Partial and full own-body illusions of epileptic origin in a child with right temporoparietal epilepsy

Partial and full own-body illusions of neurological origin have been claimed crucial to understand the contribution of bodily experience and perception to self-consciousness. Whereas partial body illusions are relatively common and well defined, much less is known about full own-body illusions, and even less is known about these illusions in children. Here we describe a 10-year-old patient with the association of partial and full own-body illusions (somatoparaphrenia and out-of-body experience) that occurred sequentially during an epileptic seizure caused by right temporoparietal epilepsy. This report shows that partial and full own-body illusions share functional and neuroanatomical properties and highlights the importance of the right temporoparietal junction for bodily self-consciousness. This is the first report of out-of-body experiences in a child with focal epilepsy.     

Brain mapping of auditory hallucinations and illusions induced by direct intracortical electrical stimulation

BackgroundThe exact architecture of the human auditory cortex remains a subject of debate, with discrepancies between functional and microstructural studies. In a hierarchical framework for sensory perception, simple sound perception is expected to take place in the primary auditory cortex, while the processing of complex, or more integrated perceptions is proposed to rely on associative and higher-order cortices.ObjectivesWe hypothesize that auditory symptoms induced by direct electrical stimulation (DES) offer a window into the architecture of the brain networks involved in auditory hallucinations and illusions. The intracranial recordings of these evoked perceptions of varying levels of integration provide the evidence to discuss the theoretical model.MethodsWe analyzed SEEG recordings from 50 epileptic patients presenting auditory symptoms induced by DES. First, using the Juelich cytoarchitectonic parcellation, we quantified which regions induced auditory symptoms when stimulated (ROI approach). Then, for each evoked auditory symptom type (illusion or hallucination), we mapped the cortical networks showing concurrent high-frequency activity modulation (HFA approach).ResultsAlthough on average, illusions were found more laterally and hallucinations more posteromedially in the temporal lobe, both perceptions were elicited in all levels of the sensory hierarchy, with mixed responses found in the overlap. The spatial range was larger for illusions, both in the ROI and HFA approaches. The limbic system was specific to the hallucinations network, and the inferior parietal lobule was specific to the illusions network.DiscussionOur results confirm a network-based organization underlying conscious sound perception, for both simple and complex components. While symptom localization is interesting from an epilepsy semiology perspective, the hallucination-specific modulation of the limbic system is particularly relevant to tinnitus and schizophrenia.     

Hemispheric asymmetries in resting‐state EEG and fMRI are related to approach and avoidance behaviour,but not to eating behaviour or BMI

Much of our behaviour is driven by two motivational dimensions—approach and avoidance. These have been related to frontal hemispheric asymmetries in clinical and resting‐state EEG studies: Approach was linked to higher activity of the left relative to the right hemisphere, while avoidance was related to the opposite pattern. Increased approach behaviour, specifically towards unhealthy foods, is also observed in obesity and has been linked to asymmetry in the framework of the right‐brain hypothesis of obesity. Here, we aimed to replicate previous EEG findings of hemispheric asymmetries for self‐reported approach/avoidance behaviour and to relate them to eating behaviour. Further, we assessed whether resting fMRI hemispheric asymmetries can be detected and whether they are related to approach/avoidance, eating behaviour and BMI. We analysed three samples: Sample 1 (n = 117) containing EEG and fMRI data from lean participants, and Samples 2 (n = 89) and 3 (n = 152) containing fMRI data from lean, overweight and obese participants. In Sample 1, approach behaviour in women was related to EEG, but not to fMRI hemispheric asymmetries. In Sample 2, approach/avoidance behaviours were related to fMRI hemispheric asymmetries. Finally, hemispheric asymmetries were not related to either BMI or eating behaviour in any of the samples. Our study partly replicates previous EEG findings regarding hemispheric asymmetries and indicates that this relationship could also be captured using fMRI. Our findings suggest that eating behaviour and obesity are likely to be mediated by mechanisms not directly relating to frontal asymmetries in neuronal activation quantified with EEG and fMRI.     

Passive avoidance behaviour deficit in the mdx mouse

Thirty per cent of boys with Duchenne muscular dystrophy (DMD) suffer from various degrees of mental retardation. Since dystrophin, the protein absent in muscles of boys with DMD, is produced also in the brain, it was postulated that the deficiency of brain dystrophin might account for the mental retardation found in DMD boys. The mdx mouse, a mouse model of DMD, fails to produce dystrophin in muscle and brain. This prompted us to study the cognitive function of these animals. Learning and memory processes were studied in 10 mdx females and 9 genetically matched controls using the passive avoidance test. Statistically significant differences in the retention of the passive avoidance response was detected between mdx and control mice, indicating an impairment in passive avoidance learning in mdx mice. Our data reinforce the view that brain dystrophin deficiency is correlated with cognitive dysfunction and indicate that mdx mice might be a model for the mental retardation found in DMD boys.     

Brainstem auditory evoked potential abnormalities in myelomeningocoele in the older child.

Brainstem auditory evoked potentials and clinical findings were examined in 18 children over the age of 5 years who were born with myelomeningocoele which was closed at birth, and whose hydrocephalus was managed by long term shunting in most of them. The potentials were compared with age and sex matched normal subjects and with four patients with hydrocephalus only. All but one had an abnormal brainstem auditory evoked potential with 72% showing a delay in the II-V and I-V interpeak latencies of more than three standard deviations. It is proposed that the abnormalities are a reflection of brainstem dysgenesis which is part of an associated Arnold-Chiari malformation, though the malformation was clinically asymptomatic in all. The usefulness of the brainstem auditory evoked potential for assessing the course of hydrocephalus and for predicting symptomatic Arnold-Chiari malformation is questioned.     

Aggressive behaviour and psychosis in a clinically referred child and adolescent sample

Background

Despite evidence of an increased risk of violence among adults suffering from psychosis, very little is currently known about the relationship between early onset psychosis and aggressive behaviour. We aimed to identify and examine overlaps between aggressive behaviour and psychosis in a referred child and adolescent sample to assess whether potential risk factors and other associated features of this co-occurring pattern can be identified at a young age.

Methods

Standardised item sheet data on young people referred to the Child and Adolescent Department of the Maudsley Hospital between 1973 and 2004 were used to contrast three groups: (1) aggressive-only (n?=?1,346), (2) psychosis-only (n?=?173), and (3) co-occurring aggression and psychosis (n?=?39) on a range of comorbid symptoms and potential risk factors.

Results

Co-occurring cases presented with elevated rates of depersonalisation/derealisation, intrusive thoughts and restlessness, and were more likely to have received past treatment compared with both psychosis-only and aggressive-only cases. Although co-occurring cases resembled the psychosis-only group in many domains, including socio-demographic background and rates of emotional symptoms, they differed from ‘pure’ psychosis cases in having high levels of special educational needs, irritability, non-aggressive antisocial behaviours, as well as being more likely to be from a low social class and have increased contact with police and child care authorities.

Conclusions

Our findings suggest that it is possible to identify early risk factors for aggression in individuals with psychosis.     

The effects of atrial natriuretic peptide on passive avoidance behaviour in rats.

The effects of rat atrial natriuretic peptide (ANP 1-28) on passive avoidance behaviour were tested following its administration into the lateral brain ventricle in rats. Different doses of ANP 1-28 were administered immediately after the learning trial of passive avoidance behaviour and the effects on the consolidation of learning were tested 24 h later. ANP 1-28, in doses in the range 50-2000 ng/rat, caused a dose-dependent increase in passive avoidance latency. Selected doses (100, 200 and 500 ng/animal) were given 30 min before the learning trial. These doses lengthened the passive avoidance latency in a dose-dependent manner. When the peptide was given 30 min before the retention trial, there was no significant alteration in passive avoidance response. The data suggest that ANP 1-28 is able to facilitate the learning and consolidation of fear-motivated passive avoidance behaviour.     

REM sleep behaviour disorder in a child with Tourette's syndrome

PURPOSE: To describe an association of Tourette's syndrome with rapid eye movement sleep behaviour disorder (RBD) in a prepubescent boy. METHODS: A four year longitudinal single-case study. RESULTS: The co-existence of Tourette's syndrome and RBD was confirmed after polysomnographic studies using the standard criteria. The authors propose possible overlap in the pathophysiological mechanisms underlying the two disorders.     

Investigating functional changes in the brain to intermittently induced auditory illusions and its relevance to chronic tinnitus

Several studies have demonstrated the neural correlates of chronic tinnitus. However, we still do not understand what happens in the acute phase. Past studies have established Zwicker tone (ZT) illusions as a good human model for acute tinnitus. ZT illusions are perceived following the presentation of a notched noise stimulus, that is, broadband noise with a narrow band‐stop filter (notch). In the current study, we compared the neural correlates of the reliable perception of a ZT illusion to that which is not. We observed changes in evoked and total theta power in wide‐spread regions of the brain particularly in the temporal‐parietal junction, pregenual anterior cingulate cortex/ventromedial prefrontal cortex (pgACC/vmPFC), parahippocampus during perception of the ZT illusion. Furthermore, we observe that increased theta power significantly predicts a gradual positive change in the intensity of the ZT illusion. Such changes may suggest a malfunction of the sensory gating system that enables habituation to redundant stimuli and suppresses hyperactivity. It could also suggest a successful retrieval of the memory of the missing frequencies, resulting in their conscious perception indicating the role of higher‐order processing in the mechanism of action of ZT illusions. To establish a more concrete relationship between ZT illusion and chronic tinnitus, future longitudinal studies following up a much larger sample of participants who reliably perceive a ZT illusion to see if they develop tinnitus at a later stage is essential. This could inform us if the ZT illusion may be a precursor to chronic tinnitus.     

Pain related behaviour during vincristine-induced neuropathy in rats.

The development of suitable animal models of neuropathic pain is essential to understand the pathophysiological mechanisms responsible for this condition. This study presents the alterations in nociception observed in rats suffering from a peripheral neuropathy induced by 10 daily repeated intravenous injections of vincristine at doses of 50 or 75 microg/kg (total dose 500 or 750 microg/ kg). The rats present both mechanical hyperalgesia, allodynia and a loss of sensitivity (thermal hypoalgesia). Conservation of good health, the fast appearance of symptoms which correspond well with human responses and the easy induction of nociceptive symptoms are favourable criteria for using this model at 50 microg/kg vincristine dose in the future.     

Recovery process of auditory perceptual disorders in a child with word deafness

The patient was a right-handed boy. Pregnancy and delivery were normal. There were no neonatal complications. His development was normal until the age of 6 years and 10 months when he suddenly fell into coma. He was admitted to a hospital, where he was diagnosed as having encephalopathy of unknown cause. It was found that he did not respond to verbal stimuli after recovery from coma. He was referred to our hospital for detailed examination of hearing at the age of 7 years, and received neuroradiological and audiological examinations including X-ray CT, positron-CT, behavioral audiometry, auditory evoked response audiometry as well as other hearing and speech tests. Pure tone audiometry showed that auditory thresholds for pure tones ranging from 125 to 8,000 Hz were normal, while speech audiometry demonstrated that he was unable to discriminate test words. However, he accurately recognized environmental sounds and noises as well as sounds produced by musical instruments. The decreased uptake of 11C-glucose at the left temporal lobe was demonstrated by positron CT, although no abnormality was showed by X-ray CT. WISC-R showed he had normal intelligence. ITPA demonstrated that the psycholinguistic ability via visual channel remained intact, whereas auditory memory and auditory closure were markedly impaired. The boy had no difficulties in reading, naming and writing. Speech therapy was started as soon as diagnosis of word deafness was made. Until 6 months after onset, he never understood and repeated what was said to him.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term follow-up of auditory agnosia as a sequel of herpes encephalitis in a child

We report a pediatric patient with auditory agnosia as a sequel of herpes encephalitis. His early development was completely normal. He uttered three words at 12 months old. Disease onset was 1 year and 2 months of age. He was discharged from the hospital seemingly with no sequel; however, he could not recover his intelligible words even at age 2 years. He was diagnosed as having auditory agnosia caused by bilateral temporal lobe injury. We began to train him at once, individually and intensively. Adult patients with pure auditory agnosia followed by two episodes of temporal lobe infarction have impairment in central hearing but not inner language. Therefore, they can communicate by reading and writing. Moreover, impairment in hearing is not always severe and is often transient. However, despite long-term (more than 15 years) energetic education and almost normal intellectual ability (Performance IQ of Wechsler Intelligence Scale for Children-Revised was 91), our patient's language ability was extremely poor. Cerebral plasticity could not work fully on our patient, whose bilateral temporal lobe was severely injured in early childhood. The establishment of a systematic training method in such patients is an urgent objective in this field.     

5-hydroxytryptamine and the mediation of pituitary-adrenocortical hormones in the extinction of active avoidance behaviour.

(1) The effect of corticosterone on the extinction of a one-way active avoidance task was correlated with hypothalamic and mesencephalic serotonin (5-HT) content. (2) Corticosterone treatment in a daily dose of 1·0 and 5·0 mg/kg i.p. facilitated the extinction of active avoidance behaviour while doses of 10·0 mg/kg corticosterone delayed it. (3) 1·0 and 2·0 mg/kg corticosterone increased the hypothalamic 5-HT content in normal and adrenalectomized animals, 5·0 mg/kg failed to influence it, and 10·0 mg/kg decreased it. (4) After 1·0, 5·0 and 10·0 mg/kg corticosterone treatment, changes in mesencephalic 5-HT followed a pattern similar to that observed in the hypothalamus. (5) Adrenocorticotrophic hormone (ACTH), in doses of 2·0 and 4·0 i.u./animal, resulted in an increased hypothalamic and mesencephalic 5-HT content in intact animals; however, there were no changes in cerebral 5-HT levels in adrenalectomized rats. (6) Decreased brain 5-HT content, brought about by parachlorophenylalanine (PCPA) (300 mg/kg), was able to prevent the behavioural effect of 1·0 and 5·0 mg/kg corticosterone. (7) PCPA treatment alone given every 72 hr caused a transitory delay in extinction 24 and 48 hr after administration; however, the tendency for extinction to occur did not change. (8) Decreased 5-HT content caused by mesencephalic raphé lesions delayed extinction. (9) Nialamide treatment (125 mg/kg), which increased brain 5-HT content, counteracted the effect of 10·0 mg/kg corticosterone on extinction. (10) These data suggest that the action of corticosterone on active avoidance behaviour is mediated, at least in part, via changed 5-HT metabolism in the brain.     

Modulation of passive avoidance behaviour by cholecystokinin octapeptides in rats

The effects of two different doses of cholecystokinin octapeptide sulphate ester and its unsulphated form on the passive avoidance behaviour were studied following intraperitoneal administration to rats. Administered immediately after the learning trial in a dose of 400 nmole/kg, both peptides resulted in significantly increased passive avoidance latencies as compared to the control. There were no effects on the latency of passive avoidance behaviour when the animals were treated 1 h before the learning trial. When the cholecystokinin octapeptides were given 23 h after the learning trial, the latency tended to be increased, but this difference was not statistically significant.