Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “brain structure”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,009 records · Page 56Linked to original sources
PubMed1998

Structural brain imaging in schizophrenia.

The subtle pathomorphology of schizophrenia is gradually being unraveled through the application of increasingly sophisticated brain imaging techniques. There is now compelling evidence of subtle brain abnormalities in patients with schizophrenia. It less clear, however, whether these reflect a widespread cortical involvement, or more selective involvement among interconnected neural systems, or more focal pathology. The extent of brain changes, their etiopathologic significance, and putative clinical correlates are reviewed in this article.

Brain↗
PubMed1988

Structural brain changes in patients with anorexia nervosa.

Twenty-five patients with anorexia nervosa were compared with 17 normal healthy control subjects in terms of their cerebral computed tomographic (CT) scan appearances. The patients displayed significantly greater ventricular and sulcal enlargement when compared to control subjects. There were no relationships between the CT scan appearance and clinical indices of illness severity or weight loss in the patient group. In 14 patients who had repeat scans after attaining normal body weight, no significant change was observed in the ventricular appearance, but there was a significant lessening in the degree of sulcal widening.

Adult↗
PubMed1996

Neuropsychological and structural brain changes in anorexia nervosa before and after refeeding.

The neuropsychological performance and Magnetic Resonance Imaging (MRI) brain appearance of a consecutive series of 46 in-patients with anorexia nervosa (AN) was compared with that of 41 normal-weight controls. The groups were matched for sex, age, estimated pre-morbid intelligence and education. AN patients who had gained at least 10% of their body weight were retested and rescanned. Controls were retested after a similar interval. The AN group performed significantly worse than the controls on tasks measuring attention, visuospatial ability and memory. On tasks assessing flexibility and learning, no group differences were evident although an examination of deficits in individuals revealed that more anorexics were impaired on both. Following treatment, the AN group improved relative to the control group only on those tasks assessing attention. Comparison of MRI measures showed a significant proportion of anorexics had enlarged lateral ventricles and dilated sulci on both cortical and cerebellar surfaces, but no dilatation was evident for the third and fourth ventricular measures. Improvements were found after treatment on some of the radiological measures but many differences remained. Relationships between morphological brain changes and cognitive impairments were weak. Lower weight, but not duration of illness, was associated with poorer performance on tasks assessing flexibility/inhibition and memory, and with greater MRI ventricular size.

Adult↗
PubMed1996

Symptomatic dystonias associated with structural brain lesions: report of 16 cases.

BACKGROUND: Symptomatic (secondary) dystonias associated isolated lesions in the brain provide insight into etiopathogenesis of the idiopathic form of dystonia and are a basis for establishing the possible correlation between the anatomy of a lesion and the type of dystonia according to muscles affected. METHODS: In 358 patients with differently distributed dystonias, a group of 16 patients (4.5%) was encountered in whom dystonia was associated with focal brain lesions. RESULTS: Of the 16 patients, 3 patients had generalized, 3 segmental and 4 hemidystonia, while the remaining 6 patients had focal dystonia. The most frequent etiologies were infarction in 7, and tumor in 4 patients. These lesions were usually found in the lenticular and caudate nucleus, thalamus, and in the case of blepharospasm in the upper brainstem. CONCLUSIONS: Our results support the suggestion that dystonia is caused by a dysfunction of the basal ganglia.

Adult↗
PubMed2000

Structural brain lesions do not influence the prognosis of juvenile myoclonic epilepsy.

OBJECTIVES: In juvenile myoclonic epilepsy (JME) neuroimaging procedures are usually unnecessary but are often performed following the first generalized tonic-clonic seizure before a specific diagnosis has been reached. Our aim was to evaluate the influence of abnormal findings on the clinical presentation and prognosis of JME. MATERIAL AND METHODS: We retrospectively analyzed all medical records of JME patients first referred in two epilepsy centers (Marseilles, Nice) between 1981 and 1998. RESULTS: Among 170 consecutive unselected newly diagnosed JME patients, neuroimaging was performed in 82 cases (MRI: 22, CT: 75, including MRI+CT: 15). In 4 subjects, specific neurological abnormalities had justified neuroimaging: severe head trauma after the onset of JME (2, both with lesions related to the trauma), multiple sclerosis with onset after JME (1, with normal MRI before the onset of multiple sclerosis and abnormal, specific findings later), severe mental retardation (1, with diffuse MRI changes but a typical electro-clinical presentation and evolution). In the other 78 cases, 9 had abnormal findings: common arachnoid cyst (3), mild diffuse cerebral atrophy and ventricular enlargement (1), mild ventricular enlargement only (3), septum lucidum cavum (1), mildly increased T2 signal in the left temporal lobe (1). Abnormal neuroimaging did not influence therapeutic decisions or prognosis. CONCLUSIONS: These data confirm that neuroimaging procedures should not be routinely performed in patients with typical JME, unless additional neurological problems, that are unrelated to the diagnosis of epilepsy, occur.

Adolescent↗
PubMed2001

Structural brain abnormalities in unselected in-patients with major depression.

OBJECTIVE: Several studies have indicated an increased frequency of cerebral atrophy and white matter lesions in patients with major depression, especially in older age groups. METHOD: Forty-four representative in-patients with major depression in which neurological disorders were clinically excluded, and 49 age- and gender-matched controls were MR scanned. RESULTS: Unexpectedly, two of the patients had severe brain pathology which could account for their psychiatric symptoms. Analysis of the remaining patients (mean age 42 years) did not reveal an increased frequency of cerebral atrophy. The number of white matter lesions increased with age to an odds ratio greater than 3 for patients aged 50, but this was not statistically significant. CONCLUSION: Brain atrophy and white matter lesions did not occur with significantly increased frequency in these relatively young unselected depressives, but the finding of severe brain pathology stresses the importance of brain imaging in late-onset psychiatric disorders.

Adult↗
PubMed2001

Brain structures and mechanisms involved in the generation of REM sleep.

This article reviews the central nervous mechanisms involved in the broad network that generates and maintains REM sleep. Experimental investigations have identified the pontine tegmentum as the critical substrate for REM sleep mechanisms. Several pontine structures are involved in the generation of each particular polygraphic event that characterizes REM sleep: desynchronization in the electroencephalogram, theta rhythm in the hippocampus, muscle atonia, pontogeniculooccipital waves and rapid eye movements. The pontine tegmentum also holds the region where cholinergic stimulation can trigger all the behavioural and bioelectric signs of REM sleep. The exact location has been investigated and amply discussed over the last few years. Studies in the authors>> laboratory, mapping the pontine tegmentum with small volume carbachol (a cholinergic agonist) microinjections, have demonstrated that the executive neurons for REM sleep generation are neither located in the dorsal part of the pontine tegmentum, nor diffusely spread through the medial pontine reticular formation: they are concentrated in a discrete area in the ventral part of the oral pontine reticular nucleus (vRPO). In turn, the vRPO has connections with structures involved in the generation of the other states of the sleep-wake cycle as well as with structures responsible for the generation of each of the different events characterizing REM sleep. This allows us to propose the vRPO as the crucial region for REM sleep generation. Related research, with invivo and invitro experiments, into the actions of different neurotransmitters on vRPO neurones indicates that not only acetylcholine but other neurotransmitters have an active key role in vRPO REM sleep generation mechanisms.

Journal Article↗
PubMed2001

Brain structures and mechanisms involved in the generation of NREM sleep: focus on the preoptic hypothalamus.

Four lines of research have greatly increased our understanding of the hypothalamic preoptic area (POA) sleep-promoting system. First, sleep-active neurons within the POA have been identified using both electrophysiological recording and immediate early gene protein (c-Fos) staining methods. Segregated sleep-active neurons were found in ventrolateral and median POA (VLPO and MnPN). Additional sleep-active neurons may be intermixed with non-sleep specific neurons in other POA regions and the adjacent basal forebrain. Second, the putative sleep factors, adenosine and prostaglandin D2, were found to excite sleep-active neurons. Other sleep factors may also modulate these sleep-active populations. Third, many sleep-active neurons are warm-sensitive neurons (WSNs). WSNs are identified by excitatory responses to small increases in local POA temperature. The same local POA thermal stimuli strongly modulate sleep propensity and EEG delta activity within sleep. Interactions between sleep regulation and thermoregulation are consistent with studies of circadian sleep propensity, prolonged sleep deprivation in rats, and species differences in sleep amounts. Fourth, sleep-active neurons were found to co-localize the inhibitory neurotransmitter, gamma-aminobutyric acid and to have projections to arousal-related neuronal subgroups in the posterior hypothalamus and midbrain. Sleep-active and arousal-related neurons exhibit reciprocal changes in discharge across the wake-NREM-REM cycle, and activation of WSNs suppresses the neuronal activity of some arousal-related neuronal groups. These studies establish mechanisms by which POA hypnogenic neurons can inhibit EEG and behavioral arousal. In addition, there is evidence that arousal-related neurotransmitters inhibit VLPO sleep-active neurons. Mutually inhibitory interactions between sleep-promoting and the arousal system provide a substrate for a <<< >>>. 2001 Harcourt Publishers Ltd

Journal Article↗
PubMed1991

Molecular cloning and analysis of small optic lobes, a structural brain gene of Drosophila melanogaster.

Mutations in the small optic lobes (sol) gene of Drosophila melanogaster cause specific cells to degenerate in the developing optic lobes, resulting in the absence of certain classes of columnar neurons. These neuronal defects lead to specific alterations in behavioral characteristics, particularly during flight and walking maneuvers. We have isolated the wild-type sol locus by microcloning and chromosomal walking and have established its genetic and molecular limits. Two major transcripts of 5.8 and 5.2 kilobases are produced from this locus by alternative splicing and are present throughout the entire life cycle. Sequence analyses of cDNAs corresponding to these two classes of transcripts predict two proteins of 1597 and 395 amino acids. The first shows similarity in its carboxyl-terminal region to the catalytic domain of a vertebrate calcium-activated neutral protease (calpain), whereas its amino-terminal region contains several zinc-finger-like repeats of the form WXCX2CX10-11CX2C. The second predicted protein contains only the first two of the zinc-finger-like repeats and is missing the calpain domain. By constructing transgenic flies carrying a single wild-type copy of the sol gene in a homozygous sol mutant background, we have restored the normal neuroanatomical phenotype to individuals that would have developed mutant brains.

Amino Acid Sequence↗
PubMed1986

Structural brain correlates of emotional disorder in multiple sclerosis.

Eighty-seven patients with definite multiple sclerosis (MS) were examined neurologically and administered the Mini-mental State examination (MMS) to assess cognitive disability at the beginning and end of a one-year study. A CT scan was performed in 37. A group of 16 patients with stable spinal cord injuries (SCI) were studied in a similar manner. Of the MS patients, 47% had a mean General Health Questionnaire (GHQ) score in the abnormal range. This was a higher rate than in SCI patients (P = 0.004). Mean depression scores were similar in MS and SCI patients, but MS patients with brain involvement were more depressed than those with cord lesions only (P = 0.05). Depression score was unrelated to functional disability but was correlated with the degree of neurological impairment (P = 0.03). Euphoric patients were more likely to have brain involvement (P = 0.006), to have progressive MS (P less than 0.0001), and to have enlarged ventricles (P = 0.04) and were more impaired cognitively (P = 0.04) than noneuphoric patients. These results suggest that depression in MS patients is partly determined by the presence of brain involvement, but that it is also an emotional reaction to the disorder. Euphoria and cognitive disorder are reflections of brain involvement.

Adult↗