal lobe psychomotor seizures without tumors. In 1947, the first nonlesional temporal lobe excisions based on EEG localization were performed in these patients, and, by 1948, anterior temporal lobectomy had become their procedure of choice. Gibbs and Lennox received the coveted Lasker Award among other honors as pioneers in establishing the modern era of epilepsy diagnosis and treatment.

The hallucinations of Frédéric Chopin.

Frédéric Chopin is the epitome of the romantic artist; he had a chronic pulmonary disease that ultimately caused his death at the age of 39. An overlooked neurological condition is discussed in this paper. We consider the possibility of a temporal lobe epilepsy, as throughout his life Chopin had hallucinatory episodes, which can accompany seizure disorders.

[Dostoevsky's epileptic experiences and his descriptions of epilepsy in the mirror of modern neurology]. / Dosztojevszkij epilepsziás tapasztalatai és epilepszia-ábrázolása a mai neurológia tükrében.

The aim of the study is to present Fyodor Mihailovich Dostoevsky's epilepsy through the results of the related historical and contemporary medical literature, further, to show how the illness is reflected in the writer's biographical data and in the famous patient characters displayed in his great romans. Nowadays it is well presumed that the writer could have had temporal lobe epilepsy with secondary generalized seizures, the symptoms of which he by no means was producing throughout his life. This can be tracked easily by his own descriptions of his seizures, from the memories of his wife and his contemporaries, as well as the symptoms of his epileptic characters in his novels. This theme has been widely dealt with by neurologists, epileptologists and literary experts all over the world. Author details the literature research, the related works and establishes her own concept concerning Dostoevsky's epilepsy.

The last myth of Giorgio De Chirico: neurological art.

Giorgio de Chirico is one of the most admired and at the same time most discredited painters of the 20th century. As the 'inventor' of metaphysical painting, he has been considered as a precursor of Surrealism, while his later works have been harshly criticized as representative of the painter's decay. The mystery and dream-like atmosphere irradiating from his works has led to speculations that de Chirico may have taken his inspiration from migraine attacks or complex partial seizures. However, a careful study of his life and his own writings suggests that while de Chirico probably suffered from recurrent malaria, he had neither migraines nor epilepsy. De Chirico also denied that dreams were a major source of his inspiration, but he insisted on his fertile inner imagery, which allowed him to put in a new, poetic, often conflictual perspective, places and objects, which he had actually seen (Hofgarten arcades, Italian piazzas, statues, antique ruins, etc.) in Athens, Munich, Florence, Turin, Ferrare, and other towns. De Chirico was accused of self-plagiarism because he commonly used his former themes in new works, sometimes in what may look like servile copies of his early paintings. This 'replay syndrome' is quite unique in modern art, which has been dominated by the obligation, dogma and cult of newness and renewal. At odds with most of his contemporaries, Andy Warhol suggested that de Chirico made such recurrent series because 'he liked it'. Indeed, as a lifelong admirer of Nietzsche, de Chirico may just have applied the philosopher's concept of the 'eternal return', in which one is supposed to live and accomplish tasks that one would want to repeat forever. In that way, de Chirico's work should not be considered as that of a genius who fell into decadence, but may appear as a continuous, organized process to which organic brain dysfunction never contributed.

Norman Geschwind's contribution to the understanding of behavioral changes in temporal lobe epilepsy: the February 1974 lecture.

Norman Geschwind catalyzed academic interest in the study of interictal behavioral changes in temporal lobe epilepsy. His contributions to this area comprise a series of 11 articles, chapters, editorials, and commentaries published between 1973 and 1984. This article summarizes, both chronologically and by behavioral topic, Geschwind's contributions and opinions on behavioral changes in temporal lobe epilepsy. A previously unpublished lecture (see article in this issue), "Personality Change in Temporal Lobe Epilepsy," from his course at Harvard Medical School on The Neurology of Behavior (1974), is also quoted to further illustrate his views on specific features of this syndrome. Notably, many of Geschwind's observations and formulations regarding this topic were highly developed in 1974, reflecting his long-standing interest in behavioral changes in epilepsy. Geschwind and his collaborators viewed temporal lobe epilepsy as an important model of behavioral change resulting from a stimulating lesion in the limbic system. This neurobiology accounted for the overarching increased interictal emotionality that underlay the increased religious interests, hypergraphia, increased aggression, increased moral and philosophical concerns, viscosity, and seriousness (lack of humor). Hyposexuality was the exception, although it was consistent with a discharging lesion altering this emotion-driven behavior. Geschwind provided a series of arguments to support the existence of this limbic syndrome and explain why alternative views (e.g., destructive lesion, psychological factors) and arguments against the syndrome's existence are inconsistent with the data.

Hippocampal sclerosis: progress since Sommer.

Hippocampal sclerosis (HS) continues to be the most common pathology identified in patients with refractory temporal lobe epilepsy undergoing surgery. Wilhelm Sommer described this characteristic pattern of neuronal loss over 120 years ago through his post-mortem studies on patients with epilepsy. Neuropathological post-mortem studies in the 20th century proceeded to contribute significantly to the understanding of this disease process, with regard to the varying patterns of HS and involvement of adjacent limbic structures. From studies of surgical temporal lobe specimens from the 1950s onwards it was recognized that an early cerebral injury could act as the precipitant for the sclerosis and epilepsy. Modern neuropathological studies have focused on aspects of neuronal injury, loss of specific neuronal groups and cellular reorganization to address mechanisms of epileptogenesis and the enigma of how specific hippocampal neuronal vulnerabilities and glial proliferation are both the effect and the cause of seizures.