Ancient Indian concepts about phenomenology,biology, and therapeutics of epilepsy

This article discusses etiology, pathogenesis, symptoms, and treatment of epilepsy, as described in Charaka Samhitā (translation: Charaka’s Compendium) and Sushruta Samhitā, the two core texts of Ayurveda, an ancient system of medicine. Ayurveda emphasized amnesia and loss of consciousness as core features of epileptic seizures (Sanskrit: apasmar; translation: apa negation, smaran memory) and recognized that seizures occur due to a disturbance in brain function or flow of “humors” to the brain. Semiology of various seizure types was well described. Epilepsy was attributed to both internal and multiple exogenous factors. Treatment of epilepsy with formulations of naturally occurring substances, their compounding and use, is described in remarkable detail. Lifestyle modifications to protect people with epilepsy are also documented. Cognitive comorbidities of epilepsy were recognized. Although none of the Ayurveda formulations have any empirical evidence supporting their safety or efficacy in the treatment of epilepsy, studies are needed to generate relevant evidence, to recognize their hazards, and to integrate traditional and complementary systems of medicine with modern health care in an informed and safe manner.     

The man behind the syndrome: Argyll Robertson,Scotland's ambassador extraordinary in the realm of ophthalmology

Abstract

The aim of this study is to find out whether bromide was able to cause conversion of epilepsy to psychosis i.e., so‐called paradoxical normalization such as has been seen in treatment with modern antiepileptic drugs. Spontaneous conversion has been known for three hundred years. Locock introduced bromide in the treatment of epilepsy in 1857. Belgrave wrote in 1868 on its effect on epileptic attacks and concommitant insanity. In 1868 Holm observed reduction of the frequency of seizures at the same time as psychotic symptoms or just dysphoria. In 1875 Voisin described a dose‐dependent intoxication with psychosis and/or neurological signs. Stark in 1875 and Bannister in 1881 were the first to clearly describe the antagonism between epileptic seizures and psychotic symptoms, an antagonism or conversion described by many authors, both in cases with high and low dosage, and with and without intoxication. Thus, the title of this paper should be answered in the affirmative.

Bromide has been used as a sedative and has rarely caused intoxication. Thus the presence of epilepsy is not a condition for the development of bromide intoxication. A case with epilepsy and fatal massive bromide intoxication is reported. It is discussed whether the pathological findings give support to Wolf's hypothesis of latent epileptic activity in subcortical pathways during “normalization”;.     

Neurology and Literature, 1860–1920 by Anne Stiles (ed.)

Abstract

Research from many perspectives has been made on the work of the French neurologist, J.‐M. Charcot (1825–1893) with particular reference to his fame for his studies and “construction”; of hysteria. What has not been demonstrated so far is the extent to which Charcot's construction can be explained by the perceived relationship between hysteria and epilepsy and Charcot's access to epileptic patients at La Salpêtrière. From the confusion that reigned concerning hysteria and epilepsy, both separately and in relation to each other, Charcot claimed to have isolated hysteria as a distinctive and universal pathology. This claim was partly based on the “grande attaque”;, representing the most intense degree of hysteria. A comparison with Gowers, the contemporary English neurologist suggests that diagnosis was the function of the practitioners’ preferences; and a linguistic analysis pinpoints Charcot's problems in describing an isolated pathology in terms of its relation to its neighbour, epilepsy.     

Does bromide cause conversion of epilepsy to psychosis?

The aim of this study is to find out whether bromide was able to cause conversion of epilepsy to psychosis i.e., so-called paradoxical normalization such as has been seen in treatment with modern antiepileptic drugs. Spontaneous conversion has been known for three hundred years. Locock introduced bromide in the treatment of epilepsy in 1857. Belgrave wrote in 1868 on its effect on epileptic attacks and concommitant insanity. In 1868 Holm observed reduction of the frequency of seizures at the same time as psychotic symptoms or just dysphoria. In 1875 Voisin described a dose-dependent intoxication with psychosis and/or neurological signs. Stark in 1875 and Bannister in 1881 were the first to clearly describe the antagonism between epileptic seizures and psychotic symptoms, an antagonism or conversion described by many authors, both in cases with high and low dosage, and with and without intoxication. Thus, the title of this paper should be answered in the affirmative. Bromide has been used as a sedative and has rarely caused intoxication. Thus the presence of epilepsy is not a condition for the development of bromide intoxication. A case with epilepsy and fatal massive bromide intoxication is reported. It is discussed whether the pathological findings give support to Wolf's hypothesis of latent epileptic activity in subcortical pathways during "normalization".     

Cortical epileptogenesis and David Ferrier

There was an increasing medical interest in the localization of representation of function in the cerebral cortex after Broca in 1861 identified a cortical area that appeared responsible for expressive speech. By the late 1860s, John Hughlings Jackson—based on clinico-pathological correlations mainly in persons with focal motor seizures—had reasoned that contralateral somatic motor function was represented in another area of the cortex. This localization was supported by Fritsch and Hitzig (1870) in experimental cortical stimulation studies in dogs. These authors also reported producing events resembling contralateral motor convulsing in their animals. Their work, and Jackson’s ideas, prompted David Ferrier, in Great Britain, to begin a program of cerebral cortical stimulation studies in various vertebrate species, trying to locate cortical sites of representation of functions other than expressive speech and motor activity. In his initial report of his investigations (1873), he noted that appropriately sited Faradic stimulation evoked immediate or delayed contralateral focal motor seizures, some of which evolved into generalized convulsions. On this basis he reasoned that focal motor and generalized seizures were expressions of the same disorder; that nearly all epilepsies originated in the cerebral cortex and not in the lower brain stem, as hitherto thought; and that the clinical pattern of epileptic seizure phenomenology depended on the function of the cortical site of origin and the extent and direction of spread of seizure activity in the brain. He not only provided experimental verification for Jackson’s reasoning about epileptic seizure mechanisms but expressed the ideas a good deal more clearly than Jackson ever managed to do. Ferrier’s achievement in this regard has tended to escape notice, lost sight of because of the great importance of his investigations into localization of cerebral function.     

Jean-Martin Charcot and the epilepsy/hysteria relationship

Research from many perspectives has been made on the work of the French neurologist, J.-M. Charcot (1825-1893) with particular reference to his fame for his studies and "construction" of hysteria. What has not been demonstrated so far is the extent to which Charcot's construction can be explained by the perceived relationship between hysteria and epilepsy and Charcot's access to epileptic patients at La Salpêtrière. From the confusion that reigned concerning hysteria and epilepsy, both separately and in relation to each other, Charcot claimed to have isolated hysteria as a distinctive and universal pathology. This claim was partly based on the "grande attaque", representing the most intense degree of hysteria. A comparison with Gowers, the contemporary English neurologist suggests that diagnosis was the function of the practitioners' preferences; and a linguistic analysis pinpoints Charcot's problems in describing an isolated pathology in terms of its relation to its neighbour, epilepsy.     

On morel's épilepsie larvee: The first Danish epileptologist Frederik hallager's opposition in 1884 against morel's psychical epileptic Equivalents*

Abstract

In 1860 B.A. Morel published some cases of masked epilepsy, i.e., paroxysmal behaviour disturbances or “epileptic equivalents”;. The majority behaved criminally. Hughlings Jackson opposed and Hallager showed that all the cases related later as épilepsie larvée could be explained as postepileptic attacks, general paralysis, paradoxical normalization, schizophrenia, mania and otherwise. True criminal behaviour was exeptional. The present author agreed. There is no need for épilepsie larvée. It is discussed whether Blumer's recent “Paroxystic neurobehaviour disorder”; will revive “Morel's disorder”;.     

Albert the Great's interpretation of neuropsychiatric symptoms in the context of scholastic psychology and physiology

Albert the Great (ca. 1193-1280) serves as an example to show how the Latin West successfully integrated Greco-Arabian psychology with Galenic physiology. He divised a model of perceptive, cognitive and mnestic powers located in different areas of the "brain cells" and interacting with the immaterial and man-specific intellect. He managed to describe anmesis, epileptic seizures and psychotic states as results of disturbed brain fuction. Finally, further aspects of Scholastic theorizing on mental disorders are discussed.     

Albert the Great's interpretation of neuropsychiatric symptoms in the context of scholastic psychology and physiology* 1

Abstract

Albert the Great (ca. 1193–1280) serves as an example to show how the Latin West successfully integrated Greco‐Arabian psychology with Galenic physiology. He divised a model of perceptive, cognitive and mnestic powers located in different areas of the “brain cells”; and interacting with the immaterial and man‐specific intellect. He managed to describe anmesis, epileptic seizures and psychotic states as results of disturbed brain fuction. Finally, further aspects of Scholastic theorizing on mental disorders are discussed.     

Embodying brainstorms: the experiential geographies of living with epilepsy

This paper examines how living with epilepsy involves the complex interaction of knowledge of the unstable body, surrounding space and social relations. Through an engagement with written testimonies, it is argued that the spatial extent of everyday life varies with willingness to take socio-emotional and material risks in terms of when and where losses of bodily control (‘seizures’) might occur. I suggest that spaces and activities once taken-for-granted become potentially ‘unsafe’ and require renegotiation as trust in the limits of the body is disrupted. Findings confirm but also build upon previous work by geographers of chronic illness and impairment by engaging characterisations of the temporalities of fluctuating symptoms and of illness as manifesting either visibly or invisibly. Furthermore, it is argued that how people respond to the complete loss of bodily control differs in key ways to people coping with partially impaired control of the body. The paper concludes by asserting the potential for using written testimony as source data to highlight the voices of people whose spaces may otherwise remain silent.     

Historical perspective: The British contribution to the understanding of neurocysticercosis

Neurocysticercosis, or brain infestation with the larval stage of Taenia solium, is the most common risk factor for epilepsy in many endemic regions of the world. Hardly any cases are seen in Western developed countries, including Britain. However, a sizeable number (n = 450) was seen among British soldiers returning from deputation to India, then a British colony, first reported by Col. MacArthur at the Queen Alexandria Military Hospital in 1931. Here, we review the influence of the perceptive observations of British Army medics on the understanding of the parasitic disorder. The majority of these people presented with epilepsy. Among the contributions of the army medics were establishing the diagnosis, initially by histological examination of subcutaneous and muscular infestation, and later by radiography, clarifying the prognosis and the role of medical and surgical treatments and uncovering the close relationship between the larval (cysticercosis) and adult (intestinal tapeworm) stages of T. solium.     

The White Paper: Wilder Penfield,the Stream of Consciousness,and the Physiology of Mind

ABSTRACT

Wilder Penfield is justly famous for his contributions to our understanding of epilepsy and of the structure-function relationship of the brain. His theory on the relationship of the brain and mind is less well known. Based on the effects of the electrical stimulation of the cortex in conscious patients, Penfield believed that consciousness and mind are functions of what he referred to as the centrencephalic integrating system. This functional system comprised bidirectional pathways between the upper brainstem, the thalami, and the cerebral cortex of both hemispheres, and was the physical substrate from which memory, perception, initiative, will, and judgment arose. It was the source of the stream of consciousness and the physical basis of mind. This paper reviews how Penfield arrived at this conception of the mind-brain relationship. Although Penfield ultimately felt that he had failed in his attempt to unify brain and mind, his work shed new light on the relationship of memory to the mesial temporal structures and to the temporal cortex; and his association of consciousness and the brainstem preceded the conceptualization of the reticular activating system by a generation. In these, as in so many aspects of neurobiology, Penfield was prescient.     

On Morel's 'épilepsie larvée: the first Danish epileptologist Frederik Hallager's opposition in 1884 against Morel's psychical epileptic equivalents

In 1860 B. A. Morel published some cases of masked epilepsy, i.e., paroxysmal behaviour disturbances or "epileptic equivalents". The majority behaved criminally. Hughlings Jackson opposed and Hallager showed that all the cases related later as épilepsie larvée could be explained as postepileptic attacks, general paralysis, paradoxical normalization, schizophrenia, mania and otherwise. True criminal behaviour was exceptional. The present author agreed. There is no need for épilepsie larvée. It is discussed whether Blumer's recent "Paroxystic neurobehaviour disorder" will revive "Morel's disorder".     

Lasthénie de Ferjol’s Syndrome: A Tribute Paid by Jean Bernard to Jules Amédée Barbey D’Aurevilly

Abstract

The idea that memories could be transferred from one organism to another by administration of a “trained”; donor brain to a naive recipient seized both scientific and public attention in the 1960's and early 1970's. Georges Ungar was one of the earliest and strongest proponents of this idea, and he provided it extensive theoretical and experimental support. This paper reviews Ungar's work on memory transfer (and in particular on the scotophobin molecule), with an analysis of its successes and failures.     

Making Distinctions: The Contribution of Hector Landouzy to Differential Diagnosis in Relation to Hysteria and Epilepsy

Hector Landouzy (1818-1864) is known for his Traité Complet de l'Hystérie (1846), which was crowned by the Académie de Médecine, but this work is not given much importance in historical accounts. It deserves more attention because it was more than an orthodox statement about the nature of hysteria. In the context of the diagnostic confusion between epilepsy and hysteria, it introduced a method of presenting criteria to facilitate diagnosis. An examination of French authors on epilepsy and hysteria in the second half of the nineteenth century suggests that this method probably set the example which was to be followed by later clinicians, including Charcot at the Salpêtrière.