Epilepsy after two different neurosurgical approaches to the treatment of ruptured intracranial aneurysm. (1/412)

One-hundred-and-fifty-two patients who underwent surgery for intracranial aneurysm were studied to determine the incidence of postoperative epilepsy in relation to the site of the aneurysm and the type of surgical approach. The overall incidence of epilepsy was 22%. Of the 116 patients treated by the intracranial approach 27.5% developed epilepsy, in contrast with only 5% of the 36 patients who had carotid artery ligation in the neck. Epilepsy occurred most frequently (35%) with middle cerebral artery aneurysms, especially if moderate or severe operative trauma was sustained and there was postoperative dysphasia.  (+info)

Evaluation and management of the child with speech delay. (2/412)

A delay in speech development may be a symptom of many disorders, including mental retardation, hearing loss, an expressive language disorder, psychosocial deprivation, autism, elective mutism, receptive aphasia and cerebral palsy. Speech delay may be secondary to maturation delay or bilingualism. Being familiar with the factors to look for when taking the history and performing the physical examination allows physicians to make a prompt diagnosis. Timely detection and early intervention may mitigate the emotional, social and cognitive deficits of this disability and improve the outcome.  (+info)

Failure of cerebellar patients to time finger opening precisely causes ball high-low inaccuracy in overarm throws. (3/412)

We investigated the idea that the cerebellum is required for precise timing of fast skilled arm movements by studying one situation where timing precision is required, namely finger opening in overarm throwing. Specifically, we tested the hypothesis that in overarm throws made by cerebellar patients, ball high-low inaccuracy is due to disordered timing of finger opening. Six cerebellar patients and six matched control subjects were instructed to throw tennis balls at three different speeds from a seated position while angular positions in three dimensions of five arm segments were recorded at 1,000 Hz with the search-coil technique. Cerebellar patients threw more slowly than controls, were markedly less accurate, had more variable hand trajectories, and showed increased variability in the timing, amplitude, and velocity of finger opening. Ball high-low inaccuracy was not related to variability in the height or direction of the hand trajectory or to variability in finger amplitude or velocity. Instead, the cause was variable timing of finger opening and thereby ball release occurring on a flattened arc hand trajectory. The ranges of finger opening times and ball release times (timing windows) for 95% of the throws were on average four to five times longer for cerebellar patients; e.g., across subjects mean ball release timing windows for throws made under the medium-speed instruction were 11 ms for controls and 55 ms for cerebellar patients. This increased timing variability could not be explained by disorder in control of force at the fingers. Because finger opening in throwing is likely controlled by a central command, the results implicate the cerebellum in timing the central command that initiates finger opening in this fast skilled multijoint arm movement.  (+info)

Functional anatomy of verbal fluency in people with schizophrenia and those at genetic risk. Focal dysfunction and distributed disconnectivity reappraised. (4/412)

BACKGROUND: PET studies of verbal fluency in schizophrenia report a failure of 'deactivation' of left superior temporal gyrus (STG) in the presence of activation of left dorsolateral prefrontal cortex (DLPFC), which deficit has been attributed to underlying 'functional disconnectivity'. AIM: To test whether these findings provide trait-markers for schizophrenia. METHOD: We used H2(15)O PET to examine verbal fluency in 10 obligate carriers of the predisposition to schizophrenia, 10 stable patients and 10 normal controls. RESULTS: We found no evidence of a failure of left STG deactivation in carriers or patients. Instead, patients failed to deactivate the precuneus relative to other groups. We found no differences in functional connectivity between left DLPFC and left STG but patients exhibited significant disconnectivity between left DLPFC and anterior cingulate cortex. CONCLUSIONS: Failure of left STG 'deactivation' and left fronto-temporal disconnectivity are not consistent findings in schizophrenia; neither are they trait-markers for genetic risk. Prefrontal functional disconnectivity here may characterise the schizophrenic phenotype.  (+info)

The SPCH1 region on human 7q31: genomic characterization of the critical interval and localization of translocations associated with speech and language disorder. (5/412)

The KE family is a large three-generation pedigree in which half the members are affected with a severe speech and language disorder that is transmitted as an autosomal dominant monogenic trait. In previously published work, we localized the gene responsible (SPCH1) to a 5.6-cM region of 7q31 between D7S2459 and D7S643. In the present study, we have employed bioinformatic analyses to assemble a detailed BAC-/PAC-based sequence map of this interval, containing 152 sequence tagged sites (STSs), 20 known genes, and >7.75 Mb of completed genomic sequence. We screened the affected chromosome 7 from the KE family with 120 of these STSs (average spacing <100 kb), but we did not detect any evidence of a microdeletion. Novel polymorphic markers were generated from the sequence and were used to further localize critical recombination breakpoints in the KE family. This allowed refinement of the SPCH1 interval to a region between new markers 013A and 330B, containing approximately 6.1 Mb of completed sequence. In addition, we have studied two unrelated patients with a similar speech and language disorder, who have de novo translocations involving 7q31. Fluorescence in situ hybridization analyses with BACs/PACs from the sequence map localized the t(5;7)(q22;q31.2) breakpoint in the first patient (CS) to a single clone within the newly refined SPCH1 interval. This clone contains the CAGH44 gene, which encodes a brain-expressed protein containing a large polyglutamine stretch. However, we found that the t(2;7)(p23;q31.3) breakpoint in the second patient (BRD) resides within a BAC clone mapping >3.7 Mb distal to this, outside the current SPCH1 critical interval. Finally, we investigated the CAGH44 gene in affected individuals of the KE family, but we found no mutations in the currently known coding sequence. These studies represent further steps toward the isolation of the first gene to be implicated in the development of speech and language.  (+info)

Are ictal vocalisations related to the lateralisation of frontal lobe epilepsy? (6/412)

The purpose was to analyse whether non-speech vocalisations in seizures originating in the frontal lobe do have lateralising value. Patients were included who had undergone presurgical evaluation with ictal video-EEG monitoring at the Epilepsy Centre, had had resective epilepsy surgery involving the frontal lobe, and who had remained seizure free>1 year postoperatively. Twenty seven patients aged 1-42 years (mean 18) met the inclusion criteria. Age at epilepsy onset ranged from 1 month to 41 years (mean 7.1 years). All selected patients had a unilateral MRI detected lesion within the frontal lobe. Fifteen patients had right sided, 12 patients had left sided epileptogenic zones. Seizures recorded during EEG-video monitoring were re-evaluated to identify the occurrence of ictal vocalisations. Pure ictal vocalisations were distinguished from ictal sound productions due to motor or vegetative seizure activity (for example, cloni or respiratory sounds). Pure ictal vocalisation occurred in 11 patients of whom nine had a left frontal epileptogenic zone (p<0.01). It is concluded that ictal vocalisation could be an additional lateralising sign in frontal lobe epilepsy. The results suggest that not only speech, but vocalisation at a subverbal level also shows a left hemispheric dominance in humans.  (+info)

Functional and social discomfort during orthodontic treatment--effects on compliance and prediction of patients' adaptation by personality variables. (7/412)

During the course of treatment orthodontic patients frequently endure a number of functional complaints and are anxious about their appearance. The aims of this longitudinal study were to follow the progress of patients' adaptation to discomfort, to elucidate the putative relationship between the type of appliance worn and functional and social discomfort experienced, to study potential predictability by their attitude to treatment and to evaluate the effects of discomfort as predictors of patients' compliance. Eighty-four patients undergoing either removable, functional, or fixed appliance treatment monitored their complaints during the first 7 days of treatment and rated them retrospectively 14 days, and 3 and 6 months after appliance insertion. The most frequent complaints were impaired speech, impaired swallowing, feeling of oral constraint and lack of confidence in public. A significant reduction in the number of complaints was observed between 2 and 7 days after insertion of the appliance. No further differences were revealed after longer periods of appliance wear. The type of appliance had an effect on impaired speech and swallowing. Patients' expectations of favourable treatment performance and appreciation of dental aesthetics were predictive of reported feeling of oral constraint and lack of confidence in public. There was a relationship between the complaints and acceptance of the appliance, as well as between lack of confidence in public and compliance with treatment. The results of this study highlight the importance of patients' attitudes to treatment and of functional and social discomfort associated with appliance wear for the theory and practice of the management of orthodontic patients, and the necessity for early intervention by clinicians.  (+info)

Repetitive speech phenomena in Parkinson's disease. (8/412)

OBJECTIVES: Repetitive speech phenomena are morphologically heterogeneous iterations of speech which have been described in several neurological disorders such as vascular dementia, progressive supranuclear palsy, Wilson's disease, and Parkinson's disease, and which are presently only poorly understood. The present, prospective study investigated repetitive speech phenomena in Parkinson's disease to describe their morphology, assess their prevalence, and to establish their relation with neuropsychological and clinical background data. METHODS: Twenty four patients with advanced Parkinson's disease and 29 subjects with mid-stage, stable idiopathic disease were screened for appearance, forms, and frequency of repetitive speech phenomena, and underwent a neuropsychological screening procedure comprising tests of general mental functioning, divergent thinking and memory. Patients with advanced Parkinson's disease had a significantly higher disease impairment, longer disease duration, and an unstable motor response to levodopa with frequent on-off fluctuations. Both groups were well matched as to their demographical, clinical, and cognitive background. Perceptual speech evaluation was used to count and differentiate forms of repetitive speech phenomena in different speech tasks. To compare the effect of the motor state, the appearance of repetitive speech phenomena was also assessed in a subgroup of patients with advanced Parkinson's disease during the on versus the off state. RESULTS: Speech repetitions emerged mainly in two variants, one hyperfluent, formally resembling palilalia, and one dysfluent, stuttering-like. Both forms were present in each patient producing repetitive speech phenomena. The repetitive speech phenomena appeared in 15 patients (28.3 %), 13 of whom belonged to the advanced disease group, indicating a significant preponderance of repetitive speech phenomena in patients with a long term, fluctuating disease course. Repetitive speech phenomena appeared with almost equal frequency during the on and the off state of patients with advanced Parkinson's disease. Their distribution among different variants of speech was disproportional, with effort demanding speech tasks producing a significantly higher number of repetitive speech phenomena over semiautomatic forms of speech. CONCLUSIONS: In idiopathic Parkinson's disease repetitive speech phenomena seem to emerge predominantly in a subgroup of patients with advanced disease impairment; manifest dementia is not a necessary prerequisite. They seem to represent a deficit of motor speech control; however, linguistic factors may also contribute to their generation. It is suggested that repetitions of speech in Parkinson's disease represent a distinctive speech disorder, which is caused by changes related to the progression of Parkinson's disease.  (+info)