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19 results

  • Clinical phenotypes of autism spectrum disorders and epilepsy comorbidity

  • T. Skrypnyk
  • Journal:
    European Psychiatry / Volume 65 / Issue S1 / June 2022
    Published online by Cambridge University Press:
    01 September 2022, pp. S230-S231
    • Article
      • You have access
      • Open access
    • PDF
    • Export citation
  • Introduction

    ASD with epileptic seizures (ES) and/or specific epileptic activity on EEG (EEG SEA) and repetitive movements and vocalizations (RMV) can be determined by different variants of genetic polymorphism or by different variants of gene expression, determined by different influences.

    Objectives

    To study the features of the clinical phenotype of ASD in preschool and school-age children with ES, EEG SEA and RMV.

    Methods

    : The study group was divided 116 children aged 2-10 years with ASD into three subgroups: subgroup A - 23 children with a history of ES, subgroup B - 35 children with EEG SEA without ES, subgroup C - 19 children with ASD having EEG SEA, RMV (motor stereotypes, motor tics and/or vocal tics). The control group consisted of 39 children with ASD non a history of ES and EEG SEA.

    Results

    : Children with ASD, complicated by severe and frequent ES are charactered by impaired social reciprocity and communication against the background of regression / stagnation of speech and motor skills development (aOR: 2,7 [1,7-4,8]). Disoders of communication and repetitive behavior in ASD in children of different ages are represented by different monoqualitative syndrome (phenotypes). Movement stereotypes predominated in children with ASD without ES and without EEG SEA (aOR: [1,8-7,9]). In children with ASD and EEG SEA, motor stereotypes and repetitive behavior were equally common ([SD] 2.1 -1, P =0.81).

    Conclusions

    : Disorders of social reciprocity, communication, repetitive behavior are diagnostically significant for ASD complicated by ES, ASD with EEG SEA.

    Disclosure

    No significant relationships.

  • Chapter 5.2 - Genetic Small-Vessel Diseases

  • from 5 - Hereditary and Genetic Causes of Stroke
  • Edited by Derya Uluduz, Istanbul Üniversitesi
  • Anita Arsovska
  • Book:
    Rare Causes of Stroke
    Published online:
    06 October 2022
    Print publication:
    01 September 2022, pp 234-239

  • Summary

    Brain infarction due to cerebral small vessel disease (SVD) accounts for up to 25% of all ischemic strokes. CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) and CARASIL (cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy) are among the monogenic hereditary cerebral SVDs. Herein, we reported a case of sporadic CADASIL-like disease and provided information about CADASIL and CARASIL, two of the most common of inheredited SVDs that are usually overlooked

  • Dissociative and Epileptic seizures: how to distinguish them?

  • A. Certo, J. Rodrigues, O. Nombora, M. Basto, E. Mendes
  • Journal:
    European Psychiatry / Volume 65 / Issue S1 / June 2022
    Published online by Cambridge University Press:
    01 September 2022, p. S481
    • Article
      • You have access
      • Open access
    • PDF
    • Export citation
  • Introduction

    Dissociative seizures (DS) are classified as dissociative convulsions within the group of dissociative disorders. Although they share many features with epileptic seizures (ES), they are not a consequence of abnormal brain discharges and may be related to psychogenic causes. DS represent a common diagnostic and are often confounded with ES.

    Objectives

    The aim of this study is to review the current evidence about the differential diagnosis between DS and ES.

    Methods

    We conducted a non-sytematic review on the topic, using Pubmed/Medline database.

    Results

    Studies emphasize a correct diagnosis before treatment of seizures. DS and ES respond differently to anticonvulsant medication and early or incorrect prescription of can even exacerbate DS. Clinical features and a neuropsychiatric history can also help. The presence of a dissociative “stigmata”, such as unexplained sensory loss, may support a non-epileptic diagnosis. EEG videorecording method is the gold standard diagnosis for DS, however often displays rhythmic movement artifacts that may resemble seizure activity and confound the interpretation. The absence of ictal EEG discharges characteristic of epilepsy is a sign of DS. However, this may not be true for some partial ES, particularly those from temporal lobes, whom also tend to report shorter duration of seizures, whereas patients with DPD often describe experiences lasting for hours or longer.

    Conclusions

    Distinguish DS from ES can be challenging. However, there are features that can help in the differential diagnosis. A correct diagnosis is essential for an adequate therapeutic approach, better prognosis, reduction of medical costs and also a referral to the right medical specialty.

    Disclosure

    No significant relationships.

  • Chapter 9 - Channelopathies

  • Nicholas Wood
  • Book:
    Neurogenetics
    Published online:
    05 May 2012
    Print publication:
    12 April 2012, pp 121-135

  • Summary

    The current classification of epileptic seizures, epilepsies, and epilepsy syndromes is considered first. The presence of progressive neurological signs is a cause for concern and suggests a degenerative disorder. Investigations may include biochemical investigation, EEG, video telemetry, cranial imaging, and DNA diagnostics. Affected males with fragile-X have an increased frequency of epilepsy. Estimates of its prevalence vary from 28% to 45%. Seizures may be generalized tonic-clonic, partial with or without secondary generalization, or of multiple types. Advances in human molecular genetic techniques have allowed positional cloning strategies to be applied to identification of the defective genes and their protein products. A number of studies have been performed on the incidence of epilepsy in the offspring of epileptic parents, and provide an empiric risk of 1. 7%-7. 3%, with a median of 4. 2% for all types of seizures, including febrile convulsions and single seizures.

  • Chapter 87 - Alzheimer disease and other neurodegenerative diseases

  • from Section 3 - Symptomatic epilepsy
  • Edited by Simon D. Shorvon, Frederick Andermann, Renzo Guerrini
  • Book:
    The Causes of Epilepsy
    Published online:
    05 March 2012
    Print publication:
    14 April 2011, pp 618-624

  • Summary

    This chapter addresses the topic of brain tumors as causes of epilepsy. It focuses on secondary brain tumors, commonly referred to as solid metastatic brain tumors, and neoplastic meningitis. Epileptic seizures in patients with cerebral metastatic disease are most likely multifactorial, however, a number of factors are considered to be contributing to the development and continuation of these seizures in a subgroup of individuals. Antiepileptic drugs are known to reduce the activity of chemotherapeutic drugs. The treatment of epilepsy in patients with secondary brain tumors should involve a multidisciplinary team that is knowledgeable about all the surgical, radiation, and therapeutic options in the management of these patients. Research needs to be focused on the best antiepileptic drug (AED) or drug combination to use in these patients so that new practice guidelines can be developed to improve patient care.

  • Chapter 31 - Organic acid, amino acids, and peroxisomal disorders

  • from Section 3 - Symptomatic epilepsy
  • Edited by Simon D. Shorvon, Frederick Andermann, Renzo Guerrini
  • Book:
    The Causes of Epilepsy
    Published online:
    05 March 2012
    Print publication:
    14 April 2011, pp 216-230

  • Summary

    The dentato-rubro-pallido-luysian atrophy (DRPLA) disorder was predominantly seen in the Japanese population. DRPLA is an autosomal dominant neurodegenerative disorder caused by abnormal repeat expansions within the DRPLA gene located on chromosome 12p13.31. Ataxia, choreoathetosis, and/or myoclonus and mental decline are the cardinal signs. Epileptic seizures usually occur in patients with an earlier onset. Unstable expanded CAG repeats in one allele in the DRPLA gene are responsible for this disorder and the size of the CAG expansion is well correlated with age of onset and severity of the disease. There are characteristic degeneration of both the dentato-rubral and pallido-luysian systems in the brain. Diffferential diagnosis includes all types of progressive myoclonic epilepsies, hereditary ataxia, and Huntington chorea. An autosomal dominant hereditary pattern and anticipation from the paternal side make the diagnosis more likely. However, a definitive diagnosis is based on genetic testing.

  • Chapter 51 - Arachnoid cysts

  • from Section 3 - Symptomatic epilepsy
  • Edited by Simon D. Shorvon, Frederick Andermann, Renzo Guerrini
  • Book:
    The Causes of Epilepsy
    Published online:
    05 March 2012
    Print publication:
    14 April 2011, pp 341-345

  • Summary

    The clinical manifestations of Urea cycle disorders are the result of acute or chronic hyperammonemia and include acute neurologic and gastrointestinal symptoms and signs. Chronic hyperammonemia may induce changes in N-methyl-D-aspartate (NMDA) receptor-mediated neurotransmission and induction of astrocytosis. Patients with partial urea cycle enzyme deficiencies may have a much later presentation, usually with hepatogastric, neurologic, or psychiatric symptoms. Seizures in the neonate are a sign of acute hyperammonemia and occur in approximately 50% of severely hyperammonemic neonates. The electroencephalographic (EEG) abnormalities may parallel the clinical course with improvement in the background and resolution of the epileptiform discharges. Measurement of blood ammonia after a protein load may help to establish the diagnosis in patients with normal baseline ammonia levels. Hemodialysis and hemofiltration can be used to lower ammonia levels acutely while measures to reverse the catabolic state are implemented by infusion of glucose and insulin.

  • Chapter 54 - Neonatal seizures and postneonatal epilepsy – causes

  • from Section 3 - Symptomatic epilepsy
  • Edited by Simon D. Shorvon, Frederick Andermann, Renzo Guerrini
  • Book:
    The Causes of Epilepsy
    Published online:
    05 March 2012
    Print publication:
    14 April 2011, pp 373-381

  • Summary

    Epileptic seizures can occur in many inborn errors of metabolism (IEMs), usually as part of a larger clinical spectrum. This chapter considers IEMs, most of which are amenable to specific metabolic treatment. Epilepsy is frequent in Glucose transporter type 1 (GLUT-1) deficiency. Hyperinsulinism/hyperammonemia syndrome (HI/HA) is a rare disorder resulting from missense mutations in glutamate dehydrogenase. Non-ketotic hyperglycinemia (NKH) results from mutations in the subunits of the glycine cleavage enzyme that degrades the neurotransmitter glycine. The congenital disorder of glycosylation (CDG) syndrome covers a group of autosomal recessive diseases, resulting from mutations in the enzymes responsible for protein glycosylation. Epileptic patients, when an IEM is suspected, should have a complete clinical examination, EEG, brain magnetic resonance imaging (MRI) with proton magnetic resonance spectroscopy, ophthalmologic examination, and abdominal ultrasonography. Practical efforts should be made to identify the IEM that can benefit from tailored metabolic therapies.

  • Chapter 55 - Cerebral palsy

  • from Section 3 - Symptomatic epilepsy
  • Edited by Simon D. Shorvon, Frederick Andermann, Renzo Guerrini
  • Book:
    The Causes of Epilepsy
    Published online:
    05 March 2012
    Print publication:
    14 April 2011, pp 382-387

  • Summary

    Down syndrome (DS) is caused by trisomy 21, and is one of the most common chromosomal disorders and etiology of congenital mental retardation. Down syndrome increases the risk of developing acute megakaryoblastic anemia (AMKL) and acute lymphoblastic leukemia (ALL). Approximately 10% of newborns with DS present with transient myeloproliferative disorder (TMD), and 10-20% with TMD develop AMKL before 4 years of age. People with DS have a greatly increased risk of early-onset Alzheimer disease (AD). Epileptic seizures occur in 5-10% of DS patients and prevalence increases with age. Children with DS may exhibit various seizures types, including myoclonic, atonic, tonic-clonic, and, rarely, partial seizures. There is no etiologic treatment for DS, but supportive care and treatment of associated conditions such as cardiac and gastrointestinal abnormalities are indicated. Approximately one-third of patients die in infancy and 50% during the first 5 years from cardiac and respiratory infections.

  • Chapter 41 - 4p (Wolf–Hirschhorn) syndrome

  • from Section 3 - Symptomatic epilepsy
  • Edited by Simon D. Shorvon, Frederick Andermann, Renzo Guerrini
  • Book:
    The Causes of Epilepsy
    Published online:
    05 March 2012
    Print publication:
    14 April 2011, pp 277-280

  • Summary

    This chapter presents the clinical features, etiology, and treatment of Sturge-Weber syndrome (SWS). SWS is a rare, sporadic, congenital disorder arising from an early developmental lesion affecting the facial skin, the eye, and the central nervous system. The association of neurological and developmental deterioration and the onset of seizures means that patients with SWS often suffer considerable disability. The effect of choroidal or ciliary body hemangioma in SWS interferes with the angle of the eye, causing elevated episcleral venous pressure or hypersecretion of fluid. Epileptic seizures are the predominant symptom of SWS and occur in about 80% of cases presenting port-wine stain (PWS) and leptomeningeal angioma. Magnetic resonance imaging (MRI) should be performed at a distance of a seizure event to avoid false interpretation of gadolinium enhancement, due to contrast leakage because of alteration of the blood-brain barrier.

  • Chapter 47 - Agenesis of the corpus callosum

  • from Section 3 - Symptomatic epilepsy
  • Edited by Simon D. Shorvon, Frederick Andermann, Renzo Guerrini
  • Book:
    The Causes of Epilepsy
    Published online:
    05 March 2012
    Print publication:
    14 April 2011, pp 305-310

  • Summary

    Inherited disorders of amino acid, organic acid, and peroxisomal metabolism are individually rare but have a high cumulative frequency. The peroxisomal disorders are subdivided into two groups: the peroxisome biogenesis disorders and the single peroxisome enzyme deficiencies. Impaired mitochondrial glutamate transport has been reported in an autosomal recessive neonatal myoclonic epilepsy. Epileptic seizures may be the inaugural or the main symptom in rare inborn errors of intermediary metabolism. Biochemical analyses in Zellweger spectrum disorders show elevated plasma very long chain fatty acids (VLCFA) and usually deficient erythrocyte membrane plasmalogens. Metabolic acidosis with ketosis is suggestive of organic acidurias such as methylmalonic aciduria, propionic aciduria, and isovaleric acidemia, and may indicate a large number of rarer and less known organic acidurias. Therapy with biotin in biotinidase deficiency and with vitamin B6 in vitamin B6-dependency represent two of the most successful therapies for inborn errors of metabolism.

  • Chapter 18 - Lafora body disease

  • from Section 3 - Symptomatic epilepsy
  • Edited by Simon D. Shorvon, Frederick Andermann, Renzo Guerrini
  • Book:
    The Causes of Epilepsy
    Published online:
    05 March 2012
    Print publication:
    14 April 2011, pp 143-146

  • Summary

    In vitro analyses of the functional properties of neuronal nicotinic acetylcholine receptor (nAChR) disclosed gain of function (i.e. an increase in acetylcholine sensitivity) of mutant receptors associated with autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) that may underlie the neuronal network dysfunction responsible for the epileptic seizures. Positron emission tomography (PET) studies in ADNFLE patients suggest a hyperactivation of the cholinergic pathway ascending from the brainstem. An accurate description of the phenotypic aspects of the patients, including precise clinical and electroencephalogram (EEG) semiology of seizures, is mandatory for a correct diagnosis. The most frequent diagnostic dilemma is distinguishing NFLE seizures from parasomnic attacks. An effect of nicotine on the seizures was elegantly demonstrated in a controlled trial and may be explained by considering that the mutant nAChRs are altered and nicotine acts as an acetylcholine receptor agonist.

  • Chapter 11 - Benign adult familial myoclonic epilepsy

  • from Section 2 - Idiopathic epilepsy
  • Edited by Simon D. Shorvon, Frederick Andermann, Renzo Guerrini
  • Book:
    The Causes of Epilepsy
    Published online:
    05 March 2012
    Print publication:
    14 April 2011, pp 85-90

  • Summary

    Epilepsy is a disease of the brain characterized by recurring unprovoked epileptic seizures, caused by a transient abnormality of neuronal activity which results in synchronized electrical discharges of neurons within the central nervous system (CNS). This chapter focuses on the most important characteristics of voltage- and ligand-gated ion channels, their role in determining neuronal excitability, and the impact of some reported mutations on epileptogenesis in idiopathic epilepsies. It describes the importance of the thalamocortical loop and thalamic ion channels for the generation of generalized seizures. The binding of transmitters and the coupling to channel opening are complex processes which can consequently be influenced by amino acid changes in many different regions of these channels. Most anticonvulsant drugs that are in clinical use today act by modulating the function of ion channels and the chapter describes how ion channel function can be altered by genetic defects associated with idiopathic epilepsies.

  • Chapter 8 - Paroxysmal paresis

  • Edited by Bettina Schmitz, Barbara Tettenborn, Johannes Gutenberg Universität Mainz, Germany, Donald L. Schomer, Harvard University, Massachusetts
  • Book:
    The Paroxysmal Disorders
    Published online:
    06 December 2010
    Print publication:
    09 September 2010, pp 89-112

  • Summary

    The gold standard case history is of particularly high importance in paroxysmal disorders because many seizures may comprise a variety of subjective symptoms or may even consist exclusively of these symptoms. Taking a seizure history is primarily for diagnostic purposes, largely to differentiate epilepsy from other seizure-like disorders but also to distinguish between different types of epileptic seizures and to understand the anatomy and etiology of these events. Hypotheses are formed, followed-up or refuted, and they determine the subsequent course of the interview. Such an in-depth dialogue also opens up perspectives beyond diagnostics. Beyond providing diagnostic clues and anatomical understanding, another frequent consequence of these interviews is indications for the best further therapeutic strategy. Verbal communication is only successful when the partners in dialogue find a common language. A dialogue is frequently necessary to get the full picture of all subjective seizure symptoms and their sequence.

  • 33 - EALES RETINOPATHY

  • from PART III: - VASCULAR CONDITIONS OF THE EYES, EARS, AND BRAIN
  • Edited by Louis R. Caplan, Julien Bogousslavsky
  • Book:
    Uncommon Causes of Stroke
    Published online:
    06 January 2010
    Print publication:
    09 October 2008, pp 235-236

  • Summary

    Sturge-Weber syndrome is characterized by a facial cutaneous nevus (port-wine stain) and a leptomeningeal angioma, often found ipsilateral to the facial lesion. Epileptic seizures, mental retardation, and focal neurological deficits are the primary neurologic abnormalities of Sturge-Weber syndrome. In a series of 52 adults with Sturge-Weber syndrome, 65% had neurologic deficits including stroke, hemiparesis, spasticity, and/or weakness. Neuroimaging, electroencephalography, and functional testing with Positron emission tomography (PET) and Single-photon emission computed tomography (SPECT) may also help to define the extent of the intracranial lesion for possible epilepsy surgery. Although gyral calcification is a classic feature of Sturge-Weber syndrome, this "tram track" appearance is not always present. Bilateral calcification is common. Calcification often becomes more apparent as the patient becomes older but is sometimes already present at birth. Daily aspirin has been tried in an effort to prevent recurrent vascular thrombosis that may cause neurologic deterioration.

  • Measurement of cerebral perfusion with arterial spin labeling: Part 2. Applications

  • GREGORY G. BROWN, CAMELLIA CLARK, THOMAS T. LIU
  • Journal:
    Journal of the International Neuropsychological Society / Volume 13 / Issue 3 / May 2007
    Published online by Cambridge University Press:
    20 March 2007, pp. 526-538

  • Arterial spin labeling (ASL) uses magnetic resonance imaging methods to measure cerebral blood flow (CBF) non-invasively. ASL CBF validly localizes brain function and may be especially useful for studies where the time frame of behavioral change is more than a few minutes, such as in longitudinal and treatment studies. ASL measures of cerebral perfusion are highly accurate in detecting lesion laterality in temporal lobe epilepsy, stenotic-occlusive disease, and brain tumors. Among lesioned patients, ASL CBF has excellent concurrent validity when correlated with CBF measured by Positron Emission Tomography or with dynamic susceptibility-weighted magnetic resonance. ASL CBF can predict tumor grading in vivo and can predict six-month response to the surgical treatment of brain tumors. ASL's capability to selectively and non-invasively tag flow in major vessels may refine the monitoring of treatment of cerebrovascular disease and brain tumors. Conclusions about the utility of ASL are limited by the small sample sizes of the studies currently in the literature and by the uncertainty caused by the effect of brain disease on transit times of the magnetic tag. As the method evolves, ASL techniques will likely become more widely used in clinical research and practice. (JINS, 2007, 13, 526–538.)

  • 17 - Antiepileptic drug interactions in handicapped and mentally retarded patients

  • from Part IV - Drug interactions in specific patient populations and special conditions
    • By Matti Sillanpää, Departments of Child Neurology and Public Health, University of Turku, Turku, Finland
  • Edited by Jerzy Majkowski, Blaise F. D. Bourgeois, Harvard University, Massachusetts, Philip N. Patsalos, Institute of Neurology, London, Richard H. Mattson, Yale University, Connecticut
  • Book:
    Antiepileptic Drugs
    Published online:
    07 September 2009
    Print publication:
    26 May 2005, pp 325-340

  • Summary

    This chapter emphasizes the context in which pharmacokinetic and pharmacodynamic interactions are likely to occur during the treatment of epilepsy in handicapped and mentally retarded patients. The diagnosis of epileptic seizures may be difficult in mentally retarded patients, because they cannot in many cases express themselves and therefore fail to tell about their perceived symptoms. The main groups of reasons for intractability of seizures are related to actions by the physician, to the patient, to the epilepsy itself, and to the drugs. Epilepsy in mental retardation commonly presents with several seizure types, drug resistance, concomitant psychiatric symptoms and syndromes with various enzyme abnormalities, which increase the risk of interactions. The outcome of drug therapy may be difficult to assess in the mentally retarded, for example in patients with infantile spasms. The impact of the newer antiepileptic drugs may consist of a better tolerability with fewer interactions.

  • 6 - Epilepsy: epidemiology, definitions, and diagnostic procedures

  • from Part II - Epilepsy diagnosis and treatment
    • By Simon Shorvon, The National Hospital for Neurology and Neurosurgery, National Society for Epilepsy, Gerrards Cross Chalfont Centre for Epilepsy, Chalfont St Peter, Buckinghamshire SL9 ORJ, England, Dominic Heaney, The National Hospital for Neurology and Neurosurgery, National Society for Epilepsy, Gerrards Cross Chalfont Centre for Epilepsy, Chalfont St Peter, Buckinghamshire SL9 ORJ, England
  • Edited by Martha J. Morrell, Columbia University, New York, Kerry L. Flynn, Columbia-Presbyterian Cancer Center, New York
  • Book:
    Women with Epilepsy
    Published online:
    02 November 2009
    Print publication:
    20 March 2003, pp 57-67

  • Summary

    This chapter outlines and defines the epidemiology and etiology of epilepsy, and explains how these issues are closely related to the present systems of defining and classifying epilepsy. It highlights the issues particularly relevant to women. Epileptic seizures are produced by an abnormal rhythmic and repetitive discharge of neurons, either localized to a particular part of the brain (the 'focal' area) or 'generalized' throughout the whole cerebral cortex. Adults may also develop idiopathic epilepsy or epilepsy that is caused by pathologies developed in childhood. Many people suspect a genetic cause for their epilepsy and are afraid that they might pass it on to their children. The chapter describes the major techniques used to investigate epilepsy. New techniques such as single-photon emission computed tomography (SPECT), positron emission tomography (PET), and functional magnetic resonance imaging (MRI) can examine the functioning of patients' brains without the need to perform invasive surgical techniques.

  • 9 - Nonepileptic seizures

  • from Part II - Epilepsy diagnosis and treatment
    • By Steven C. Schachter, Beth Israel Deaconess Medical Center, Comprehensive Epilepsy Center, 300 Brookline Avenue, Boston, MA 02215, USA
  • Edited by Martha J. Morrell, Columbia University, New York, Kerry L. Flynn, Columbia-Presbyterian Cancer Center, New York
  • Book:
    Women with Epilepsy
    Published online:
    02 November 2009
    Print publication:
    20 March 2003, pp 89-98

  • Summary

    Nonepileptic seizures are behavioral events that look to other people like epileptic seizures or are events that create internal sensations that may also occur in people who have epileptic seizures. This chapter focuses on psychogenic nonepileptic seizures, which are referred to simply as nonepileptic seizures. The patient with nonepileptic seizures may have a history of having experienced one or more significant traumatic events, such as sexual or physical abuse. Electroencephalogram (EEG) monitoring is the best way to make an accurate diagnosis of nonepileptic seizures. This test involves recording the brain rhythms of the patient for a prolonged period, typically for one or more days, usually in the hospital and while video images of the patient are also being recorded. Treatment begins when the results of EEG monitoring (including the findings of the provocative tests, if done) are discussed with the patient.