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PubMed2004

The human basis pontis: motor syndromes and topographic organization.

Clinical-anatomic correlations were performed in 25 patients with focal infarcts in the basilar pons to determine whether pontine lacunar syndromes conform to discrete clinical entities, and whether there is topographic organization of the motor system within the human basis pontis. Twelve clinical signs were scored on a 6-point scale, neuroimaging lesions were mapped and defined with statistical certainty, and structure-function correlation was performed to develop a topographic map of motor function. Clinical findings ranged from major devastation following extensive lesions (pure motor hemiplegia) to incomplete basilar pontine syndrome and restricted deficits after small focal lesions (ataxic hemiparesis, dysarthria-clumsy hand syndrome, dysarthria-dysmetria and dysarthria-facial paresis). The syndromes are not absolutely discrete, and are distinguished from each other by the relative degree of involvement of each clinical feature. Structure-function correlations indicate that strength is conveyed by the corticofugal fibres destined for the spinal cord, whereas dysmetria results from lesions involving the neurons of the basilar pons that link the ipsilateral cerebral cortex with the contralateral cerebellar hemisphere. Facial movement and articulation are localized to rostral and medial basilar pons; hand coordination is medial and ventral in rostral and mid-pons; and arm function is represented ventral and lateral to the hand. Leg coordination is in the caudal half of the pons, with lateral predominance. Swallowing is dependent upon the integrity of a number of regions in the rostral pons. Gait is in medial and lateral locations throughout the rostral- caudal extent of the pons. Dysmetria ipsilateral to the lesion constitutes a disconnection syndrome, as it occurs when the hemipontine lesion is extensive and interrupts pontocerebellar fibres traversing from the opposite, intact side of the pons. The heterogeneity of manifestations reflects the well-organized topography of motor function in the human basis pontis, in agreement with the anatomic organization of the motor corticopontine projections in the monkey. Higher order impairments including motor neglect, paraphasic errors and pathological laughter result from rostral and medial pontine lesions, and may result from disruption of the pontine component of associative corticopontocerebellar circuits.

Adult↗

PubMed2005

The Advantages of Traditional Chumash Healing.

Chumash healing has been practiced in California for approximately 13 000 years. Chumash healers treat their patients with prayer, laughter, dreaming, phytotherapy, aromatherapy, healing ceremonies and other techniques. Healing involves first healing the spirit, then healing the body. Chumash people still maintain their unique identity. Chumash Healers still practice the ancient healing arts in California. This lecture is a brief introduction to Chumash Healing.

Journal Article↗

PubMed2003

Williams-Beuren syndrome: a challenge for genotype-phenotype correlations.

Many human chromosomal abnormality syndromes include specific cognitive and behavioural components. Children with Prader-Willi syndrome lack a paternally derived copy of the proximal long arm of chromosome 15, and eat uncontrollably; in Angelman syndrome lack of a maternal contribution of 15q11-q13 results in absence of speech, frequent smiling and episodes of paroxysmal laughter; deletions on 22q11 can be associated with obsessive behaviour and schizophrenia. The neurodevelopmental disorder Williams-Beuren syndrome (WBS), is caused by a microdeletion at 7q11.23 and provides us with one of the most convincing models of a relationship that links genes with human cognition and behaviour. The hypothesis is that deletion of one or a series of genes causes neurodevelopmental abnormalities that manifest as the fractionation of mental abilities typical of WBS. Detailed molecular characterization of the deletion alongside well-defined cognitive profiling in WBS provides a unique opportunity to investigate the neuromolecular basis of complex cognitive behaviour, and develop integrated approaches to study gene function and genotype-phenotype correlations.

Animals↗

PubMed2005

Maternal disruption of Ube3a leads to increased expression of Ube3a-ATS in trans.

Angelman syndrome (AS) is a neurogenetic disorder characterized by severe mental retardation, 'puppet-like' ataxic gait with jerky arm movements, seizures, EEG abnormalities, hyperactivity and bouts of inappropriate laughter. Individuals with AS fail to inherit a normal active maternal copy of the gene encoding ubiquitin protein ligase E3A (UBE3A). UBE3A is transcribed predominantly from the maternal allele in brain, but is expressed from both alleles in most other tissues. It has been proposed that brain-specific silencing of the paternal UBE3A allele is mediated by a large (>500 kb) paternal non-coding antisense transcript (UBE3A-ATS). There are several other examples of imprinting regulation involving antisense transcripts that share two main properties: (i) the sense transcript is repressed by antisense and (ii) the interaction between sense and antisense occurs in cis. We show here that, in a mouse model of AS, maternal transmission of Ube3a mutation leads to increased expression of the paternal Ube3a-ATS, suggesting that the antisense is modulated by sense rather than the reciprocal mode of regulation. Our observation that Ube3a regulates expression of Ube3a-ATS in trans is in contrast to the other cases of sense-antisense epigenetic cis-interactions and argues against a major role for Ube3a-ATS in the imprinting of Ube3a.

Angelman Syndrome↗

PubMed2000

A prospective cohort study of childhood behavioral deviance and language abnormalities as predictors of adult schizophrenia.

Language and behavioral deviance in early childhood in preschizophrenia individuals suggests that the pathologic processes predisposing to schizophrenia are present from early in life. However, the etiologic antecedents of such impairments, and the degree to which they predict adult schizophrenia, have not been conclusively demonstrated. To address this, we examined language and behavioral predictors of adult psychiatric outcome in a population cohort (72 individuals with schizophrenia or schizoaffective disorder, 63 of their unaffected siblings, and 7,941 with no diagnosis) evaluated prospectively with behavioral examinations and a speech and language evaluation at 8 months, 4 years, and 7 years of age. Psychiatric outcome was ascertained via adult treatment contacts, and diagnoses were made by chart review according to DSM-IV criteria. Social maladjustment at age 7 was found to predict adult schizophrenia, and focal deviant behaviors (e.g., echolalia, meaningless laughter) at ages 4 and 7 were significantly associated with both schizophrenia and sibling status. Unintelligible speech at age 7 was a highly significant predictor of adult schizophrenia (odds ratio = 12.7), and poor expressive language ability predicted both schizophrenia and unaffected sibling outcome. Early behavioral and language dysfunction did not differentially characterize preschizophrenia subjects with a history of fetal hypoxia or an early age of first treatment contact. Given that unaffected siblings show similar signs of deviance, such problems may indicate genotypic susceptibility to the disorder, or shared environmental influences, or both.

Adult↗

PubMed1998

Major depression: behavioral markers of depression and recovery.

The concepts of psychosocial and psychomotor inhibition characteristic of major depression are based primarily on clinical observations. It is possible to describe and define these two types of inhibition by means of a systematic, quantitative ethological (behavioral) approach, which singles out precise and significant behavior markers. This investigation focuses on the behavioral features of psychosocial and psychomotor inhibition in 11 hospitalized depressed subjects and their changes during clinical recovery. The hypothesis that major depression is characterized by a significant reduction of social interaction is tested (psycho-intellectual inhibition is not addressed). Results show significant behavioral differences between depressed and recovered subjects with depression being characterized by a significant reduction of social interaction, whereas self occupation and body mobility are reduced to a lesser degree. Behavior markers for depression include nonspecific gaze, withdrawal, no mouth movements, no eye region movements, and social inactivity. Behavior markers for recovery include socially interested, social smile, verbal social initiative, speech, nod, raised eyebrows, wrinkled eyebrows, social laughter, gesticulation, drum one's fingers, point, and help. Findings point to tendencies toward two types of major depression and two types of recovery. A companion paper (Schelde, this journal) addresses theoretical issues.

Adult↗

PubMed1996

Successful treatment of giggle incontinence with methylphenidate.

PURPOSE: Giggle incontinence, the second most common type of childhood enuresis unrelated to disease, is notoriously difficult to treat. However, the association of laughter or emotion precipitated alteration of muscle tone is suggestive of a functional relationship to cataplexy, a part of the narcoleptic syndrome complex that may respond to stimulant medication. MATERIALS AND METHODS: Two boys and 5 girls (mean age 10.9 years) with giggle incontinence, a positive family history of giggle incontinence (4 patients) and no evidence of urological disease were treated with methylphenidate for 1 to 5 years. RESULTS: All patients responded positively with complete cessation of enuresis to varying dose schedules of methylphenidate. CONCLUSIONS: These results suggest that giggle incontinence is a centrally mediated and likely hereditary disorder that may share a common pathophysiological basis with the narcolepsy/cataplexy syndrome.

Adolescent↗

PubMedDate not supplied

Communication patterns and conflict in marital dyads.

Responses--pauses, laughter, and interruptions (postulated to be communication techniques of couples with more equal power in decision making) and questions, silence time, and longer decision time (hypothesized to be communication techniques of couples in a dominant-submissive power structure)--of 68 middle-class suburban couples who volunteered to take the Inventory of Marital Conflicts were analyzed. Although study hypotheses were not supported, a high intercorrelation was revealed among communication variables hypothesized to be characteristic of power-sharing couples.

Adult↗

PubMed1988

Rett syndrome: a survey of North American patients.

Parents of 63 North American girls with Rett syndrome filled out retrospective questionnaires in a project of the International Rett Syndrome Association, a parent group. No consistent pattern was revealed of possible etiological factors related to environmental insults; however, additional information gathered supported a genetic etiology. The survey included one pair of identical twins and one child with consanguineous parents. There were 46 male sibs and 34 female sibs. These data weigh against any theory relating etiology to a gene on the X chromosome which is lethal to males in utero. Figures were gathered on a number of clinical items. These were: onset of symptoms between 6 and 18 months of age, 83%; autistic withdrawal, 73%; never walked independently, 23%; hyperventilators with abdominal swelling, 63%; night laughter, 83%. The average age of walking of those who walked was 19 months and the average onset of seizure disorders was between 3 1/2 and 4 years of age. This paper ends by discussing the limitations of a parent questionnaire.

Adolescent↗

PubMed2006

The behavioural phenotype of Angelman syndrome.

BACKGROUND: The purpose of this review is to examine the notion of a behavioural phenotype for Angelman syndrome and identify methodological and conceptual influences on the accepted presentation. METHODS: Studies examining the behavioural characteristics associated with Angelman syndrome are reviewed and methodology is described. RESULTS: Potential bias in the description of the phenotype emerges with the use of case and cohort studies with the absence of comparison groups. A trend in the literature from a direct gene effect to a socially mediated effect on laughter is evident. CONCLUSION: Evidence for a behavioural phenotype of Angelman syndrome has begun to emerge. However, by adopting the concept of a 'behavioural phenotype', attention may become biased towards the underlying biological basis of the syndrome, with developmental and environmental factors being overlooked.

Adolescent↗

PubMed1996

The last post? Defending nursing against the postmodernist maze.

Is postmodernism in many ways the empiricist-liberal tradition at the inevitable end of its intellectual and political tether? Or is postmodernism the 'laughter of genius' that art and argument in their traditional forms are dead? Can postmodernism be applied to social and economic issues whilst carrying a denial of the manner by which Western thought has shaped these issues? Can postmodernism provide moral pathways to help us with contemporary ethical issues? How can postmodernist thought encompass the activities of nurses, particularly in the area of psychiatric care? Can nurses afford postmodernist suppositions in the face of suffering and pain? If postmodernism exists, does it exist everywhere (as does nursing) or is it a more localized event?

Attitude to Health↗

PubMed1998

Normal growth in Angelman syndrome due to paternal UPD.

We describe 2 patients with Angelman syndrome (AS) due to paternal uniparental disomy (UPD). One patient is a female aged 30 years and the other a male aged 4 1/2 years. Both have the characteristic wide mouth and big chin, moderate mental retardation, virtually no speech but some 30 words of sign language and a happy disposition with outbursts of laughter. Ataxia is minimal in both patients, manifesting mainly when they are excited or running. Both patients are tall (height around 90th percentile), have a head circumference around 75th percentile and are overweight (weight over the 97th percentile). These cases add to the knowledge of the possibility of normal or increased growth parameters, particularly weight, in AS when the genetic mechanism is paternal UPD.

Adult↗

PubMed1979

An autopsy case of multiple leucoencephalitis showing hemiatrophy of the brain.

A 39-year-old female died 25 years after the onset of epileptic seizure. In the clinical course, she suffered epileptic seizures, left hemiparesis and muscular atrophy of the left upper extremity, psychological character change, dementia, forced laughter and hallucinatory and delusional states. Pathologically, severe changes were found in the right hemisphere consisting of lesions of white matter with myelin loss, especially in the frontal, temporal and occipital lobes. Gliosis was diffusely observed in the white matter excepting areas with severe changes. In some parts of the cortex, the cytoarchitecture was destroyed and in this area, blood vessels numerously increased. In the left occipital white matter, perivascular infiltration mainly consisting of lymphocytes was observed with numerous fat granule cells and gemystocytic astrocytes around them. The present case may belong to the category of multiple leucoencephalitis, however, it had many characteristic features, such as a long clinical course (25 years) and pathologically revealed hemiatrophy of the brain.

Adult↗

PubMedDate not supplied

Partial seizures evolving to infantile spasms.

We describe the clinical and electroencephalographic (EEG) manifestations of four patients with simultaneous EEG-video-telemetry recording (VTR) documented partial seizures evolving to infantile spasms. Clinical manifestations of the partial seizures included cessation of activity, staring, automatisms, increased limb tone, and laughter. In each case, partial seizures were followed by a cluster of infantile spasms. Infantile spasms preceded by partial seizures have not been previously documented.

Electroencephalography↗

PubMed1994

The effects of the presence of a third person on the physician-older patient medical interview.

OBJECTIVE: To compare communication in triadic (three-person) and dyadic (two-person) older patient medical interviews and to determine the influence of the presence of a third person on the physician-older patient relationship. DESIGN: Matched sample of dyadic and triadic audiotaped outpatient medical visits. Audiotapes were coded with the Multi-dimensional Interaction Analysis (MDIA) system. SETTING: Hospital-based medical primary care group practice in a major urban teaching institution. PARTICIPANTS: Patients 60 years and older who were making their first visit to study physicians. In a sample of 96 audiotaped initial medical visits, 15 encounters involved three persons. These 15 cases were matched with 15 dyadic interviews for gender and race of the patient and for gender and race of the physician. MAIN OUTCOME MEASURES: Content, interactional processes, and specific language and communication behaviors of older patients, physicians, and third persons in the medical encounter, as measured by the MDIA system. RESULTS: The specific content and the quality of interactional processes of physicians were not affected by the presence of a third person. However, older patients raised fewer topics in all content areas (medical, personal habits, psychosocial, and physician-patient relationship) in triads than in dyads. Overall, patients were less responsive (ie, the quality of their questioning, informing, and supportiveness was poorer) on patient-raised topics in triads than in dyads. Patients were rated as less assertive and expressive, and there was less joint decision-making and shared laughter in triads than in dyads. Patients were frequently excluded from conversations in visits in which a third person was present. CONCLUSIONS: The presence of a third person in the medical encounter changes the interactional dynamics of older patient medical interviews and may influence the development of a trusting and effective physician-older patient relationship.

Adult↗

PubMed1989

The 'happy puppet' syndrome of Angelman: review of the clinical features.

Thirty six children with typical features of Angelman's syndrome, including global developmental delay, ataxia, episodes of paroxysmal laughter, seizures, and microcephaly were studied. The series included three sibships of three affected sisters, two affected brothers, and two affected sisters, respectively. The facial appearance is characterised by a prominent jaw, a wide mouth, and a pointed chin. Tongue thrusting is common. The movement disorder consists of a wide based, ataxic gait with frequent jerky limb movements and flapping of the hands. Tone is variable in the limbs with normal reflexes, and the plantar responses are usually flexor. The syndrome is being diagnosed more often, and attention is drawn to its diagnostic aspects.

Adolescent↗

PubMed1994

X linked mental retardation with non-deletional alpha thalassaemia (ATR-X): further delineation of the phenotype.

Two sibs with non-deletional alpha thalassaemia and mental retardation (ATR-X) have been ascertained showing variable neurological features. The proband had a complex neurological picture with recurrent apnoea, complex partial seizures, and prolonged periods of semiconsciousness between 12 and 17 months of age. Episodes of spontaneous laughter were also a feature. An EEG was initially normal. Hb H inclusions were present but rare in this family. The sole genital anomaly was deficiency of the foreskin, a feature not previously described in ATR-X.

Abnormalities, Multiple↗

PubMed2003

Angelman syndrome: a review of the clinical and genetic aspects.

Angelman syndrome (AS) is a neurodevelopmental disorder characterised by severe learning difficulties, ataxia, a seizure disorder with a characteristic EEG, subtle dysmorphic facial features, and a happy, sociable disposition. Most children present with delay in developmental milestones and slowing of head growth during the first year of life. In the majority of cases speech does not develop. Patients with AS have a characteristic behavioural phenotype with jerky movements, frequent and sometimes inappropriate laughter, a love of water, and sleep disorder. The facial features are subtle and include a wide, smiling mouth, prominent chin, and deep set eyes. It is caused by a variety of genetic abnormalities involving the chromosome 15q11-13 region, which is subject to genomic imprinting. These include maternal deletion, paternal uniparental disomy, imprinting defects, and point mutations or small deletions within the UBE3A gene, which lies within this region. UBE3A shows tissue specific imprinting, being expressed exclusively from the maternal allele in brain. The genetic mechanisms identified so far in AS are found in 85-90% of those with the clinical phenotype and all interfere with UBE3A expression.

Angelman Syndrome↗