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PubMed1993

Minor structural brain changes in young drug abusers. A magnetic resonance study.

Twenty-three drug abusers and seventeen controls underwent clinical neurological examinations and magnetic resonance imaging (MRI) of the brain. The drug abuse encompassed cannabis, inhalants, opiates, psychedelics, amphetamines, and cocaine but not necessarily all drugs in all persons. The drug abuse was always combined with heavy alcohol consumption. One drug abuser had abnormal neurological findings which consisted of lower limb ataxia and 3 others had mild imbalance. MRI examinations did not show differences in width of the third, fourth or lateral ventricles nor the diameter of the cerebral aqueduct but the drug abusers had significantly smaller vermes cerebelli compared to controls. White matter changes also occurred more often in the drug abuser group. These findings are not consistent with known side-effects of the narcotic drugs but more probably a result of very high alcohol consumptions in parallel with drug abuse. Alcohol is clearly a much more potent brain toxic agent than are the most commonly abused narcotic drugs.

Adult↗
PubMed1997

Structural brain changes in PTSD. Does trauma alter neuroanatomy?

Although the impetus for studying hippocampal morphology and functioning in PTSD was the finding that stress could result in hippocampal damage in rodent and primate models, it is far from proven that the findings to date in PTSD represent defects that have been caused by trauma. It is equally possible that the findings represent a preexisting anomaly which might serve as a risk factor for the development of PTSD following trauma exposure. To resolve this dilemma, it is necessary to study persons at high risk for trauma (e.g., soldiers) prior to trauma exposure and ag in after exposure. Such methods will permit the determination not only of whether trauma alters hippocampal morphology, but also, if so, of whether this effect is limited to persons with PTSD. At the present time, the field would be well advised to proceed vigorously but with appropriate caution along these lines of research. As just outlined, sample sizes have been small, and potentially confounding variables have abounded in most studies. The next few years of research may well continue to replicate the finding of abnormal hippocampal morphology in PTSD. However, it would not be surprising to find that other brain regions are also involved and that these represent part of a broader risk spectrum for the development of psychopathology under stress. Until these issues are clarified, the neuroanatomical findings to date in PTSD should be viewed as tentative, tantalizing, and in need of additional study.

Brain↗
PubMed1993

Studies of brain structures involved in diffuse noxious inhibitory controls in the rat: the rostral ventromedial medulla.

1. Previous electrophysiological, pharmacological and anatomical evidence had suggested a possible participation of rostral ventromedial medulla (RVM) in the supraspinal part of the loop underlying diffuse noxious inhibitory controls (DNICs). In order to test this hypothesis, two experimental series were performed during which DNICs were compared in control sham-operated rats and rats with lesions of the RVM and of an adjacent candidate for such a role, the nucleus gigantocellularis reticularis (Gi). 2. In the first experimental series, lesions were induced, in anaesthetized animals, by injections of quinolinic acid (0.3-0.8 microliter of a 360 nmol/microliter solution) into the RVM or Gi. In the control animals (n = 10), the vehicle alone (artificial cerebrospinal fluid) was injected. Histological lesion reconstructions were performed after each electrophysiological experiment. Three groups of animals were considered: in the first group (n = 5), the lesion was centered on the RVM, including the two caudal thirds of nucleus raphe magnus (NRM) and adjacent reticular areas; in the second group (n = 5), the lesions extended more rostrally and involved the rostral pole of NRM; in the third group (n = 5), the lesion extended more laterally and dorsally and included nucleus reticularis gigantocellularis pars alpha (GiA), nucleus reticularis paragigantocellularis lateralis (LPGi) and the Gi. In each case, all the neuronal cell bodies within the lesioned area were destroyed. 3. In the second experimental series, electrolytic lesions of the total rostrocaudal extent of the NRM (n = 5) were induced, in anesthetized animals, by passing cathodal current (5 mA, 8 s). In the control animals (n = 5), the electrode was lowered but current was not applied. 4. One week after lesioning, the animals were anaesthetized, paralysed, artificially ventilated and recordings were made from convergent neurones in trigeminal nucleus caudalis. These neurones gave responses due to activation of A and C fibres when percutaneous electrical stimuli were applied to their receptive fields. DNICs were triggered by immersion of each paw in a 50 degrees C water-bath. Both the general properties of the convergent neurones and the inhibitions of the C fibre-evoked responses produced by these heterotopic noxious stimuli were compared in the different groups of animals. 5. The sizes of receptive field, spontaneous activities, thresholds for C fibre-evoked responses and responses to C fibre activation were not different in the control and lesioned animals. The percentage inhibitions of the C fibre-evoked responses both during and in the 44s following the conditioning periods were also very similar in the different groups of animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Studies of the brain structures involved in diffuse noxious inhibitory controls: the mesencephalon.

1. Diffuse noxious inhibitory controls (DNIC) were compared in control sham-operated rats and in rats with lesions of mesencephalic structures involved in the modulation of pain, namely the periaqueductal gray (PAG), cuneiformis nucleus (CNF), and parabrachial nucleus (PB). 2. Lesions were induced by ibotenic acid: 4 micrograms (0.2 microliter) injected bilaterally in the PAG or the CNF-PB area or 10 micrograms (0.5 microliter) injected unilaterally in the CNF or PB. Control animals were microinjected with the vehicle (artificial CSF) alone. Histological controls were performed at the end of each electrophysiological experiment. Only the animals in which the target structure (PAG, CNF, or PB) was completely destroyed in its entire rostrocaudal length were selected. With the exception of the cell bodies of the trigeminal mesencephalic nucleus, all neurons were destroyed in these regions. 3. At least 1 wk after the microinjection procedure, recordings were made from convergent neurons in both the right and left trigeminal nucleus caudalis. These neurons were activated by both noxious and nonnoxious stimuli applied to their excitatory receptive fields and gave responses due to activation of both A- and C-fibers after percutaneous electrical stimulation of their receptive fields. These types of response were inhibited by applying noxious conditioning stimuli to heterotopic areas of the body, namely immersing a paw in a 50 degrees C water bath. A virtually total block of the responses was observed during the application of the noxious conditioning stimulus, and this was followed by long-lasting poststimulus effects. 4. The general properties of neurons (sizes of receptive fields, spontaneous activity, thresholds to obtain C-fiber-evoked responses, responses to C-fiber activation) were all found to be similar in the control and the lesioned animals. The percentage inhibition of the C-fiber-evoked responses of the trigeminal convergent neurons elicited by the noxious conditioning stimuli were found to not be significantly different in any group of animals; in all the animals, inhibitions exceeded 85% during the immersion of either paw and were followed by long-lasting poststimulus effects. 5. We conclude that the PAG, CNF, and PB, three structures that are putatively involved in the modulation of pain, do not participate directly in the supraspinal part of the loop subserving DNIC. The involvement of other structure(s) and a possible indirect modulation of DNIC are discussed. It is also concluded that the PAG, CNF, and PB do not participate directly in the tonic descending inhibitory controls, which are presumed to modulate the activity of convergent neurons.

Anesthesia↗
PubMed1992

Structural brain correlates of neurologic abnormalities in multiple sclerosis.

We examined the relationship between cerebral magnetic resonance imaging (MRI) findings and urinary dysfunction in 70 consecutive patients with definite multiple sclerosis. MRI-weighted lesion scores for seven different brain regions were recorded according to the number and size of cerebral lesions. Thirty-two subjects (46%) had urinary symptoms and 38 (54%) were asymptomatic. Subjects with urinary symptoms exhibited greater overall functional disability and a higher midbrain MRI-weighted lesion score than asymptomatic patients. No statistically significant group differences were found for the other brain regions.

Adolescent↗
PubMed1993

Structural brain abnormalities in catatonia.

In this study, the ventricle to brain ratios of catatonic subjects were compared and evaluated with respect to the underlying diagnoses. Catatonic individuals with the diagnosis of schizophrenia were more likely to have greater ventricle to brain ratios than other catatonic subjects. The association of large ventricles with chronic, deteriorating psychosis is maintained and the heterogeneity of the syndrome of catatonia is apparent. It is possible that the presence of large ventricles may be useful to predict the chronicity of disability for some cases of catatonia.

Adult↗
PubMed2001

Structural brain abnormalities associated with deletion at chromosome 22q11: quantitative neuroimaging study of adults with velo-cardio-facial syndrome.

BACKGROUND: Velo-cardio-facial syndrome (VCFS) is associated with deletions in the qll band of chromosome 22, learning disability and psychosis, but the neurobiological basis is poorly understood. AIMS: To investigate brain anatomy in adults with VCFS. METHOD: Magnetic resonance imaging was used to study 10 patients with VCFS and 13 matched controls. We carried out three analyses: qualitative; traced regional brain volume; and measurement of grey and white matter volume. RESULTS: The subjects with VCFS had: a high prevalence of white matter hyperintensities and abnormalities of the septum pellucidum; a significantly smaller volume of cerebellum; and widespread differences in white matter bilaterally and regional specific differences in grey matter in the left cerebellum, insula, and frontal and right temporal lobes. CONCLUSIONS: Deletion at chromosome 22q11 is associated with brain abnormalities that are most likely neurodevelopmental and may partially explain the high prevalence of learning disability and psychiatric disorder in VCFS.

Adult↗
PubMed2003

Endogenous melanocortin antagonist in fish: structure, brain mapping, and regulation by fasting of the goldfish agouti-related protein gene.

Agouti-related protein (AGRP) is a naturally occurring antagonist of melanocortin. In mammals, central AGRP expression is restricted to the arcuate nucleus in which it plays a key role in the control of energy balance by antagonizing melanocortin effects at melanocortin 4 receptors. In goldfish, melanocortin 4 receptor is profusely expressed within the main brain areas for the control of energy balance, and central administration of agonist or antagonist analogs inhibits or stimulates food intake, respectively. Here we demonstrate that the goldfish genome has a homologous gene to mammalian AGRP. Detailed brain mapping by in situ hybridization shows that AGRP is exclusively expressed in the ventrobasal hypothalamic lateral tuberal nucleus, the teleostean homolog of the arcuate nucleus. Fasting up-regulates its mRNA levels in the lateral tuberal nucleus. In the periphery, AGRP is expressed in several tissues including ovary, muscle, and ventral skin, suggesting that AGRP might regulate peripheral actions of melanocortin peptides. The results provide the first evidence for an endogenous melanocortin antagonist in nontetrapod species and suggest that hypothalamic overexpression during fasting might regulate the inhibitory effects of melanocortin peptides on food intake in goldfish.

Agouti-Related Protein↗
PubMed1992

Neuropsychological and structural brain lesions in multiple sclerosis: a regional analysis.

Quantified lesion scores derived from MRI correlate significantly with neuropsychological testing in patients with multiple sclerosis (MS). Variables used to reflect disease severity include total lesion area (TLA), ventricular-brain ratio, and size of the corpus callosum. We used these general measures of cerebral lesion involvement as well as specific ratings of lesion involvement by frontal, temporal, and parieto-occipital regions to quantify the topographic distribution of lesions and consequent effects upon cognitive function. Lesions were heavily distributed in the parieto-occipital regions bilaterally. Neuropsychological tests were highly related to all generalized measures of cerebral involvement, with TLA being the best predictor of neuropsychological deficit. Mean TLA for the cognitively impaired group was 28.30 cm2 versus 7.41 cm2 for the cognitively intact group (p less than 0.0001). Multiple regression analyses revealed that left frontal lobe involvement best predicted impaired abstract problem solving, memory, and word fluency. Left parieto-occipital lesion involvement best predicted deficits in verbal learning and complex visual-integrative skills. Analysis of regional cerebral lesion load may assist in understanding the particular pattern and course of cognitive deficits in MS.

Adult↗
PubMed2006

Structural brain abnormalities in early-onset schizophrenia.

BACKGROUND: Few studies investigated brain abnormalities in early onset schizophrenia. OBJECTIVE: To assess computed tomography (CT) abnormalities in patients with childhood or adolescence onset schizophrenia. METHOD: CT scans of patients with childhood (6 to 11 years old) (N=6) or adolescence (12-17 years old) (N=9) schizophrenia were compared to normal controls. Patients were diagnosed based on the DSM-III-R criteria. Ventricular enlargement was measured by the Ventricle to Brain Ratio (VBR) and Cortical Atrophy (pre-frontal prominence) was measured by the Pre-Frontal Atrophy Index (PFAI). RESULTS: There was a significant difference in VBR, but not in PFAI, between subjects and controls [8.26+/-2.79, and 5.71+/-3.26 (p=0.029)], and [2.72+/-1.77, and 3.21+/-1.53 (p=0.424)], respectively. There were no differences of VBR and PFAI between children and adolescents with schizophrenia. CONCLUSION: Compared to controls, patients with child or adolescent onset schizophrenia exhibit more pronounced ventricular enlargement. There were no differences regarding prefrontal atrophy.

Adolescent↗
PubMed1986

The structural brain mutant Vacuolar medulla of Drosophila melanogaster with specific behavioral defects and cell degeneration in the adult.

The mutant Vam (Vacuolar medulla) has vacuoles in the distal medulla, caused by age-dependent cell degeneration in the lamina and the medulla. Lamina monopolar neurons L1 and L2 degenerate, but whether the degeneration is confined only to these cells is uncertain. The cell degeneration commences at eclosion and the vacuoles begin appearing about 1/2 h after eclosion. This is accompanied by the disappearance of the electroretinogram transients and a loss of the optomotor response. Vam males or homozygous Vam females one day after eclosion or later, show no measurable optomotor response to horizontal or vertical movement and no landing response. However, they are able to turn towards dark stripes larger than 20 degrees in width. This indicates that motion-dependent visual responses are not a prerequisite for landmark fixation in Drosophila. The mutant's apparent defects suggest that the loss of motion-dependent visual functions is due to the loss of certain cell types linking the lamina to the distal medulla. The role of lamina neurons in optomotor responses and fixation behavior is discussed.

Animals↗
PubMedDate not supplied

The relationship between structural brain imaging and histopathologic findings in schizophrenia research.

The suggestion that schizophrenia may involve a neurodegenerative process has emanated from the highly replicated finding of ventricular enlargement in brain images of patients with this disorder. These investigations have provided a direct impetus for recent histopathologic studies seeking evidence of a neurodegenerative process in the brains of subjects with schizophrenia. Whereas most postmortem studies have reported the presence of atrophy and/or neuronal loss in several corticolimbic regions of subjects with schizophrenia, no quantitative study, to date, has detected an increase in the number of glial cells. For this reason the changes observed in postmortem schizophrenic brain are not consistent with a typical adult pattern of neuronal degeneration, such as that seen in Huntington's disease. Because several studies have reported various changes in layer II of the anterior cingulate, prefrontal, and entorhinal cortices, the histopathologic findings described are compatible with the idea that schizophrenia involves a disturbance of the "inside-out" migration or differentiation of cortical neurons that normally occurs during ontogenesis. A neurodevelopmental perturbation early in life could result in discrete alterations of corticolimbic circuitry that eventually contribute to the appearance of schizophrenic symptoms during adolescence and adulthood.

Adult↗