Brain structure deficits

Nenadic, I., H. Sauer, and C. Gaser, Distinct pattern of brain structural deficits in subsyndromes of schizophrenia delineated by psychopathology. Neuroimage, 2009. 

FIG. 5. The number of errors on an inclined plane response flexibility problem (Thompson et al 1990) is shown for the same groups of animals as seen in Fig. 4. Saline-treated controls made the fewest errors. Animals exposed to the neurotoxin MAM were slower to abandon a previously learned solution to try new routes to food. However, animals treated postnatally with naltrexone, an opiate receptor antagonist reported to induce dendritic arborization and spine formation, showed performance similar to controls. Decreases in neuron number, such as seen with MAM exposure prenatally, have adverse effects on tests of rat intelligence. Treatments that induce dendritic arborization and synapse formation can ameliorate these deficits. The ability to modify brain structure permits direct testing of the causal role of variation in brain structure and behavioural performance. 

The experiments reported here deal with three different topics (1) the search for brain structures primarily involved in lead-induced neurobehavioural dysfunction, (2) the influence of the time span between indirect maternal exposure and age at behavioural testing in the rat, and (3) the role of lead in central and peripheral visual processes in monkeys. The results indicate that there are differences in the effects of lead exposure and hippocampal lesions, that permanent post-weaning lead exposure does not add to the neurobehavioural deficit due to indirect maternal exposure, and that in monkeys parameters of the visual evoked potentials and electroretinograms are altered by lead. 

Association of Pain, neuropathic pain is defined as pain initiated or caused by a primary lesion, dysfunction in the nervous system". Neuropathy can be divided broadly into peripheral and central neuropathic pain, depending on whether the primary lesion or dysfunction is situated in the peripheral or central nervous system. In the periphery, neuropathic pain can result from disease or inflammatory states that affect peripheral nerves (e.g. diabetes mellitus, herpes zoster, HIV) or alternatively due to neuroma formation (amputation, nerve transection), nerve compression (e.g. tumours, entrapment) or other injuries (e.g. nerve crush, trauma). Central pain syndromes, on the other hand, result from alterations in different regions of the brain or the spinal cord. Examples include tumour or trauma affecting particular CNS structures (e.g. brainstem and thalamus) or spinal cord injury. Both the symptoms and origins of neuropathic pain are extremely diverse. Due to this variability, neuropathic pain syndromes are often difficult to treat. Some of the clinical symptoms associated with this condition include spontaneous pain, tactile allodynia (touch-evoked pain), hyperalgesia (enhanced responses to a painful stimulus) and sensory deficits. 

Nasrallah HA, Varney N, Coffman JA, et al Opiate antagonism fails to reverse post-ECT cognitive deficits. J Clin Psychiatry 47 555-556, 1986 Nasrallah HA, Coffman JA, Olson SC Structural brain-imaging findings in affective disorders an overview. J Neuropsychiatry Clin Neurosci 1 21-26, 1989 Naylor GJ, Smith AHW Defective genetic control of sodium-pump density in manic depressive psychosis. Psychol Med 11 257-263, 1981 Naylor GJ, McNamee HB, Moody JP Erythrocyte sodium and potassium in depressive illness. J Psychosom Res 14 173-177, 1970 Naylor GJ, McNamee HB, Moody JP Changes in erythrocyte sodium and potassium on recovery from depressive illness. Br J Psychiatry 118 219-223, 1971 Naylor GJ, Dick DAT, Dick EG, et al Lithium therapy and erythrocyte membrane cation carrier. Psychopharmacologia 37 81-86, 1974 Naylor GJ, Smith AHW, Dick EG, et al Erythrocyte membrane cation carrier in manic-depressive psychosis. Psychol Med 10 521-525, 1980... 

L. J. Seidman, E. M. Valera and N. Makris, Structural brain imaging of attention-deficit/ hyperactivity disorder. Biol Psychiatry, 2005, 57,1263-1272. 

Brain lesions that produce depression can be divided into structural and biochemical types. Any disease that produces a mass lesion or deficit in the frontal lobes can cause a depressive syndrome. Typically, occurrence and severity are correlated with proximity to the tip of the frontal lobe rather than to the extent of motor function loss. The most extensively studied lesions are strokes, but tumors and plaques related to multiple sclerosis can both produce similar results. 

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