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A case study of the cognitive and behavioral deficits of temporal lobe damage in herpes simplex encephalitis
Abstract
Herpes simplex viral encephalitis is a fairly common nonepidemic encephalitis which produces severe neurological sequelae in survivors. Most viral infections of the central nervous system produce diffuse damage, but the herpes simplex virus demonstrates a predilection for localization in the temporal and orbitofrontal regions of the brain. This case study illustrates the highly significant language difficulties, marked memory deficits, and propensity for physical aggression following temporal lobe damage brought about by herpes encephalitis, and presents the usefulness of a new diagnostic measure in delineating such a variable cognitive pattern.
... However, magnetic resonance imaging (MRI), along with the clinical presentation, has been found to be a sensitive and efficacious means of diagnosing HSE (Whitley & Kimberlin, 2005). The infection localizes itself in the brain rather than causing diffuse damage, causing focal necrosis in the temporal, limbic, and orbitofrontal structures of the brain Greer, Lyons-Crews, Mauldin, & Brown, 1989;Whitley & Kimberlin, 2005). Specifically, HSE can cause damage to the hippocampus, amygdala, and areas of the frontal lobe (Lezak et al., 2004). ...
... Due to the focal damage that HSE can cause in the aforementioned brain regions, it often causes some degree of neurological impairments for the survivors, leading to cognitive and behavioral deficits Raschilas et al., 2002;Whitley & Kimberlin, 1999, 2005. The deficits reported in the neuropsychological profile of survivors of HSE as a result of this neurological impairment include deficits in memory, language, visuospatial abilities, executive functioning, inhibition, and social behavior (Greer et al., 1989;Hokkanen et al., 1996;Lezak et al., 2004;Pietrini, Nertempi, Vaglia, Revello, & Pinna, 1988;Stewart, Parkin, & Hunkin, 1992;Wilson, Baddeley, & Kapur, 1995). ...
... Memory deficits for both visual and verbal stimuli are pronounced in HSE survivors due to damage to the temporal lobes (Greer et al., 1989;Hokkanen et al., 1996;Wilson et al., 1995), with damage to the hippocampus detrimentally affecting patients' ability to learn new information (Lezak et al., 2004). Hokkannen and colleagues compared the cognitive deficits of HSE patients to a control group and also with patients who suffered from other types of acute encephalitis 1 month after the onset. ...
This study describes a patient with herpes simplex encephalitis. Brain MRI showed the expected finding of medial temporal damage. Neuropsychological assessment results were consistent with the location of damage, with profound memory impairment and mildly impaired naming, but normal visuospatial and executive skills. The patient also showed a typical testing pattern of insufficient effort and possible malingering, which was concerning as she was seeking disability compensation. In spite of this, we chose to place greatest weight on the finding of deficits consistent with the type, location, and severity of brain damage, considering this to be true cognitive impairment.
... This was strongly suspected to be herpetic in origin because of the positive vesical culture and the characteristic involvement of the eyes. Greer, Lyons-Crews, Mauldin, and Brown (1989) recently commented on the cognitive and behavioral deficits of temporal lobe damage in herpes encephalitis. They described a 14-year-old boy, who was apparently normal till the second grade when he was admitted to hospital with herpes simplex encephalitis. ...
... He later developed significant and persistent language, social, and memory deficits. Herpes virus appears to have a predilection for the temporal lobes (Greer et al., 1989). Several studies have implicated the temporal lobes in the pathogenesis of autism (e.g., Heltzer & Griffin, 1981). ...
... Thalidomide's binding to the CRBN-DDB1-CUL4A complex inhibits its associated ubiquitin ligase activity and disrupts downstream pathways involved in physical and mental development [4]. The CRBN protein also binds to the UL14 protein of the herpes simplex virus type 1 (HSV1) [9], a virus with a neurotropism for the hippocampus (HPC) [10][11][12]. CRBN's abundance in HPC neurons with prominent expression in the hilus and granule cell layer of the dentate gyrus [13], correlates with the topography of HSV1's selective regional damage to the HPC [10]. Thus, CRBN may be a target for HSV1 mediated HPC injury and participate in the pathogenesis of the memory deficits in patients who survive HSV1 encephalitis [10][11][12]. ...
... CRBN's abundance in HPC neurons with prominent expression in the hilus and granule cell layer of the dentate gyrus [13], correlates with the topography of HSV1's selective regional damage to the HPC [10]. Thus, CRBN may be a target for HSV1 mediated HPC injury and participate in the pathogenesis of the memory deficits in patients who survive HSV1 encephalitis [10][11][12]. The observation that activation of the NF-E2-related factor 2 (Nrf2)/antioxidant response element site in the promoter region of crbn is responsible for the in vitro increase in crbn expression during hypoxic stress, suggests that crbn has a role in the selective vulnerability of HPC neurons to hypoxic ischemic injury [14]. ...
A nonsense mutation in the human cereblon gene (CRBN) causes a mild type of autosomal recessive non-syndromic intellectual disability (ID). Animal studies show that crbn is a cytosolic protein with abundant expression in the hippocampus (HPC) and neocortex (CTX). Its diverse functions include the developmental regulation of ion channels at the neuronal synapse, the mediation of developmental programs by ubiquitination, and a target for herpes simplex type I virus in HPC neurons. To test the hypothesis that anomalous CRBN expression leads to HPC-mediated memory and learning deficits, we generated germ-line crbn knock-out mice (crbn(-/-)). We also inactivated crbn in forebrain neurons in conditional knock-out mice in which crbn exons 3 and 4 are deleted by cre recombinase under the direction of the Ca(2+)/calmodulin-dependent protein kinase II alpha promoter (CamKII(cre/+), crbn(-/-)). crbn mRNA levels were negligible in the HPC, CTX, and cerebellum (CRBM) of the crbn(-/-) mice. In contrast, crbn mRNA levels were reduced 3- to 4-fold in the HPC, CTX but not in the CRBM in CamKII(cre/+), crbn(-/-) mice as compared to wild type (CamKII(cre/+), crbn(+/+)). Contextual fear conditioning showed a significant decrease in the percentage of freezing time in CamKII(cre/+), crbn(-/-) and crbn(-/-) mice while motor function, exploratory motivation, and anxiety-related behaviors were normal. These findings suggest that CamKII(cre/+), crbn(-/-) mice exhibit selective HPC-dependent deficits in associative learning and supports the use of these mice as in vivo models to study the functional consequences of CRBN aberrations on memory and learning in humans.
... In contrast, other studies have found connections between various viral infections and the development of autism (Table 1). Gregg (1941) first linked congenital rubella virus infection to defects in the, 1941;Desmond et al, 1970;Stubbs, 1976;Chess, 1971Chess, , 1977Herpes simplex virusJorgensen et al, 1982Herpes simplex virusDeLong et al, 1981;Gillberg, 1986;Greer et al, 1989;Ghaziuddin et al, 1992, 1975Intrauterine human parvovirusAnlar et al, 1994Cytomegalovirus (CMV)Stubbs, 1978;Markowitz, 1983;Ivarsson et al, 1990;ined the relationship between prenatal rubella and autism and found that autistic children had an altered immune response to rubella vaccination indicating that they had been congenitally infected with rubella virus.Chess (1971Chess ( , 1977) conducted studies linking congenital rubella to autism.Chess (1971)found that children who had congenital rubella had an increased incidence of autism. The prevalence rates were 412 children with the complete syndrome of autism (Kanner's classical criteria) plus 329 children with a partial autism syndrome (displaying a significant number of signs of autistic behavior) for a total of 741 children with autism per 10,000 children having congenital rubella. ...
... In contrast,Gillberg (1986)described the development of the classical symptoms of autism over a 70-day period following herpes encephalitis in a 14-year-old girl. This was followed by a report byGreer et al (1989)who described the development of autism in another older child, a 14-year-old male, whose autistic symptoms continued after the acute signs of herpes encephalitis had diminished.Ghaziuddin et al (1992)documented two patients who in all likelihood were infected in utero or soon after birth with HSV and developed herpes encephalitis. Both children developed autism as defined in the Diagnostic ...
Autistic disorder (autism) is a behaviorally defined developmental disorder with a wide range of behaviors. Although the etiology of autism is unknown, data suggest that autism results from multiple etiologies with both genetic and environmental contributions, which may explain the spectrum of behaviors seen in this disorder. One proposed etiology for autism is viral infection very early in development. The mechanism, by which viral infection may lead to autism, be it through direct infection of the central nervous system (CNS), through infection elsewhere in the body acting as a trigger for disease in the CNS, through alteration of the immune response of the mother or offspring, or through a combination of these, is not yet known. Animal models in which early viral infection results in behavioral changes later in life include the influenza virus model in pregnant mice and the Borna disease virus model in newborn Lewis rats. Many studies over the years have presented evidence both for and against the association of autism with various viral infections. The best association to date has been made between congenital rubella and autism; however, members of the herpes virus family may also have a role in autism. Recently, controversy has arisen as to the involvement of measles virus and/or the measles, mumps, rubella (MMR) vaccine in the development of autism. Biological assays lend support to the association between measles virus or MMR and autism whereas epidemiologic studies show no association between MMR and autism. Further research is needed to clarify both the mechanisms whereby viral infection early in development may lead to autism and the possible involvement of the MMR vaccine in the development of autism.
... Beyin ile ilişkili enfeksiyöz yada otoimmun ensefalitler de bu tıbbi durumlardan olabilir Özellikle üç yaştan sonra ortaya çıkan otistik belirtilerin nedenleri araştırılırken bu konuda akılda tutulmalıdır 15 . Konu ile ilgili yazın incelendiğinde özellikle temporal bölgeyi içeren ensefalit durumlarında olgularda otistik belirtilerin gözlendiği bildirilmiştir 16 . Limbik ensefalitler de temporal bölge ile ilişkili otoimmun kökenli ensefalitlerdir. ...
Childhood disintegrative disorder (CDD) is a neuropsychiatric syndrome characterized as autism spectrum disorder in DSM 5 which is described by regression in the areas of communication, social interaction skills and motor behavior that develop normally in the first years of life. Autoimmune limbic encephalitis occurs with clinical manifestations of limbic system involvement such as subacute memory malformation, various neuropsychiatric symptoms, behavioral disturbances, and temporal lobe seizures. In this paper; an 7-year-old girl who applied with CDD findings, and diagnosed with limbic encephalitis after physical examination with symptoms persisted after IVIG treatment, was reported. Although autistic symptoms due to limbic encephalitis may be rarely seen in the clinic, autistic symptoms that are particularly acute or subacute are important neurological diagnoses that should be kept in mind in the differential diagnosis of psychiatric patients.
... From prenatal period to adulthood, many researchers have found evidence of altered immune mediators in ASD patients both peripherally and centrally. 5 Maternal immune activation as a response to viral and bacterial infections [6][7][8][9] and maternal antifetal autoantibodies have been associated with increased risk for ASD. 10 Studies evaluating cellular immunity reported altered lymphocyte count, reduced T lymphocyte counts and functions as well as imbalanced helper/suppressor lymphocyte ratio. [11][12][13][14] Growing attention is being paid to altered levels of cytokines and chemokines in plasma or serum but unfortunately consistent findings couldn't have been obtained. ...
Objective: Although autism spectrum disorder (ASD) is one of the most studied neurodevelopmental disorders, its etiology has not been fully elucidated. A growing body of evidence suggest the role of neuroinflammation in the etiology of ASD. Neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR) are markers of systemic inflammation. In this study, we aimed to evaluate NLR and PLR in children with ASD comparison to healthy controls. Methods: We reviewed the medical files of children with ASD in the ages of 2 to 5. The ASD group were consisted of drug-naïve 64 children who had complete blood count within a month of assessment. Age and sex matched 64 healthy children without any psychiatric disorders were recruited from the healthy child outpatient unit of the hospital. Results: NLRs were significantly higher in ASD. Children with ASD had significantly higher neutrophil counts but lower platelet and lymphocyte counts compared to those of healthy controls. NLR was found to be a predictor of ASD. Conclusions: Increased NLRs support the hypothesis of the involvement of neuroinflammation in the under-lying physiopathology of ASD. Even though recent evidence is not enough to suggest that in young children increased NLR levels may be used as screening and early intervention predictor, it should be kept in mind and may inspire new studies. Further longitudinal studies with larger sample size and homogeneous groups regarding the age and subtypes may clarify the inflammatory involvement in ASD. © 2018, Cukurova University, Faculty of Medicine. All rights reserved.
... From prenatal period to adulthood, many researchers have found evidence of altered immune mediators in ASD patients both peripherally and centrally. 5 Maternal immune activation as a response to viral and bacterial infections [6][7][8][9] and maternal antifetal autoantibodies have been associated with increased risk for ASD. 10 Studies evaluating cellular immunity reported altered lymphocyte count, reduced T lymphocyte counts and functions as well as imbalanced helper/suppressor lymphocyte ratio. [11][12][13][14] Growing attention is being paid to altered levels of cytokines and chemokines in plasma or serum but unfortunately consistent findings couldn't have been obtained. ...
Objective: Although autism spectrum disorder (ASD) is one of the most studied neurodevelopmental disorders, its etiology has not been fully elucidated. A growing body of evidence suggest the role of neuroinflammation in the etiology of ASD. Neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR) are markers of systemic inflammation. In this study, we aimed to evaluate NLR and PLR in children with ASD comparison to healthy controls. Methods: We reviewed the medical files of children with ASD in the ages of 2 to 5. The ASD group were consisted of drug-naïve 64 children who had complete blood count within a month of assessment. Age and sex matched 64 healthy children without any psychiatric disorders were recruited from the healthy child outpatient unit of the hospital. Results: NLRs were significantly higher in ASD. Children with ASD had significantly higher neutrophil counts but lower platelet and lymphocyte counts compared to those of healthy controls. NLR was found to be a predictor of ASD. Conclusions: Increased NLRs support the hypothesis of the involvement of neuroinflammation in the underlying physiopathology of ASD. Even though recent evidence is not enough to suggest that in young children increased NLR levels may be used as screening and early intervention predictor, it should be kept in mind and may inspire new studies. Further longitudinal studies with larger sample size and homogeneous groups regarding the age and subtypes may clarify the inflammatory involvement in ASD. (Anatolian Journal of Psychiatry 2018; 19:xx-xx) Keywords: Neutrophil-lymphocyte ratio, platelet-lymphocyte ratio, autism spectrum disorder, inflammation Yüksek nötrofil-lenfosit oranı otizm spektrum bozukluğunu öngörebilir mi? ÖZ Amaç: Otizm spektrum bozukluğu (OSB), üzerinde en çok çalışılan nörogelişimsel bozukluklardan biri olmasına rağmen, etiyolojisi tam olarak aydınlatılamamıştır. OSB'nin altta yatan patofizyolojisinde nöroinflamasyonun rol oynadığına ilişkin çalışmalar ve bulgular giderek artmaktadır. Nötrofil-Lenfosit oranı (NLO) ve trombosit-lenfosit oranı (TLO) sistemik inflamasyonun göstergeleridir. Bu çalışmada, OSB'li çocuklarda sağlıklı kontrollere göre NLO ve TLO'yu değerlendirmeyi amaçladık. Yöntem: Bu çalışmada OSB tanısı olan 2-5 yaşları arasındaki çocukların tıbbi dosyaları gözden geçirilmiştir. Hasta grubu, daha öncesinde ilaç kullanımı olmayan ve tanı konulduğu bir ay içinde tam kan sayımı yapılan 64 çocuktan oluşmaktadır. Sağlam çocuk polikliniğinden psikiyatrik bozukluğu olmayan, yaş ve cinsiyetleri benzer 64 çocuk sağlıklı kontrol olarak çalışmaya alınmıştır. Sonuç: OSB'li çocuklarda, NLO anlamlı olarak yüksek bulunmuştur. Olgu grubunda, sağlıklı kontrollere kıyasla nötrofil sayısı daha yüksek, lenfosit ve trombosit sayısı daha düşük bulunmuştur. NLO değerlerinin OSB'yi yordadığı saptanmıştır. Tartışma:
... Les appuis pour l'hypothèse d'une étiologie autoimmune s'accumulent depuis plus de deux décennies (Chess, 1977 ; Stubbs et al, 1976 Stubbs et al, , 1977 Stubbs et al, , 1978 Stubbs et al, , 1985 Singh et al, 1988 Singh et al, , 1991 Todd et al, 1985; Warren et al, 1985Weizmanetal, 1982;.Yonket al, 1990). Comme c'est maintenant reconnu pour plusieurs autres maladies auto-immunes du système nerveux central (sclérose en plaques, chorée de Sydenham ), la condition semble découler souvent d'une infection (Chess, 1971Chess, , 1977 Gill berg, 1986; Greer et al, 1989; Stubbs et al, 1 978, 1983 ; Peterson et Torrey, 1976). Parmi les facteurs de risque, il y a le syndrome Xfragile , les complications obstétricales, la sclérose tubéreuse de Bourneville, la phénylcétonurie, l'hypsarythmie , la rubéole congénitale (Rapin et Allen, 1983), la neurofibromatose, les spasmes infantiles, la rubéole, l'infection herpétique postnatale, 1 'acidose lactique, les désordres des purines, l'hydrocéphalie, le syndrome de Mobius, la dystrophie musculaire de Duchesne (Harris, 1 998). ...
Comment regrouper les syndromes comportementaux par catégories d'âge? Certains syndromes congénitaux
ne se manifestent que plusieurs années après la naissance (ex : schizophrénie juvénile). Certains syndromes
posent parfois problème avant l'âge scolaire, mais deviennent un handicap majeur, et ne sont diagnostiqués,
qu'à l'arrivée de l'enfant à l'école (ex : maladie de Gilles de la Tourette). Tout regroupement des syndromes comportementaux sera donc forcément relativement arbitraire. Toutefois, parce que le matériel à couvrir est énorme, nous avons néanmoins décidé de nous y risquer. Nous présenterons dans le présent chapitre quelques syndromes congénitaux à manifestation précoce tels l'alcoolisme foetal, le syndrome de Rett, l'autisme, la schizophrénie infantile, et les syndromes neurogènes comportant des comportements violents ou automutilatoires. Il s'est développé, dans la littérature nord-américaine une tendance à nommer l'autisme «désordre envahissant du développement ». Nous nous permettons de juger que cette désignation est tout à fait inappropriée. De nombreux désordres développementaux sont au moins aussi «envahissants» que l'autisme, comme le lecteur pourra aisément le constater à la lecture du présent chapitre. Parce que les chutes, et les abus traumatiques (coups, secousses) de la tête sont un risque pour le jeune enfant, nous traiterons ici aussi de la question du traumatisme crâniocérébral.
... More than 40 years ago, a higher risk for autism was reported in the offspring of maternal rubella infection cases (Chess 1971). Since then, prenatal exposure to different virus have been linked to increased risk for ASD, including herpes simplex virus (DeLong et al. 1981;Ghaziuddin et al. 1992;Gillberg 1986;Greer et al. 1989), cytomegalovirus (Ivarsson et al. 1990;Markowitz 1983;Stubbs 1978;Yamashita et al. 2003), measles (Ring et al. 1997;Singh and Jensen 2003), and viral meningitis (Barak et al. 1999;Ring et al. 1997). Moreover, a larger study showed an increase in the prevalence of autism in children born to mothers hospitalized for viral infections during the first trimester of pregnancy or for bacterial infections during the second trimester . ...
Autism spectrum disorders (ASD) are a group of severe pervasive neurodevelopmental disorders characterized by a highly variable impairment in social interaction and verbal and nonverbal communication, a stereotyped repetitive behavior, learning problems, and aloofness. ASD is frequently accompanied by a core neurobehavioral symptoms and immunological derangements, including aberrant sensitivity to sensory stimulation, anxiety and cellular immune deregulation. Currently, the involvement of the neuroimmune pathology in autism remains unclear and we consider that a better understanding would be useful for earlier clinical and therapeutic intervention. The main aim of this chapter is to review the most current aspects regarding the antibody response in autism occurring either in the periphery or into the brain and how they can influence the abnormal development of the offspring and modulate the nontypical behaviors frequently observed in autism.
... More than 40 years ago, a higher risk for autism was reported in the offspring of maternal rubella infection cases (Chess 1971). Since then, prenatal exposure to different virus have been linked to increased risk for ASD, including herpes simplex virus (DeLong et al. 1981;Ghaziuddin et al. 1992;Gillberg 1986;Greer et al. 1989), cytomegalovirus (Ivarsson et al. 1990;Markowitz 1983;Stubbs 1978;Yamashita et al. 2003), measles (Ring et al. 1997;Singh and Jensen 2003), and viral meningitis (Barak et al. 1999;Ring et al. 1997). Moreover, a larger study showed an increase in the prevalence of autism in children born to mothers hospitalized for viral infections during the first trimester of pregnancy or for bacterial infections during the second trimester . ...
In recent years, an increasing number of mouse and rat models of autism has been validated. These models have shown face validity, exhibiting alterations in behavior similar to those observed in autistic individuals. Moreover, some of these models were aimed to study different putative etiological factors of autism spectrum disorder (ASD), successfully showing construct validity. More recently, these animal models have been proved valuable to assess the contribution of neuroinflammation to ASD. On the one hand, eliciting inflammation in the central nervous system (CNS) during development was shown to result in behavioral alterations in mice similar to those observed in autistic individuals. On the other hand, neuroinflammation and malfunction of the immune system have been observed in different animal models of autism. The use of animal models has then contributed to stress the role and effects of neuroinflammation to the pathophysiology of autism.
... Despite reduced mortality with acyclovir [14], dose has not been associated with HSE outcomes [13] nor has there been an appreciable reduction in morbidity [15,16]. Even those who receive prompt treatment still a chance of experiencing detrimental side effects, including behavioral modifications, amnesia, emotional changes, aphasia, and other cognitive deficits [17][18][19][20][21][22][23][24]. A variety of rehabilitation methods have helped to improve recovery in activities of daily living and semantic processing, such as positive reinforcements or extinction techniques [25], associations (motor imagery strategy) [26], and community-based programs [27]. ...
... Sachdev & Smith, 1992). In a recent example, temporal lobe damage resulting from herpes simplex viral encephalitis in a 14-year old boy resulted in a new syndrome of aggression (Greer & Lyons-Crews, 1989). Charles Whitman, the notorious University of Texas sharpshooting killer of 14, was found upon autopsy to be suffering from a tumour pressing on the amygdala (Joseph, 1990). ...
... Prenatal exposure to rubella (Chess, 1971(Chess, , 1977Stubbs, 1976), herpes simplex virus (DeLong et al., 1981;Ghaziuddin et al., 1992;Gillberg, 1986;Greer et al., 1989), cytomegalovirus (Ivarsson et al., 1990;Markowitz, 1983;Stubbs, 1978;Yamashita et al., 2003), measles (Ring et al., 1997;Singh and Jensen, 2003) or viral meningitis (Barak et al., 1999;Ring et al., 1997) greatly increases the risk for ASD. This led to the claim that prenatal viral infection is the principal nongenetic cause of autism (Ciaranello and Ciaranello, 1995). ...
Recent reports have given a central role to environmental factors in the etiology of autism spectrum disorders (ASD). However, most proposed perinatal factors seem to converge into the activation of the immune system, suggesting that an early inflammatory response could be a unifying factor in the etiology ASD. Here I review the evidence of early immune activation in individuals with ASD, and the chronic peripheral and central alterations observed in the inflammatory response in ASD. This evidence shows that ASD is associated with altered neuroinflammatory processes and abnormal immune responses in adulthood. How these immune alterations can affect developmental programming of adult behavior or directly affect behavior later in life is discussed in the context of both clinical and animal models of research. Recent studies in rodents clearly support a role of elevated cytokines in the behavioral symptoms of ASD, both during development and in adulthood.
... The herpes simplex virus selectively affects the temporal and orbitofrontal regions of the brain. A high number of patients with this sort of encephalitis also show aggressive and disruptive behavior (Greer, Lyons-Crews, Mauldin, & Brown, 1989). ...
The biological basis of psychopathy has not yet been fully elucidated. Few studies deal with structural neuroimaging in psychopaths. The aim of this article is to review these studies in order to contribute to our understanding of the biological basis of psychopathy. Data in the literature report a reduction in prefrontal gray matter volume, gray matter loss in the right superior temporal gyrus, amygdala volume loss, a decrease in posterior hippocampal volume, an exaggerated structural hippocampal asymmetry, and an increase in callosal white matter volume in psychopathic individuals. These findings suggest that psychopathy is associated with brain abnormalities in a prefrontal–temporo-limbic circuit—i.e. regions that are involved, among others, in emotional and learning processes. Additionally, data indicate that psychopathic individuals cannot be seen as a homogeneous group.
The associations between structural changes and psychopathic characteristics do not enable causal conclusions to be drawn, but point rather to the important role of biological brain abnormalities in psychopathy. To gain a comprehensive understanding of this, psychopathy must be viewed as a multifactorial process involving neurobiological, genetic, epidemiological and sociobiographical factors. Copyright
... 1,2,3 In this case, we believe that meningoencephalitis produced brain lesions in neural circuits involved in global development disorders (those for which pathogenic mechanisms are established during development) and thus mimicked a picture of autism. An autistic syndrome has been reported after herpes virus infections in teenagers, 4 and there have been reported relationships between autism and congenital infections (rubella, toxoplasmosis, and cytomegalovirus). 5 To date, there was no case report on atypical autism after pneumococcal meningoencephalitis. ...
... However, other parts of the brain may also be involved and the infection may take the form of meningitis and diffuse encephalitis [13]. Most cases of autism and herpes encephalitis reported in the literature have described damage to the temporal lobes [10]. However, in the present report, damage to the frontal lobes was primary. ...
Autism is a childhood onset neurodevelopmental disorder characterized by reciprocal social deficits, communication impairment, and rigid ritualistic interests, with the onset almost always before three years of age. Although the etiology of the disorder is strongly influenced by genes, environmental factors are also important. In this context, several reports have described its association with known medical conditions, including infections affecting the central nervous system. In this report, we describe an 11-year-old Asian youngster who developed the symptoms of autism following an episode of herpes encephalitis. In contrast to previous similar reports, imaging studies suggested a predominant involvement of the frontal lobes. At follow-up after three years, he continued to show the core deficits of autism. This case further supports the role of environmental factors, such as infections, in the etiology of autism, and suggests that in a minority of cases, autistic symptoms can develop in later childhood.
Behavioral pediatrics is a multidisciplinary field that involves many healthcare specialists
revolving around the practicing pediatrician and primary care clinician; also, various additional, associated fields of training have developed such as developmental-behavioral pediatrics, neurodevelopmental pediatrics, pediatric psychodermatology and medical care for those of all ages with developmental disabilities (1-16). Experts in psychiatry and psychology work closely with pediatric clinicians in a variety of professional relationships, including co-located and non-co-located mental health settings (17-24). Pediatricians can provide a wide variety of care to children and adolescents with complex disorders, depending on their training as well as interests, and this book seeks to provide au courant perspectives in behavioral pediatrics (25-29). Behavioral health screening remains an important task of pediatricians and behavioral pediatricians as they evaluate their pediatric patients (30-40).
Comportamenti violenti sono stati per lungo tempo associati a lesioni focali o a danno diffuso del sistema nervoso centrale (SNC). Ogni condizione che porti a psicosi o mania prevede, come possibile sintomo concomitante, l’aggressività. Condizioni patologiche organiche che non compromettano direttamente l’integrità anatomica cerebrale possono essere causa di comportamento aggressivo, dovuto a diffusi effetti sulla funzionalità del SNC. Irritabilità e aggressività sono un grande bacino di malattia in molti pazienti neurologici e organici e aumentano le difficoltà di famiglie e caregiver.
Autism spectrum disorders (ASD) are a group of severe pervasive neurodevelopmental disorders (PDD) affecting between 1 and 3% of pediatric populations. It is characterized by a highly variable impairment in social interaction and verbal and nonverbal communication, as well as by a stereotyped repetitive behavior, learning problems, and aloofness. ASD behavioral symptoms are frequently accompanied by immunological derangements, including cellular immune dysregulation, chronic inflammatory states, and neuroimmune alterations. Currently, the involvement of the immune pathology in autism remains unclear, and we consider that a better understanding would be useful for earlier clinical and therapeutic interventions. The main aim of this chapter is to review the most current aspects regarding the etiology of autism, with particular reference to the contribution of inflammatory events occurring in the periphery and into the brain, and how they can influence the abnormal development of the offspring and modulate the typical behaviors frequently observed in autism.
Export Date: 18 October 2014
Background/aim:
The etiology of autism spectrum disorder (ASD) is unknown, even though it is hypothesized that a viral infection could trigger this disorder. The aim of this study was to evaluate the seropositivity rate and antibody level of Herpes Simplex Virus 1 (HSV1) and Herpes Simplex Virus 2 (HSV2) in children with ASD compared to same-aged healthy controls.
Patients and methods:
We compared seropositivity rate and levels of antibodies to HSV1/2 in 54 children with ASD (19 with autistic disorder and 35 with non-autistic ASD) and in 46 controls.
Results:
Seropositivity rate and levels of anti-HSV1/2 were not dissimilar between cases and controls. Exposure to HSV2 was minimal.
Conclusion:
Rate of contact with HSV1 and HSV2 assessed by the mean of detection of specific antibodies was similar between children with ASD and healthy controls.
Background/Aim: The etiology of autism spectrum disorders (ASD) still eludes investigators. Several viral infections have been associated with ASD etiopathogenesis but few studies have ever focused on the role of HHV-6 and HHV-8, two members of the herpesviridae family. The aim of the present study was to evaluate seropositivity rate and levels of antibodies to HHV6 and HHV-8 in children with ASD compared to controls.
We measured and compared seropositivity rate and levels of antibodies to HHV-6 and HHV-8 in 30 children with ASD (14 with autistic disorder and 16 with non-autistic disorder ASD) and in 28 healthy controls of the same age.
Seropositivity rate and levels of the two antibodies were similar in cases and controls. Seropositivity rate and levels of antibodies were not correlated with disease severity in children with ASD.
Levels and seropositivity rate of antibodies to HHV-6 and HHV-8 do not differ between children with ASD and controls.
Cases of autistic disorder (autism) have frequently been reported in association with congenital rubella and other infections. These observations stimulated further investigation into markers of immune function in autism. Postinfectious and autoimmune mechanisms of pathophysiology have been proposed. This review comprehensively addresses immune findings to date, including the role of viruses, neuroimmune factors, cellular and humoral immunity, immunogenetics, and immunotherapy in relation to autism. Although numerous immune abnormalities have been identified in autism, inconsistent results have often been reported. To date, research in this area has largely involved small, uncontrolled studies. In order to bring clarity to this field, high-quality, systematic research is needed to explore the role of neuroimmunologic factors in autism.
Autism spectrum disorders (ASD) are disorders of the central nervous system characterized by impairments in communication and social reciprocity. Despite thousands of studies on this topic, the etiopathogenesis of these disorders remains unclear, apart from a general belief that they derive from an interaction between several genes and the environment. Given the mystery surrounding the etiopathogenesis of ASD it is impossible to plan effective preventive and treatment measures. This is of particular concern due to the progressive increase in the prevalence of ASD, which has reached a figure as high as 1:88 children in the USA. Here we present data corroborating a novel unifying hypothesis of the etiopathogenesis of ASD. We suggest that ASD are disorders of the immune system that occur in a very early phase of embryonic development. In a background of genetic predisposition and environmental predisposition (probably vitamin D deficiency), an infection (notably a viral infection) could trigger a deranged immune response which, in turn, results in damage to specific areas of the central nervous system. If proven, this hypothesis would have dramatic consequences for strategies aimed at preventing and treating ASD. To confirm or refute this hypothesis, we need a novel research approach, which unlike former approaches in this field, examine the major factors implicated in ASD (genetic, infections, vitamin D deficiency, immune system deregulation) not separately, but collectively and simultaneously.
Human and non-human primate research has shown that pathological processes affecting the temporal lobe, particularly the amygdala and hippocampus, are related to the development of the autistic syndrome. This case report describes a young male child with left temporal oligodendroglioma, who demonstrated a constellation of autistic behaviors meeting DSM-III-R criteria for pervasive developmental disorder. Abnormalities in social interaction, affective expression and communication were particularly evident. Some of the symptoms improved after tumor resection, while other signs of qualitative abnormalities in development emerged or persisted. This case adds evidence to the hypothesis that damage to mesial-temporal structures at an early developmental period may lead to the autistic syndrome.
Autism is held to be the result of the failure of a central cognitive processor which is necessary for flexible multidimensional association of sensorial stimuli, memory, and motivational states. Failure of this processor produces rigid, invariant, rote behavior, thought and language and aberrant modulation of emotion. It is argued that this central processing function is critically dependent on the hippocampus. Thus autism is postulated to be the developmental syndrome of hippocampal dysfunction. The hippocampus is postulated to be necessary for normal development in the child of language syntax, semantics, and pragmatics; the capacity for creativity and generativity in language and behavior, and combinatorial possibilities in general; for the integration of motivational states with experience and learning; and for the construction of a complex, useful and flexible structure of meaning. These constructs may become independent of hippocampus for use, but hippocampus is still required to modify or add to them. Finally, this analysis suggests a specific hypothesis of hippocampal organization which I advance as an hypothesis: that the hippocampus can be modelled as a multidimensional system in which the unique intersection of all input dimensions is the resultant.
Autism is a perplexing condition because of its unique presenting signs and high degree of variability. Evidence is presented that the basic underlying information processing disorder is a dysfunction of the appreciation of the emotional significance of incoming stimuli and attaching motivational value to the stimuli. It is proposed that this dysfunction occurs when the amygdaloid nucleus and/or its connections are disrupted, resulting in the variability of the presentation of this syndrome among individuals. Herpes simplex encephalitis sometimes results in signs of autism. The virus has a predilection to attack specific areas of the brain, which provides information on the probable underlying neurological dysfunction in autism.
A highly topical subject, violence, its consequences as well as its causes, deserve more attention on behalf of the public health authorities. On one hand, nowadays, the concepts in this field tend to become more global than before; however, on the other hand the epidemiological, etiological and therapeutic approaches benefit also from considering more limited behavior categories and age groups. In this review of the international literature, the authors focus their attention on intentional (excluding accidents) and interpersonal (excluding self-destructive behavior) violence. They consider by priority adolescents (10 to 19) and young adults (15 to 24). After a general introduction to the theme and the presentation of the relevant concepts and definitions, the authors, as a complement to their earlier publication on violence, develop epidemiological aspects concerning mortality, morbidity and the sources of information about these two topics. Their view is partly a critical one, including considerations on risk factors and risk predictors. The etiological aspects are developed along three axes : biomedical components, mainly of neuro-psychiatric and neurological nature ; family violence ; the broader social environment. The following part is devoted to care and prevention. In the discussion, several of the main issues considered in the conceptual, epidemiological, etiological as well as curative and preventive approaches are brought up again, with a perspective on presenting new proposals for further consideration and developments as well as on broadening the initial debate of the introduction.
A 2-year-old boy meeting the criteria for autistic disorder was diagnosed 2 years later with a visual agnosia characterised by a combination of certain aspects of associative and apperceptive agnosia. MRI then revealed a severe encephalomalacia of the right temporal lobe and bilateral temporo-occipital areas. This association is discussed in terms of a clinical and aetiological relation between autistic disorder and visual agnosia.
Autism is a neurodevelopmental disorder that is defined behaviorally by severe deficiencies in reciprocal social interaction, verbal and nonverbal communication, and restricted interests. The amygdala is involved in the regulation of social behaviors and may be an important site of pathology for the social dysfunction seen in autism. This review focuses on lesion, postmortem, and neuroimaging studies that investigate the amygdala and related structures in this disorder. Other brain regions potentially involved in the neuropathology of autism are also briefly discussed. Although supportive evidence exists for amygdala dysfunction in autism, the currently available data are inconsistent and additional research is needed.
To evaluate cognitive outcome in unselected patients with previously diagnosed viral meningitis.
Twenty-one unselected patients were examined neurologically, psychiatrically, and psychometrically 25+/-12 months after the acute stage of viral meningitis. The results were compared with the results of twenty-one healthy controls.
Despite of a very good clinical outcome in the post-meningitis group patients performed significantly worse on tasks concerning non-verbal memory functions (BVRT), attention and speed of cognitive performance (WMS-3) even when there was no sign of parenchymal involvement. Forty percent of the patients were categorised as suffering from mild to moderate cognitive impairment.
Viral meningitis in adults results in mild cognitive impairment in a significant proportion of patients that is not identified by clinical examination or cognitive screening tests. Nevertheless, even mild deficits in non-verbal learning and cognitive speed might lead to overstrain and handicap in complex situations of daily living and working. We therefore recommend that the neuropsychiatric evaluation of all patients with intracranial infections include neuropsychological testing.
Infections of the central nervous system can damage the brain and cause abnormal behavior. In this article, the authors examine how behavior is affected by damage to different parts of the brain. They then focus on damage caused by specific infections of the brain and how these can result in abnormal behavior with legal consequences. Examples of such infections include neurosyphilis, encephalitis lethargica, herpes simplex encephalitis, and various other viral encephalitides, both acute and chronic. The AIDS dementia complex, which results from HIV infection of the brain, causes behavioral abnormalities in addition to motor and cognitive impairments. In some cases of violence and other criminal behavior, this can be a consequence of central nervous system infection, and the authors suggest that criminal sanctions in such events are inappropriate in the absence of volitional criminal intent.
Viral encephalitis, a condition in which a virus infects the brain and produces an inflammatory response, affects approximately 20,000 individuals per year in the United States. The viral encephalidities include sporadic and epidemic acute viral encephalidities and subacute and chronic/progressive viral encephalitis or encephalomyelitis. In people who survive these conditions, postencephalitic impairments of elemental neurologic, cognitive, emotional, and behavioral function are common. This article will provide a brief overview of the diagnosis and acute management of acute viral infections of the central nervous system. The neurologic and neuropsychiatric features, neuropathologies, and treatments of two of the more common types of acute viral encephalitis in North America--herpes simplex encephalitis and West Nile encephalitis--will be reviewed. The current and future role of psychiatrists and neuropsychiatrists in the care and study of individuals with these conditions will be discussed.
Previous research has identified a relationship between autistic disorder (autism) and specific congenital infections. Three cases of congenital or perinatal cytomegalovirus (CMV) infection occurring in association with autism are described. Hypothetical mechanisms relating congenital infection, such as CMV, to the development of autism are discussed. A better understanding of the immunologic response to certain congenital infections may provide important information pertaining to the pathophysiology and etiology of autism in vulnerable individuals.
The purpose of this work was to investigate the association between infections in the first 2 years and subsequent diagnosis of autism spectrum disorders.
We conducted a case-control study among children born at Kaiser Permanente Northern California from 1995 to 1999. Case subjects (n = 403) were children with an autism diagnosis recorded in Kaiser Permanente databases. Control subjects (n = 2100) were randomly sampled from the remaining children without autism and frequency matched to case subjects on gender, birth year, and birth hospital. Information on infections and covariates were obtained from Kaiser Permanente and birth certificate databases.
Overall, infection diagnoses in the first 2 years of life were recorded slightly less often for children with autism than control children (95.0% vs 97.5%). Among specific diagnoses, upper respiratory infections were significantly less frequently diagnosed and genitourinary infections more frequently diagnosed in children with autism. In the first 30 days of life, the frequency of having an infection was slightly higher among children with autism (22.6% vs 18.7%).
Children with subsequent diagnoses of autism do not have more overall infections in the first 2 years of life than children without autism. Data suggest that children with autism may have modestly elevated rates of infection in the first 30 days and that, during the first 2 years, children with autism may be at higher risk for certain types of infections and lower risk for others. Additional studies that explore the associations between prenatal and early childhood infections and autism may help clarify the role of infection and the immune system in the etiology of autism spectrum disorder.
A syndrome consisting of "agnostic" disturbances, strong "oral" tendencies, and marked emotional changes resulted from bilateral temporal lobectomy in 3 rhesus monkeys. The "agnostic" disturbances appeared in the form of hyper-attention to seen objects, with repeated manipulation of all objects irrespective of importance. This manipulation tended to take an "oral" form. Social behavior was markedly decreased, behavior characteristic of anger, fear, etc. largely disappeared, and a persistence of attentive action appeared. The "agnostic" symptoms were primarily visual, but some evidence appeared for the meaninglessness of perceptions in other sensory fields. Slight visual disturbances present after operation could not have accounted for the agnostic disturbances. This report, given as preliminary evidence, is detailed for one animal over a period of 4 months. The data from the other two animals were confirmatory. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The effects of intracerebral infection with herpes simplex virus on the subsequent behavior of two strains of mice were examined. Infected Nya: NYLAR mice were hyperactive and did not show any deficits in the acquisition or reversal of a spatial learning task. In contrast, infected Nya: (SW) mice were hypoactive and made more errors than controls during both phases of the learning tasks. These differences in the nature of the sequelae to infection were related to an overall higher virus titer in the brains of Nya:(SW) mice, an effect particularly marked in the cerebral hemispheres. The results suggest that herpes encephalitis may produce a variety of behavioral syndromes, depending in part on the genetic background of the host. The relevance of these findings to clinical disorders produced by viral infection is discussed.
Herpes encephalitis, a viral attack on the brain, contracted in Vietnam through the veteran's sexual activities, is certainly not the familiar learning disability. Yet the documented, neurologically induced reading dysfunction offered implications that the clinician could not avoid. First, similarities between the symptoms existed. Visual-perceptual inaccuracies persisted. Furthermore, their severity varied with his frustrations and mental states on different days. He was frustrated with his difficulty in evoking the oral equivalents of objects or concepts he knew. Wide discrepancies existed between encoding and deconding skills. He was inconsistent with skills. Perseverations persisted. Blending was difficult. Sound-symbol concepts could be verbalized but not applied. Second, although recovery from encephalitis varies, this reported case responded to remedial principles that are recognized in the field of learning disabilities. These included the cooperation of cross disciplines, ongoing diagnostic teaching, multisensory reinforcements, individualized instruction, and sequential skills development.
A recall and recognition memory study of Korsakoff and post-herpes encephalitis patients employing percentage correct recall and the statisticd′ derived from signal detection theory supports Lhermitte's contention that these two patient groups represent two distinct organic amnesia syndromes. Post-herpes encephalitis patients show little evidence of encoding and storage of information. In contrast recognition memory of Korsakoff and normal control subjects was essentially similar for truly novel information. Recognition memory for English words was markedly impaired for Korsakoff patients and worsened with increased semantic organization of the material. In light of our findings it would seem advisable to utilize homogeneous groups, with respect to brain pathology, when studying memory processes in organic patients.
Autistic children were compared with control children on tasks in which retention was tested by different methods. In three tests of recall, using named pictures, written words and spoken words as test stimuli, autistic children were impaired in comparison with age-matched normal children and with controls matched for verbal ability. In one test of forced-choice recognition of pictures, autistic children were impaired in comparison with ability-matched controls. In three tests of cued recall, using named pictures, written words and spoken words as test stimuli, and acoustic, graphemic and semantic cues, autistic children were not impaired in comparison with normal age-matched controls. In one test of paired-associate learning using non-related word pairs as test stimuli autistic children were not impaired in comparison with normal age-matched controls. These experimental paradigms were similar to some that have been used to investigate the amnesic syndrome in man. Thus findings on paired-associate learning differ in autistic and amnesic subjects, but findings on recall, recognition and cued recall are comparable. A possible parallel between autism and amnesia is discussed.
In order to address the issue of quantitative versus qualitative differences more fully, the authors' laboratory has conducted evaluations of neurological and neuropsychological status in 21 patients with global amnesia of seven different etiologies affecting various brain regions. This paper reviews the neuropathological changes that characterize each etiology, presents the computed tomographic (CT) brain scans of illustrative cases, describes and compares patterns of cognitive deficit within and among groups, and reaches the tentative conclusion that the etiologies of amnesia that they studied differ quantitatively but not qualitatively with respect to mnemonic capabilities involved in fact learning.
Computed tomographic (CT) scans were obtained from eight infants and young children with herpes simplex virus encephalitis. In two cases the initial scan showed diffuse edematous changes as a mass effect without laterality. Unilateral localized low attenuation in the initial scan was evident 4 days after the onset in one patient, and high attenuation in the initial scan appeared on the 6th day in another patient, but in general, it was not possible to establish an early diagnosis of herpes simplex virus encephalitis from CT scan. In the longitudinal study the calcification with ventriculomegaly appeared in 3 of 5 survivors, and gyriform calcification in 2 of 3 patients, respectively. The appearance of multicystic encephalomalacia was evident in one patient 6 months after the onset of neonatal herpes simplex encephalitis. It is shown that the CT findings of neonates and young children with herpes simplex encephalitis are different from those of older children and adults, and the importance of longitudinal CT studies was stressed in clarifying the pathophysiology of the central nervous system involvement in survivors.
This article has no abstract; the first 100 words appear below.
HUMAN Central-nervous-system infection with Herpesvirus hominis (herpes-simplex virus), first described in 1941,¹ is by no means rare. A number of reports describe the clinical, pathological and epidemiological aspects of encephalitis caused by this virus and its frequency in nonbacterial Central-nervous-system infections.²³⁴⁵ Because of its sporadic occurrence and difficulties in establishing diagnoses during life, knowledge of the disease has been based upon histologic study. However, accurate and rapid diagnosis during life is required if treatment with 5-iodo 2′-deoxyuridine (IUDR) is contemplated. This report reviews 49 patients with Central-nervous-system disease associated with herpes-simplex virus studied in this laboratory in the past twenty-five . . .
*From the Department of Virus Diseases, Walter Reed Army Institute of Research (requests for reprints should be addressed to Colonel Edward L. Buescher, M.C., USA, at the Department of Virus Diseases, Walter Reed Army Institute of Research, Washington, D. C., 20012).
Presented in part before the annual meeting of the American College of Physicians, New York City, April 18, 1966.
We are indebted to Drs. Charles Adair, Clifton Arrington, Joseph A. Bellanti, Robert E. Blount, Jr., Francis C. Cadigan, Jr., Irving Crawford, Harry E. Dascomb, Richard T. Johnson, Bernard Portnoy, Aaron F. Rasmussen and Howard A. Weinberger, who at various times supervised the Diagnostic Section of the Department of Virus Diseases, thus leading to the accumulation of cases analyzed here, and Clarence L. Parker and Oliver Dandridge for technical assistance.
Source Information
WASHINGTON, D.C.
† Formerly, virologist, Department of Virus Diseases, Walter Reed Army Institute of Research (present address, Department of Virology, SEATO Medical Research Laboratory, APO San Francisco 96346).
‡ Chief, Department of Virus Diseases, Walter Reed Army Institute of Research; clinical associate professor of pediatrics, Georgetown University School of Medicine.
§ Chief, Department of Bacteriology, Walter Reed Army Institute of Research; clinical associate professor of medicine, George Washington University School of Medicine.
¶ Formerly, virologist, Department of Virus Diseases, Walter Reed Army Institute of Research (present address, Division of Biological Standards, National Institutes of Health, Bethesda, Maryland).
the subject of this study was a 43-year old man who developed a disorder of memory following herpes simplex encephalitis six years earlier. Recent memory was severely affected in contrast to the preservation of both intellect and immediate and remote memory. The impairment of recent memory functions was evident on tasks using verbal material whereas memory for motor tasks such as maze learning and the rendering of new compositions for the piano was preserved. The deficit in remembering verbal items varied with (1) the type of retrieval (recall vs. recognition), (2) the modality of stimulus presentation (acoustic vs. visual), and (3) the way in which learning was attempted (serial presentation vs. self-ordering and classification). Evidence of proactive interference in memory formation was demonstrated by intrusion errors.
Two cases of congenital cytomegalovirus infection associated with autism are reported. The viral hypothesis of autism is discussed along with a brief review of the literature. Suggestions are made for future research.
In seeking the neurologic substrate of the autistic syndrome of childhood, previous studies have implicated the medial temporal lobe or the ring of mesolimbic cortex located in the mesial frontal and temporal lobes. During an acute encephalopathic illness, a clinical picture developed in three children that was consistent with infantile autism. This development was reversible. It was differentiated from acquired epileptic aphasia, and the language disorder was differentiated aphasia. One child has rises in serum herpes simplex titers, and a computerized tomographic (CT) scan revealed an extensive lesion of the temporal lobes, predominantly on the left. The other two, with similar clinical syndromes, had normal CT scans, and no etiologic agent was defined. These cases are examples of an acquired and reversible autistic syndrome in childhood, emphasizing the clinical similarities to bilateral medial temporal lobe disease as described in man, including the Klüver-Bucy syndrome seen in postencephalitic as well as postsurgical states.
A case of probable herpetic viral encephalitis is presented. The clinical picture following the acute phase of disease was dominated by severe fluent aphasia, prominent oral tendencies, visual agnosia, and a decrease in fear reactions. Most of these symptoms, with the obvious exception of aphasia, are similar to those observed by Kluver and Bucy in rhesus monkeys that underwent bitemporal lobectomy. These manifestations may be explained by the tendency of the herpes simplex virus to invade the temporal lobes. "Agnosia" in the auditory field and changes in vocal behavior were observed by H. Kluver and P. C. Bucy (1939, Archives of Neurology and Psychiatry, 42, 949-1000) in some of their bitemporal monkeys. The association of sensory aphasia, as observed in this case, with the auditory "agnosia" observed in some bitemporal monkeys, is discussed.
Introduction
During the past 5 years we have observed 6 patients with encephalitis in the wards of the Massachusetts General Hospital. Each patient presented a distinctive clinical picture with which our medical staff had not been familiar. Therefore, as might be expected, the disease occasioned considerable difficulty in diagnosis for the reason that in each instance the illness had been acute and without evident cause and had occurred at a time when there was no epidemic of encephalitis. Psychological disturbances were outstanding features during the acute phase of the illness or as major sequelae, a quality which tends to distinguish it clinically from several other types of encephalitis. In some of the patients, serologic tests were adequate to establish the presence of an infection caused by herpes simplex virus; in others, the existence of an "inclusion-body" encephalitis was demonstrated pathologically.Our data provide no clue as to the manner in
Five basic theories about the personality of epileptics are outlined, and the extent to which they have been affirmed or refuted by clinical and psychological investigations is considered. The findings of studies which have used the Rorschach test are shown to be contradictory, and the inadequacies of this test for research purposes are pointed out. It is argued that progress in this field depends on a recognition and study of the complex environmental and pathophysiological factors involved, and on the development of reliable criteria with which to classify epileptics.
Delayed recovery from herpes (letter) Pediatric Infec-tious Disease, 4, 703 Reading recovery following herpes encephalitis
- E S Roach
- J Abramson
Roach, E. S., & Abramson, J. (1985). Delayed recovery from herpes (letter). Pediatric Infec-tious Disease, 4, 703. Rogers, C. D., & Peters, P. (1979). Reading recovery following herpes encephalitis. Journal of Learning Disabilities, 12, 572-575.
Stanford-Binet Intelligence Scale Chicago: Riverside
- R. L. Thorndike