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Query: UMLS:C0004352 (autism)
 32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of electroconvulsive therapy (ECT) in adolescence are presented and the literature on the use of ECT in childhood and adolescence is reviewed. ECT was effective in children and adolescents with bipolar disorder and depression. Inadequate information exists to make a judgment regarding schizophrenia, delirium, and anorexia nervosa. ECT is not effective in autism and chronic organic brain syndromes. Complications cited include organicity and seizures in the period immediately after ECT, anxiety reactions, and disinhibition. Long-term memory deficit or cognitive impairment has not been found, although further research to rule out residual impairment is needed.
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PMID:A review of ECT for children and adolescents. 222 48

Electroencephalographic study was performed in 30 children of 1-3 years old from the group with the high risk of schizophrenia. Clinical observation of the patients was performed in the period of EEG recording and follow-up study was also made during 10-12 years. Three groups of patients were picked out with the differences in both clinical and electrophysiologic indices. Bundle beta-activity was registered on EEG in the cases of an active schizophrenic process. A presence of the spindles of the sleep and their dominance on EEG were characteristic for children with nonprocessual disorders of psychopathic-like type with disinhibition of the drives. Hypersynchronism of delta- and theta-activities were observed in the cases of schizotypic diathesis and an early children's autism with the predominance of paroxysmal somato-autonomic disorders.
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PMID:[Electroencephalographic correlates of schizophrenic type mental disorders at an early age in childhood]. 1020 41

Midline lesion of the cerebellum was performed in young 10-day-old DA/HAN strained (pigmented) rats. Once adults, the lesioned animals were subjected to a series of behavioral tests and their performances were compared with those of control (nonlesioned) rats. Compared with controls, the spontaneous motor activity of the lesioned rats was higher, they showed persevering behavior and did not pay attention to environmental distractors. In anxiety and social discrimination tests, disinhibition tendencies were obvious, which suggested that the animals were less dependent on the context. These abnormalities were most likely due to early midline lesion of the cerebellum and not to a deficit in maternal care before weaning, since the dams took care of the lesioned and control pups similarly. From these results, it can be concluded that the cerebellar vermis is involved in motor control, attentional capabilities and emotional behavior. Given that the lesioned rats observed in this study presented obvious autistic-like symptoms, and since a number of autistic subjects have cerebellar deficits and, particularly, a hypoplasia of vermal lobules, our results may strengthen the idea that the cerebellar vermis is involved in autism, as already suggested in the guinea pig (Caston J, et al. Eur J Neurosci 1998;10:2677-2684).
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PMID:Effects of early midline cerebellar lesion on cognitive and emotional functions in the rat. 1086 41

A 69-year-old right-handed woman developed a transcortical motor aphasia with hyperlexia following resection of a glioma in the left medial frontal lobe. Neurological examination revealed grasp reflex in the right hand and underutilization of the right upper extremity. An MRI demonstrated lesions in the left medial frontal lobe including the supplementary motor area and the anterior part of the cingulate gyrus, which extended to the anterior part of the body of corpus callosum. Neuropsychologically she was alert and cooperative. She demonstrated transcortical motor aphasia. Her verbal output began with echolalia. Furthermore hyperlexia was observed in daily activities and during examinations. During conversation she suddenly read words written on objects around her which were totally irrelevant to the talk. When she was walking in the ward with an examiner she read words written on a trash bag that passed by and signboards which indicated a name of a room. Her conversation while walking was intermingled with reading words, which was irrelevant to the conversation. She also read time on analog clocks, which were hung on a wall in a watch store. In a naming task, she read words written on objects first and named them upon repeated question about their names. When an examiner opened a newspaper in front of her without any instructions she began reading until the examiner prohibited it. Then she began reading again when an examiner turned the page, although she remembered that she should not read it aloud. She showed mild ideomotor apraxia of a left hand. Utilization behavior, imitation behavior, hypergraphia, or compulsive use of objects was not observed throughout the course. Hyperlexic tendency is a prominent feature of this patient's language output. Hyperlexia was often reported in children with pervasive developmental disorders including autism. There are only a few reports about hyperlexia in adults and some of them were related to diffuse brain dysfunction. Hyperlexia of our patient was associated with echolalia but not with the other "echo" phenomena, which may be because the lesion was unilateral on the left side. Dysfunction of the left supplementary motor area could lead to disinhibition of regulatory mechanism of verbal output in response to auditory and visual stimuli.
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PMID:[Hyperlexia in an adult patient with lesions in the left medial frontal lobe]. 1096 60

Low serotonin activity in man has been related to impulsive, self-destructive violence but not to instrumental aggression aimed at dominance. A relationship has also been suggested between aggression and high catecholaminergic activity. Several studies have reported signs of aberrant dopaminergic function in attention deficit hyperactivity disorder, autism, and schizophrenia. In 22 violent offenders undergoing pretrial forensic psychiatric investigation, interpersonal and behavioral features of psychopathy, measured by the Psychopathy Checklist Revised (PCL-R), were significantly predicted by low cerebrospinal fluid (CSF) concentrations of 5-HIAA and high CSF concentrations of HVA in multivariate regression models. CSF concentrations of MHPG did not contribute to the model. This seems to link the outward-directed aggression of psychopathy to serotonergic hypofunctioning and high dopamine turnover, which might account for disinhibition of destructive impulses.
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PMID:CSF studies in violent offenders. I. 5-HIAA as a negative and HVA as a positive predictor of psychopathy. 1151 52

Social anxiety disorder is well suited to the spectrum concept because it has trait-like qualities of early onset, chronicity, and no empirically derived threshold that demarcates normal from clinically significant trait social anxiety. Social anxiety disorder has been shown to respond to relatively specific pharmacologic and cognitive-behavioral therapies, which makes identification of other conditions that may lie on the social anxiety disorder spectrum important because of possible treatment implications. Biologic markers associated with social anxiety disorder also may be shared by similar but nonidentical traits, such as behavioral inhibition and detachment. Clarification of the trait spectrums associated with specific biologic systems offers an opportunity for improving the understanding of the origin of these conditions. Strong evidence exists that at least some forms of shyness, avoidant personality disorder, and selective mutism lie on a social anxiety disorder spectrum. For several other disorders that share a prominent focus on social comparison, significant subgroups of patients seem to have features of social anxiety disorder. These disorders include major depression (especially the atypical subtype), body dysmorphic disorder, and eating disorders. Several other disorders marked by social dysfunction or inhibition, including substance use disorders (especially alcoholism), paranoid disorder, bipolar disorder, autism, and Asperger's disorder, also may show some overlap with social anxiety disorder features (e.g., social anxiety as a cause or complication of substance abuse, social avoidance in paranoid disorder, social disinhibiton in bipolar disorder, and social communication deficits in autism and Asperger's disorder). Social anxiety disorder also is associated with other anxiety disorders in general and other phobias in particular. In respect to traits, a growing body of evidence links behavioral inhibition to the unfamiliar to a social anxiety disorder spectrum with some specificity. Biologic measures of dopamine system hypoactivity have been linked to social anxiety disorder, trait detachment, and general deficits in reward and incentive function. It remains to be clarified, however, whether this brain system function is best characterized by a social anxiety disorder spectrum or some variant that incorporates social reward deficits or social avoidance behavior. Social anxiety disorder, shyness, and behavioral inhibition all seem to have a genetic component, but more research is needed to attempt to identify a more specifically heritable temperament associated with these conditions. Finally, the emergent concept of a social anxiety spectrum needs maturation. Although the notion of a single social anxiety disorder spectrum currently has some clinical use, the authors believe that exclusive focus on the notion of a single continuum with two extremes--from social disinhibition in mania to the most severe form of social anxiety, avoidant personality disorder--is premature and limiting in respect to etiologic research. An alternative approach is to conceptualize multiple, probably overlapping spectra in this area of social psychopathology. Individual dimensions might be based on various core phenomenologic, cognitive, or biologic characteristics. A bottom-up biologic approach holds promise for identifying spectra with a common etiology that might respond to specific treatments. Taking a pluralistic view of the concept of spectrum at this stage may help accelerate our understanding of social anxiety and related disorders.
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PMID:The social anxiety spectrum. 1246 59

The neurobiologic basis of autism is reviewed, with discussion of evidence from genetic, magnetic resonance imaging, neuropathology, and functional neuroimaging studies. Although autism is a behaviorally valid syndrome, it is remarkably heterogeneous and involves multiple developmental domains as well as a wide range of cognitive, language, and socioemotional functioning. Although multiple etiologies are implicated, recent advances have identified common themes in pathophysiology. Genetic factors play a primary role, based on evidence from family studies, identification of putative genes using genome-wide linkage analyses, and comorbidities with known genetic mutations. The RELN gene, which codes for an extracellular protein guiding neuronal migration, has been implicated in autism. Numerous neuropathologic changes have been described, including macroencephaly, acceleration and then deceleration in brain growth, increased neuronal packing and decreased cell size in the limbic system, and decreased Purkinje cell number in the cerebellum. Abnormalities in organization of the cortical minicolumn, representing the fundamental subunit of vertical cortical organization, may underlie the pathology of autism and result in altered thalamocortical connections, cortical disinhibition, and dysfunction of the arousal-modulating system of the brain. The role of acquired factors is speculative, with insufficient evidence to link the measles-mumps-rubella (MMR) vaccine with autism or to change immunization practices.
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PMID:The neurobiology of autism: new pieces of the puzzle. 1258 44

The repetitive, stereotyped and obsessive behaviours, which are core diagnostic features of autism, are thought to be underpinned by executive dysfunction. This study examined executive impairment in individuals with autism and Asperger's disorder using a verbal equivalent of an established pseudo-random number generating task. Different patterns of disinhibition emerged in the autism (n = 12) and Asperger's disorder (n = 12) groups. Consistent with previous research, the autism group repeated single numbers (e.g. 2, 2, 2) more frequently than the control group. In contrast to past research suggesting intact executive abilities, this study found that the Asperger's disorder group generated more repetitive number patterns (e.g. 45, 45) than the controls. Executive functioning in children with Asperger's disorder may be particularly vulnerable to a lack of visual cueing and concrete rules. Qualitative differences in executive dysfunction between these groups may implicate differential disruption within the fronto-striatal circuitry.
Autism 2006 Jan
PMID:Pseudo-random number generation in children with high-functioning autism and Asperger's disorder: further evidence for a dissociation in executive functioning? 1652 11

A central aspect of the cerebellar cognitive affective syndrome is the dysregulation of affect that occurs when lesions involve the 'limbic cerebellum' (vermis and fastigial nucleus). In this case series we describe neuropsychiatric disturbances in adults and children with congenital lesions including cerebellar agenesis, dysplasia, and hypoplasia, and acquired conditions including cerebellar stroke, tumor, cerebellitis, trauma, and neurodegenerative disorders. The behaviors that we witnessed and that were described by patients and families included distractibility and hyperactivity, impulsiveness, disinhibition, anxiety, ritualistic and stereotypical behaviors, illogical thought and lack of empathy, as well as aggression and irritability. Ruminative and obsessive behaviors, dysphoria and depression, tactile defensiveness and sensory overload, apathy, childlike behavior, and inability to appreciate social boundaries and assign ulterior motives were also evident. We grouped these disparate neurobehavioral profiles into five major domains, characterized broadly as disorders of attentional control, emotional control, and social skill set as well as autism spectrum disorders, and psychosis spectrum disorders. Drawing on our dysmetria of thought hypothesis, we conceptualized the symptom complexes within each putative domain as reflecting either exaggeration (overshoot, hypermetria) or diminution (hypotonia, or hypometria) of responses to the internal or external environment. Some patients fluctuated between these two states. We consider the implications of these neurobehavioral observations for the care of patients with ataxia, discuss the broader role of the cerebellum in the pathogenesis of these neuropsychiatric symptoms, and revisit the possibility of using cerebellar stimulation to treat psychiatric disorders by enhancing cerebellar modulation of cognition and emotion.
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PMID:The neuropsychiatry of the cerebellum - insights from the clinic. 1778 22

Bipedal locomotion and fine motility of hand and larynx of humans introduced musculoskeletal adaptations, new pyramidal, corticostriatal, corticobulbar, nigrostriatal, and cerebellar pathways and expansions of prefrontal, cingular, parieto-temporal and occipital cortices with derived new brain capabilities. All selectively degenerate in aged homo sapiens following 16 syndromic presentations: (1) Parkinsonism: nigrostriatal control for fast automatic movements of hand, larynx, bipedal posture and gait ("simian gait and hand"). (2) Frontal (highest level) gait disorders (lower body parkinsonism, gait apraxia, retropulsion): prefrontostriatal executive control of bipedal locomotion. (3) ataxia: new synergistic coordination of bipedal gait and fine motility. (4) Dyskinesias (chorea, dystonia, tremor...): intrusions of simian basal ganglia motor subroutines. (5) motoneuron diseases: new proximo-distal and bulbar motoneurones, preserving older ones (oculomotor, abdominal...). (6) Archaic reflexes: prefrontal disinhibition of old mother/tree-climbing-oriented reflexes (sucking, grasping, Babinski/triple retraction, gegenhalten), group alarms (laughter, crying, yawning, grunting...) or grooming (tremor=scratching). (7) Dysautonomia: contextual regulation (orthostatism...). (8) REM sleep disorders of new cortical functions. (9) Corticobasal syndrome: melokinetic control of hand prehension-manipulation and language (retrocession to simian patterns). (10) Frontal/temporal lobe degeneration: medial-orbitofrontal behavioural variant: self monitoring of internal needs and social context: apathy, loss of personal hygiene, stereotypia, disinhibition, loss of concern for consequences of acts, social rules, danger and empathy; dorsolateral executive variant: inadequacy to the context of action (goal, environmental changes...); progressive non-fluent aphasia: executive and praxic processing of speech; temporal variant: abstract concepts for speech, gestures and vision (semantic dementia, progressive nonfluent aphasia) (11) Temporomesial-limbic-paralimbic-associative cortical dementias (Alzheimer's disease, Lewy body, progressive amnesia): processing of explicit cognition: amnesic syndrome, processing of hand, larynx and eye: disorientation, ideomotor apraxia, agnosia, visuospatial processing, transcortical aphasia. (12) Focal posterior atrophy (Benson, progressive apraxia): visuomotor processing of what and where. (13) Macular degeneration: retinal "spot" for explicit symbols. (14) "Psychiatric syndromes": metacognition, self monitoring and regulation of hierarchical processing of metacognition: hallucinations, delusions, magic and mystic logic, delusions, confabulations; drive: impulsivity, obsessive-compulsive disorders, mental automatisms; social interactions: theory of mind, autism, Asperger. (15) Mood disorders: control on emotions: anxio-depressive and bipolar disorders, moria, emotional lability. (16) Musculoskeletal: inclusion body myositis: muscles for bipedal gait and fine motility. Paget's disease: bones for bipedal gait and cranium. Understanding of the genetic mechanisms underlying the evolution of these recent human brain regions and paleoneurology my be the key to the focal, asymmetrical or systemic character of neurodegeneration, the pathologic heterogeneity/overlap of syndromic presentations associating gait, hand, language, cognition, mood and behaviour disorders.
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PMID:Paleoneurology: neurodegenerative diseases are age-related diseases of specific brain regions recently developed by Homo sapiens. 1870 90


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