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Cortical Atrophy (cortical + atrophy)
Selected AbstractsEstrogen replacement therapy is associated with less progression of subclinical structural brain disease in normal elderly women: a pilot studyINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 7 2002Ian A. Cook Abstract Background Cortical atrophy, central atrophy, deep white-matter hyperintensities, and periventricular hyperintensities are reported in normal aging. Objectives We examined the effects of estrogen replacement therapy (ERT) on these forms of ,subclinical structural brain disease' (SSBD) in normal, postmenopausal women in a pilot, naturalistic, longitudinal study of 15 subjects. Methods Two assessments were performed at least two years apart, with volumetric magnetic resonance imaging (MRI) and neuropsychological testing. Results Women receiving open-label ERT showed significantly less progression of SSBD than those who did not. Conclusions The association between reduced SSBD progression and ERT suggests this intervention could help preserve normal brain structure in healthy elderly women. Copyright © 2002 John Wiley & Sons, Ltd. [source] A novel ARX phenotype: rapid neurodegeneration with Ohtahara syndrome and a dyskinetic movement disorderDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 3 2010MICHAEL ABSOUD ARX mutations are associated with variable clinical phenotypes. We report a new neurodegenerative phenotype associated with a known ARX mutation and causing early abnormal neurodevelopment, a complex movement disorder, and early infantile epileptic encephalopathy with a suppression-burst pattern (Ohtahara syndrome). A male infant presented at age 5 months with a dyskinetic movement disorder, which was initially diagnosed as infantile spasms. Clinical deterioration was accompanied by progressive cortical atrophy with a reduction in white matter volume and resulting in death in the first year of life; such a rapidly progressive and severe phenotype has not previously been described. ARX mutation testing should be undertaken in children aged less than 1 year with Ohtahara syndrome and a movement disorder, and in infants with unexplained neurodegeneration, progressive white matter loss, and cortical atrophy. [source] Complex visual hallucination and mirror sign in posterior cortical atrophyACTA PSYCHIATRICA SCANDINAVICA, Issue 1 2006T. Yoshida Objective:, In posterior cortical atrophy (PCA), visual hallucinations are rare symptoms and mirror sign has not been described. Method:, Single case report. Results:, We reported a 60-year-old woman with PCA who reported complex visual hallucinations, such as a man walking in her room, and mirror sign, which was the perception of a stranger staring at her when she looked into a mirror. She could not recognize images of herself in the mirror correctly, although she could recognize that a person standing next to her and the images of that person reflected in the mirror were the same person. Conclusion:, Early complex visual hallucinations in this patient appeared to be more characteristic of dementia with Lewy body than Alzheimer's disease (AD). It is hard to explain mirror sign in this patient as being because of either prosopagnosia, Balint's syndrome or advanced AD. This patient may have other underlying cognitive dysfunction. [source] Atypical posterior cortical atrophy: a diagnostic and treatment dilemmaACTA PSYCHIATRICA SCANDINAVICA, Issue 1 2006Dr Peter Williamson No abstract is available for this article. [source] Comprehensive studies of cognitive impairment of the elderly with type 2 diabetesGERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 3 2006Takashi Sakurai Type 2 diabetes mellitus is associated with cognitive dysfunction and increases the risk of dementia for the elderly. The aim of the study presented here was to provide a brief review of how disturbance of glucose and metabolic homeostasis may be implicated in the cognitive decline of patients with type 2 diabetes. Several risk factors such as nutrition, cerebrovascular disorders and the neurotoxic effects of hyperglycemia may combine for the formation of mechanisms of cognitive decline in the diabetic elderly. It should be noted that cognitive deficits of diabetes are accompanied by neuroradiological changes in the brain, so that cognitive dysfunction both with and without brain structural changes may overlap during cognitive decline of the diabetic elderly. Recently, we conducted two studies to explore, by means of brain imaging, hierarchical relationships among clinical profiles of diabetes, cognitive function, white matter hyperintensity and brain atrophy. The results suggested that subcortical brain atrophy and hyperintensity constitute predictors of the rate of progression of cognitive dysfunction in the diabetic elderly, while cortical atrophy is associated with high diastolic blood pressure and lower HbA1c. These hypotheses may explain in part the underlying mechanisms of cognitive impairment in the diabetic elderly. Prospective intervention studies are needed, however, to clarify the mechanism of cognitive dysfunction of the diabetic elderly and what the targets are for preventive measures. [source] A child with spider bite and glomerulonephritis: a diagnostic challengeINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 4 2000Jennifer M. Lung MD A previously healthy 7-year-old white boy presented to St. Louis Children's Hospital with a 1-day history of headache, malaise, temperature of 38.7 °C, and a progressively erythematous, tender calf with central dusky purpura. On the morning of admission, his mother noticed a 2-mm crust on the patient's right calf with a 3-cm × 3-cm area of surrounding erythema. No history of recent trauma or bite was obtained. He had suffered two episodes of nonbloody, nonbilious emesis during the last day. In addition, over the previous 12 h, he presented brown urine without dysuria. His mother and brother had suffered from gastroenteritis over the previous week without bloody diarrhea. On initial physical examination, there was a 6-cm × 11-cm macular tender purpuric plaque with a central punctum on the right inner calf, which was warm and tender to the touch, with erythematous streaking towards the popliteal fossa ( Fig. 1). The inguinal area was also erythematous with tender lymphadenopathy and induration, but without fluctuance. Laboratory studies included an elevated white blood cell count of 20,800/,L with 6% bands, 86% segs, and 7% lymphocytes, hemoglobin of 12.5 g/dL, hematocrit of 35.1%, and platelets of 282,000/,L. The prothrombin time/activated partial tissue thromboplastin was 10.4/28.0 s (normal PT, 9.3,12.3 s; normal PTT, 21.3,33.7 s) and fibrinogen was 558 mg/dL (normal, 192,379 mg/dL). Urinalysis showed 1+ protein, 8,10 white blood cells, too numerous to count red blood cells, and no hemoglobinuria. His electrolytes, blood urea nitrogen (BUN), and creatine were normal. The urine culture was negative. Blood culture after 24 h showed one out of two bottles of coagulase negative Staphylococcus epidermidis. Figure 1. (A) 7-year-old boy with painful purpura of the calf The patient's physical examination was highly suggestive of a brown recluse spider bite with surrounding purpura. Over the next 2 days, the surrounding rim of erythema expanded. The skin within the plaque cleared and peeled at the periphery. The coagulase negative staphylococci in the blood culture were considered to be a contaminant. Cefotaxime and oxacillin were given intravenously. His leg was elevated and cooled with ice packs. The patient's fever resolved within 24 h. The lesion became less erythematous and nontender with decreased warmth and lymphadenopathy. The child was discharged on Duricef for 10 days. Because the patient experienced hematuria rather than hemoglobinuria, nephritis was suggested. In this case, poststreptococcal glomerulonephritis was the most likely cause. His anti-streptolysin-O titer was elevated at 400 U (normal, <200 U) and C3 was 21.4 mg/dL (normal, 83,177 mg/dL). His urine lightened to yellow,brown in color. His blood pressure was normal. Renal ultrasound showed severe left hydronephrosis with cortical atrophy, probably secondary to chronic/congenital ureteropelvic junction obstruction. His right kidney was normal. [source] Temporal Discrimination Learning in Abstinent Chronic AlcoholicsALCOHOLISM, Issue 6 2002Regina McGlinchey-Berroth Background: Converging evidence from varied experimental paradigms has demonstrated that the cerebellum is involved in the timing of learned behavior. Given the documented neurological changes secondary to chronic alcoholism, particularly cerebellar degeneration, the ability of recovered chronic alcoholics to learn a temporal discrimination was assessed by using delayed eyeblink classical conditioning. Methods: Twelve abstinent alcoholic participants and 12 matched control participants were randomly presented 2 clearly discriminable tone conditioned stimuli that were individually paired with 2 different interstimulus intervals. Results: The data revealed a significant alteration in the abstinent alcoholics' peak latency measure at the long interstimulus intervals and an overall impairment in their level of acquisition of conditioned responses. No group differences in extinction were observed. Conclusions: It was speculated that cerebellar cortical atrophy caused by years of alcohol abuse resulted in the peak latency alteration and that atrophy extending into deep cerebellar nuclei caused the overall impairment in conditioned response acquisition. [source] Language Processing in Frontotemporal Dementia: A Brief ReviewLINGUISTICS & LANGUAGE COMPASS (ELECTRONIC), Issue 1 2008Jonathan E. Peelle Frontotemporal dementia (FTD) is a neurodegenerative condition that presents with a number of distinct behavioral phenotypes. Here we review language-processing deficits in three subgroups of FTD patients: progressive nonfluent aphasia (PNFA), semantic dementia (SD), and nonaphasic FTD patients with a disorder of social and executive functioning (SOC/EXEC). These three clinical subgroups have contrasting patterns of regional cortical atrophy that can be linked to their language impairments. PNFA patients' disease includes left ventral inferior frontal cortex, resulting in impaired grammatical processing. SD patients demonstrate a profound impairment for semantic knowledge related to atrophy of the left temporal lobe. SOC/EXEC patients' frontal atrophy tends to be more right lateralized and is associated with declines in executive functioning. SOC/EXEC patients' limited executive resources impact language processing in a variety of ways, including slowed grammatical processing and impaired narrative discourse. FTD patients therefore provide converging evidence regarding dissociable components of language processing and their neuroanatomical bases. [source] MRI and cognitive impairment in Parkinson's disease,MOVEMENT DISORDERS, Issue S2 2009Naroa Ibarretxe-Bilbao PhD Abstract Patients with Parkinson's disease (PD) may present impairment in cognitive functions even at early stages of the disease. When compared with the general population, their risk of dementia is five to six times higher. Recent investigations using structural MRI have shown that dementia in PD is related to cortical structural changes and that specific cognitive dysfunctions can be attributed to atrophy in specific structures. We review the structural MRI studies carried out in PD using either a manual region of interest (ROI) approach or voxel-based morphometry (VBM). ROI studies have shown that hippocampal volume is decreased in patients with PD with and without dementia; in addition, hippocampal atrophy correlated with deficits in verbal memory. VBM studies have demonstrated that dementia in PD involves structural changes in limbic areas and widespread cortical atrophy. Findings in nondemented patients with PD are less conclusive, possibly because cognitively heterogeneous groups of patients have been studied. Patients with PD with cognitive impairment and/or visual hallucinations present greater brain atrophy than patients without these characteristics. These findings suggest that cortical atrophy is related to cognitive dysfunction in PD and precedes the development of dementia. Structural MRI might therefore provide an early marker for dementia in PD. © 2009 Movement Disorder Society [source] Corticobasal degeneration as cause of progressive non-fluent aphasia: Clinical, radiological and pathological study of an autopsy caseNEUROPATHOLOGY, Issue 6 2006Masaki Takao A Japanese male developed gradual loss of spontaneous speech at age 60. Three years later meaningful speech had deteriorated to the point that it had become restricted to monotonous utterances. Neuropsychological examination at age 62 showed that he had severe non-fluent aphasia. A brain MRI demonstrated mild cortical atrophy with ischemic lesions in the cerebral white matter. He was diagnosed as having primary progressive aphasia. At age 63, he was admitted to the hospital to reevaluate the neurological condition. Neurologic examination showed severe non-fluent aphasia, hyperreflexia, snout and sucking reflexes. No alien hand was observed. He was able to walk, dress, wash himself and use chopsticks as well as name real objects. At age 65, 99mTc-hexamethylpropyleneamine oxime single photon emission computed tomography (HMPAO-SPECT) revealed diffuse cerebral hypoperfusion that was particularly prominent in the left frontal lobe. An MRI showed progressive cortical atrophy with the definite atrophy of the left paracentral gyrus. The hippocampal formation and putamen were also atrophic. He died of pneumonia at age 67. The brain weighed 810 g with atrophy of the frontal lobe, globus pallidus, enlargement of the lateral ventricles and depigmentation of the substantia nigra. Microscopic examination showed severe neuronal loss and gliosis in the cerebral cortex, globus pallidus interna and substantia nigra. Ballooned neurons were observed in the cerebral cortex. Gallyas-Braak method revealed numerous astrocytic plaques and argentophilic threads in the cerebrum. Clinical diagnosis of corticobasal degeneration sometimes is difficult in individuals with atypical clinical presentations. More exact clinical and radiological criteria may warrant a diagnosis of corticobasal degeneration. [source] Progressive neuronal degeneration of childhood: prenatal diagnosis by MRIPRENATAL DIAGNOSIS, Issue 4 2005Jocelyne de Laveaucoupet Abstract We report two cases in the same family of progressive neuronal degeneration of childhood,Alpers syndrome,with prenatal MRI findings in one case. The first infant presented at birth with severe microcephaly, then rapidly evolved to progressive encephalopathy with refractory epilepsy, leading to death at 10 months. Biochemical investigations including liver function tests were normal. CT and MRI showed severe diffuse brain atrophy. The diagnosis of progressive neuronal degeneration of childhood was made on the clinical and imaging data. The second pregnancy was marked by gradual decrease of fetal cerebral biometry and a prenatal MRI performed at 32 weeks showed diffuse cortical atrophy, as observed in the sibling. The infant died at 5 months. Neuropathological findings were consistent with Alpers syndrome. Copyright © 2005 John Wiley & Sons, Ltd. [source] Benzodiazepines in catatonia associated with systemic lupus erythematosusPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 6 2006HUNG-YU WANG md Abstract, Neuropsychiatric disturbances are found in 50,70% of systemic lupus erythematosus (SLE) patients. However, there are rare cases of catatonia being described in SLE. Some studies have shown the effectiveness of high-dose steroid, plasma exchange and electroconvulsive therapy (ECT) in lupus catatonia. Herein are described two SLE patients with catatonia who had good response to i.v. diazepam (i.e. relief of catatonia symptoms). Patient 1, with mild cortical atrophy, had great improvement in catatonia symptoms on i.v. diazepam 150 mg during a period of 5 days. Patient 2, without cortical atrophy, had quick response to i.v. diazepam 10,20 mg. Both patients had no recurrence during 6-month follow up. In conclusion, benzodiazepines may play an important role in the treatment of catatonia associated with SLE if patients refuse ECT treatment. [source] A 3-year magnetic resonance imaging study of cortical lesions in relapse-onset multiple sclerosisANNALS OF NEUROLOGY, Issue 3 2010Massimiliano Calabrese MD Objective We assessed the occurrence, extent, and frequency of formation of cortical lesions (CLs) in patients with relapsing-remitting (RR) and secondary progressive (SP) multiple sclerosis (MS), and their relationship with cortical atrophy and disability progression. Methods One-hundred seven MS patients (76 RRMS and 31 SPMS), enrolled in a prospective, longitudinal magnetic resonance imaging (MRI) study, were assessed clinically and by brain MRI (including a double inversion recovery sequence) 3 years after study initiation. CL number and volume, T2 white matter (WM) lesion volume, gray matter fraction, and expanded disability status scale (EDSS) were measured. Results At baseline, CLs were detected in 64.4% of RRMS and 74.2% of SPMS patients. During follow-up, 132 new CLs were found in 44 RRMS patients (57.9%; 0.8 new CL/patient/yr) and 61 in 15 SPMS patients (48.4%; 1.0 new CL/patient/yr). Among these patients, only 31 also showed at least 1 new WM lesion. CL number and volume increases were higher in the 52 patients with a clinical worsening compared with those without (p < 0.001). Baseline CL volume correlated with baseline EDSS (r = 0.36, p < 0.001) and EDSS changes over time (r = 0.51, p < 0.001). Baseline CL volume was an independent predictor of EDSS accumulation and GM volume change at follow-up in both patient groups. In SPMS patients, baseline T2 WM lesion volume was another independent predictor of EDSS worsening. Interpretation In relapse-onset MS, CLs accumulate over time and are associated with disability progression. The quantification of CLs might represent an additional useful paraclinical tool to monitor MS evolution. ANN NEUROL 2010;67:376,383 [source] Brain herniations in patients with intracerebral hemorrhageACTA NEUROLOGICA SCANDINAVICA, Issue 4 2009J. Kalita Objectives,,, To study the types, frequency and clinical correlates of brain herniations in patients with intracerebral hemorrhage (ICH). Methods,,, In 24 patients with ICH (putaminal 22 and thalamic 2) features of raised intracranial pressure (ICP), such as hyperventilation, extensor rigidity, pupillary asymmetry and pyramidal signs on the non-hemiplegic side, were recorded. Depth of coma was assessed by using the Glasgow Coma Scale (GCS) and severity of stroke by using the Canadian Neurological Scale (CNS). On MRI, evidence of herniation, horizontal and vertical shifts and the edema,hematoma complex were measured and compared with that of 15 matched controls. The clinical signs of herniation correlated with radiological parameters. Results,,, The mean age of the patients was 57.7 years, six of them were women. Cerebral herniations were present in 11 (46%) patients. Subfalcian herniation (in six) was the commonest followed by uncal (in three). Combination of subfalcian and uncal herniations was present in one and subfalcian, uncal and tonsillar herniations in another. Herniations had significant correlation with the GCS, pupillary abnormalities, cortical atrophy, hematoma size and the edema,hematoma complex. One-month mortality was related to the GCS score, pupillary abnormalities and the edema,hematoma complex. Horizontal shift was related to the GCS score. Conclusion,,, In patients with ganglionic ICH, subfalcian herniation was the commonest. Herniation was associated with increased mortality. Horizontal shift correlated with clinical features of raised ICP and outcome. [source] | ||||||||||||||||||||||