Obsessive-Compulsive Disorder and Tourette's Syndrome
eBook - ePub

Obsessive-Compulsive Disorder and Tourette's Syndrome

The Science of Mental Health

  1. 350 pages
  2. English
  3. ePUB (mobile friendly)
  4. Available on iOS & Android
eBook - ePub

Obsessive-Compulsive Disorder and Tourette's Syndrome

The Science of Mental Health

About this book

First published in 2002. Obsessive-compulsive disorder (OCD) and Tourette's syndrome (TS) are treated together in this volume because symptoms of each often co-occur and because there are substantial overlaps in genetic risks and possibly in the neurobiology underlying these disorders.

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Yes, you can access Obsessive-Compulsive Disorder and Tourette's Syndrome by Steven E. Hyman in PDF and/or ePUB format, as well as other popular books in Éducation & Santé mentale en psychologie. We have over one million books available in our catalogue for you to explore.

Information

Obsessive-Compulsive and Other Behavioural Changes with Bilateral Basal Ganglia Lesions

A Neuropsychological, Magnetic Resonance Imaging and Positron Tomography Study
by D. Laplane1, M. Levasseur2, B. Pillon3, B. Dubois3, M. Baulac1, B. Mazoyer2, S. Tran Dinh4, G. Sette2, F. Danze5, J. C. Baron2

SUMMARY

Eight patients are reported who shared the combination of bilateral basal ganglia lesions and a frontal lobe-like syndrome. The main features were inertia and loss of drive, with preservation of intellectual function. Some patients showed stereotyped activities with compulsive and obsessive behaviour which were sometimes highly elaborate in pattern. Extrapyramidal clinical signs were absent or mild. Brain damage, related to anoxic or toxic encephalopathy, was demonstrated by CT scans and MRI. The lesions appeared to be confined to the lentiform nuclei, particularly affecting the pallidum, although there was generalized brain atrophy in 2 cases. Positron emission tomography (PET) in 7 patients revealed hypometabolism of the prefrontal cortex relative to other parts of the brain. The PET studies suggest dysfunction of the prefrontal cortex as a result of damage to the lentiform nuclei. These clinical, anatomical and functional observations emphasize the role of the circuits linking the prefrontal associative cortex and some specific areas of the neostriatum, including the pallidum. The existence of distinct nonoverlapping circuits in the motor field or in the associative field can explain the fact that basal ganglia lesions may give rise to a clinical picture that is either purely motor, purely behavioural (as in some of our patients), or both. Similarities existed between some symptoms found in our patients and certain features of major psychiatric illnesses such as severe depression, catatonic schizophrenia, and obsessive-compulsive disorder. This raises the hypothesis that some aspects of these psychiatric disorders could be related to structural and physiological disturbances in the systems linking the frontal associative cortex and the basal ganglia.

INTRODUCTION

The symptoms reported in cases of damage to the lentiform nucleus generally consist of motor disturbances (Marsden, 1982). We have previously reported instances where patients with bilateral lesions of the lentiform nuclei without or with very mild extrapyramidal symptoms, presented unusual behavioural abnormalities (Laplane et al., 1981, 1982, 1984). The symptoms, which were summarized as a loss of drive’, included a marked decrease in spontaneous activity, a loss of affect, and a notable reduction of spontaneous thought content. Also remarkable was the observation that their inertia was apparently reversible by external stimulation, such as the incitement by a relative. Moreover, on neuropsychological testing, intellectual capacities were largely preserved, except for a memory defect in 1 of the 3 cases.
The attributability of these disturbances to lesions of the lentiform nuclei was strongly suggested by the CT scan findings, but doubt remained as to the possibility of diffuse or multifocal brain damage, in spite of the normality of EEG recordings and the absence of other visible lesions on the scan images. In addition, the question was raised as to how these limited subcortical lesions could induce such behavioural changes. The hypothesis of a functional impairment of the prefrontal cortex was made on the basis of strong clinical resemblances between our patients’ symptoms and a frontal lobe syndrome. This similarity, and the absence of motor disturbance, led to the suggestion that the lesions might have affected the ‘association’ circuits linking some compartments of the basal ganglia and the prefrontal cortex. Finally, the additional presence, in 2 of these 3 patients, of obsessive-compulsive behaviour was noteworthy, representing a likely example, if confirmed by further cases, of psychiatric symptoms being produced by focal brain impairment.
Since then, 2 other cases have been reported by Ali-Cherif et al. (1984) and we have now been able to examine 5 new similar cases. It was possible to perform magnetic resonance imaging (MRI) and positron emission tomography (PET) in 7 of our 8 cases, and in the light of this additional material, some progress can be made towards the understanding of the clinical features.

Material and Methods

All 8 patients were selected on the basis of symptoms of inertia, reversible under stimulation and the presence of lesions of the lentiform nuclei on CT scans.

Neuropsychological testing

Intellectual function and memory. The following tests were selected: the Wechsler Verbal Scale, the Raven’s 1938 Progressive Matrices (PM 38) and the Wechsler Memory Scale. Patients were allowed unlimited time to perform these tests.
Frontal lobe function. The simplified version of the Wisconsin Card Sorting test (Nelson, 1976), tests of verbal fluency (names of animals in 1 min. words beginning with the letter M in 1 min) (Benton, 1968), and a graphic series (Luria, 1966) were chosen because they were known to be sensitive to frontal lobe dysfunction. Behavioural abnormalities (prehension, imitation and utilization), observed in patients with frontal lobe lesions (Lhermitte, 1983: Lhermitte et al., 1986) were also evaluated.
Linguistic, gestural and drawing tests. These included the naming of objects, writing a sentence on dictation, calculation, execution of symbolic gestures, and the copying of a cube or the Rey-Osterrieth complex figure.
The 15 objects test (B. Pillon et al., unpublished). This visual discrimination task, consisting of 15 superimposed images of objects, was chosen in order to evaluate cognitive slowing.
Objective personality tests. The Minnesota Multiphasic Personality Inventory (MMPI) or a self-rating depression scale (Pichot et al., 1984) was used.

Magnetic resonance imaging

In 7 patients (Cases 2–8), MRI was performed on a superconducting MR imager operating at a Held strength of 1.5 T. Coronal and horizontal (Virschow’s plane) 5 mm slices were taken every 7.5 mm. T1 and T2 weighted sequences were used. Real-size printed photographs were obtained from the films and were compared with atlases (Salamon and Huang, 1980, f...

Table of contents

  1. Cover
  2. Half Title
  3. Title Page
  4. Copyright Page
  5. Table of Contents
  6. Introduction
  7. Body Dysmorphic Disorder
  8. Body Dysmorphic Disorder: A Review of Conceptualizations, Assessment, and Treatment Strategies
  9. The Epidemiology and Cross-National Presentation of Obsessive-Compulsive Disorder
  10. Prevalence of Obsessive-Compulsive Disorder in the British Nationwide Survey of Child Mental Health
  11. Tourette’s Disorder: Epidemiology and Comorbidity in Primary School Children
  12. A Family Study of Gilles de la Tourette Syndrome
  13. A Family Study of Obsessive-Compulsive Disorder
  14. Course of Tic Severity in Tourette Syndrome: The First Two Decades
  15. Body Dysmorphic Disorder: 30 Cases of Imagined Ugliness
  16. Obsessive-Compulsive Disorder in Children and Adolescents
  17. A 40-Year Follow-up of Patients with Obsessive-Compulsive Disorder
  18. Prospective, Longitudinal Study of Tic, Obsessive-Compulsive, and Attention-Deficit/Hyperactivity Disorders in an Epidemiological Sample
  19. Toward a Neurobiology of Obsessive-Compulsive Disorder
  20. Obsessive-Compulsive and Other Behavioural Changes with Bilateral Basal Ganglia Lesions: A Neuropsychological, Magnetic Resonance Imaging, and Positron Tomography Study
  21. Tourette’s Syndrome: When Habit-Forming Systems Form Habits of Their Own?
  22. Functional Neuroimaging and the Neuroanatomy of Obsessive-Compulsive Disorder
  23. Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections: Clinical Description of the First 50 Cases
  24. Tourette’s Syndrome and “PANDAS”: Will the Relation Bear Out? Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infection
  25. A Functional Magnetic Resonance Imaging Study of Tic Suppression in Tourette Syndrome
  26. A Functional Neuroanatomy of Tics in Tourette Syndrome
  27. Regional Brain Volume Abnormalities and Long-Term Cognitive Outcome in Preterm Infants
  28. Orbital Frontal and Amygdala Volume Reductions in Obsessive-Compulsive Disorder
  29. Tourette Syndrome: Prediction of Phenotypic Variation in Monozygotic Twins by Caudate Nucleus D2 Receptor Binding
  30. A Multicenter Investigation of Fixed-Dose Fluoxetine in the Treatment of Obsessive-Compulsive Disorder
  31. Effectiveness of Psychological and Pharmacological Treatments for Obsessive-Compulsive Disorder: A Quantitative Review
  32. Effectiveness of Exposure and Ritual Prevention for Obsessive Compulsive Disorder: Randomized Compared with Nonrandomized Samples
  33. Acknowledgments