Diagnosis and prevention of atherosclerotic cerebral infarction

Atherosclerotic disease accounts for approximately 25% of ischemic strokes. Atherosclerotic stroke is caused mainly by embolic events from the carotid artery bifurcation or the aortic arch, although intracranial thrombosis can occur, more often in African Americans, Asians, and diabetes patients. Primary prevention of stroke is critical for patients with risk factors for atherosclerosis, including hypertension, diabetes, smoking and hypercholesterolemia. Stroke can be prevented in patients with established atherosclerotic disease by identification and management of patients with carotid artery stenosis by non-invasive testing. Particular attention must be paid to patients with transient symptoms of brain ischemia.     

Advances in prevention and treatment of cerebral palsy

In recent years there have been a number of advances in understanding of predisposing and protective factors in the development of cerebral palsy in infants. Multiple gestation births, maternal infection, and maternal and fetal thrombophilic conditions all predispose to the development of CP in the infant. Opportunities for prevention of CP may develop from an improved understanding of these factors and their mechanisms of operation. Similar progress has been made in the evaluation of treatments for CP and the effects of these treatments on the individual's impairment, function, and disability. Selective posterior rhizotomy and Botulinum toxin A are now widely used in the treatment of spasticity. The challenge remains to determine how effectively these promising interventions can alter long-term function and quality of life outcomes in children and adults with CP.     

Generalized anxiety disorder: acute and chronic treatment

Clinical and epidemiological data suggest that generalized anxiety disorder (GAD) is a chronic illness causing patients to suffer for many years leading to significant distress in daily life functioning. The literature suggests the several conclusions. GAD is a disorder in need of appropriate treatment and often has a chronic course with comorbid conditions, such as major depression and other anxiety disorders. Benzodiazepines, while effective anxiolytic agents acutely, when prescribed for >4 weeks cause rebound anxiety and following prolonged therapy may lead to withdrawal symptoms. Antidepressants cause significant anxiety relief compared with placebo and for psychosocial treatment cognitive-behavioral therapy is an efficacious psychosocial treatment. Many GAD patients are in need of long-term medication management. Furthermore, there is limited data for patients diagnosed with GAD the treatment outcome with the combination of medication and psychotherapy both acutely and long-term; how to best sequence these treatments; for those patients who do not meet remission criteria what is the ideal approach for augmentation; and for patients with treatment-refractory GAD the empirical evidence is lacking on medication switching and augmentation strategies. Research is needed in the area of developing treatment strategies for patients suffering from treatment-refractory GAD. There is still an urgent need to explore treatment combinations and duration strategies in the management of patients suffering with GAD.     

Modifying acute pain by matching cognitive style with cognitive treatment

To test whether congruence between cognitive style and cognitive coping would facilitate the attenuation of pressure pain, 30 verbalizers and 30 visualizers were assigned in equal numbers (ns = 10) to pleasant imagery, rational thoughts, and expectancy conditions. Separate 2 X 3 (cognitive style X experimental condition) analyses of covariance on pain tolerance and subjective discomfort indicated that imagery was superior to expectancy in raising tolerance. These findings are discussed in terms of the flexibility of cognitive coping and the content of the images and thoughts which were used.     

Assessment and treatment of adult acute responses to traumatic stress following mass traumatic events

Assessment and treatment of acute responses to traumatic stress has received much attention since September 11, 2001. This article elucidates principles of early intervention with adults in the immediate (within 48 hours) and early recovery phase (within the first week). The principles have been drawn from research on risk and recover factors, stress and traumatic stress theory, and expert consensus recommendations. The debriefing model is discussed, and principle interventions of psychological first aid, pharmacology, and mass trauma systems are described. This article concludes with brief guidelines for longer-term interventions and recommendations for future research.     

Patterns of cerebral organization

An analysis of the concurrent incidence of aphasia and spatial disorder in 270 patients with unilateral brain damage suggests that the two functions are statistically independent. These data can also be used to estimate the distribution of left, right, and bilateral representation of linguistic and spatial functions in the population. In right-handers, sex affects the pattern of cerebral asymmetries, while the familial history of sinistrality has a stronger effect on the pattern of cerebral asymmetries in left-handers. These findings suggest that complementary specialization exists only as a statistical norm: It is suggested that differences in complementary and noncomplementary specialization may underlie individual differences in cognitive skills.     

The effects of acute 17beta-estradiol treatment on gene expression in the young female mouse hippocampus

Previous studies have demonstrated that treatment with 17beta-estradiol (E(2)) improves both spatial and nonspatial memory in young female mice. Still unclear, however, are the molecular mechanisms underlying the beneficial effects of E(2) on memory. We have previously demonstrated that a single post-training intraperitoneal (i.p.) injection of 0.2 mg/kg E(2) can enhance hippocampal-dependent spatial and object memory consolidation (e.g., Gresack & Frick, 2006b). Therefore, in the present study, we performed a microarray analysis on the dorsal hippocampi of 4-month-old female mice injected i.p. with vehicle or 0.2 mg/kg E(2). Genes were considered differentially expressed following E(2) treatment if they showed a greater than 2-fold change in RNA expression levels compared to controls. Overall, out of a total of approximately 25,000 genes represented on the array, 204 genes showed altered mRNA expression levels upon E(2) treatment, with 111 up-regulated and 93 down-regulated. Of these, 17 of the up-regulated and 6 of the down-regulated genes are known to be involved in learning and memory. mRNA expression changes in 5 of the genes were confirmed by real-time quantitative PCR analysis, and protein changes in these same genes were confirmed by Western blot analysis: Hsp70, a heat shock protein known to be estrogen responsive; Igfbp2, an IGF-I binding protein; Actn4, an actin binding protein involved in protein trafficking; Tubb2a, the major component of microtubules; and Snap25, a synaptosome-specific protein required for neurotransmitter release. The types of genes altered indicate that E(2) may induce changes in the structural mechanics of cells within the dorsal hippocampus that could be conducive to promoting memory consolidation.     

The neuropsychology of paramedian thalamic infarction

A longitudinal study of three patients with CT-scan documented paramedian thalamic infarctions (bilateral, primarily right, unilateral left) is reported and the neuropsychology of human paramedian thalamic infarction is reviewed. The neuropsychological deficits following these selected lesions, the nature of the clinical memory disorder, and the neuroanatomy of memory are discussed. The significance of cortical/subcortical relationship in explaining observed behavioral changes is emphasized. Brain damage with maximum involvement in the dorsomedial nuclei and mamillothalamic tracts appears to cause primarily a memory disorder and frontal-limbic behavioral changes, the severity and profile of deficits depending on lesion extent and location. Both anterograde and remote memory loss may be present. Asymmetry in memory at the level of the thalamus was observed, following the left-verbal, right-nonverbal dichotomy.