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Biomedical subjects

P Hedera

Publications and source records attributed to P Hedera.

At least 37 records · Page 2Linked to original sources
PubMed1998

Sex and electroencephalographic synchronization after photic stimulation predict signal changes in the visual cortex on functional MR images.

PURPOSE: We evaluated factors that influence MR signal changes during photic stimulation of the visual cortex. We also tested the hypothesis that functional MR imaging response corresponds to electroencephalographic (EEG) synchronization after photic stimulation. METHODS: Thirty-eight healthy subjects, 20 men and 18 women, underwent photic stimulation of the visual cortex. They were studied with a 1.5-T MR unit, and photic stimulation was induced via 8-Hz LED goggles. Seven subjects with and seven without detectable functional MR imaging response to photic stimulation underwent further studies with 16-channel EEG after 2- to 30-Hz stroboscopic stimulation. RESULTS: Thirteen men and 18 women had a significant increase in MR signal in the visual cortex; seven men showed no visual cortex activation during more than two repeated studies. Six of seven volunteers with increased functional MR imaging signal after photic stimulation also showed signs of EEG synchronization when an 8-Hz stroboscopic flash was used; six of seven subjects with no functional MR imaging lacked EEG synchronization at 8-Hz stimulation. CONCLUSIONS: Men were more likely than women to have undetectable MR signal changes after photic stimulation. This finding should be considered when interpreting results of functional MR imaging studies. EEG with stroboscopic examination is a good predictor of functional MR imaging sensitivity to changes in regional cerebral blood flow induced by sensory stimulation.

Adult↗
PubMed1997

Neuroimaging of vessel amyloid in Alzheimer's disease.

Despite extensive recent advances in understanding Alzheimer's disease (AD) we are unable to noninvasively establish a definite diagnosis during life and cannot monitor the cerebral deposition of amyloid beta protein (A beta) in living patients. We evaluated the use of 10H3, a monoclonal antibody Fab targeting A beta protein 1-28 labeled with Tc-99m. Six subjects with probable AD were studied using single-photon emission computed tomography (SPECT) at times from 0-24 hours following injection. Curves of radioactivity in blood demonstrate a half-life of the injected Fab of 2-3 hours. Images show uptake around the head in the scalp or bone marrow in all subjects. There is no evidence of cerebral uptake of the antibody. Scalp biopsies in all six patients demonstrate diffuse staining with 10H3 of the scalp, a pattern indistinguishable from that found in controls. Evidence of amyloid deposition in the scalp in AD is not seen with other anti-A beta antibodies, suggesting that 10H3 is cross-reacting with another protein. Further studies with anti-A beta antibodies will require longer-lived radionuclides to detect cerebral uptake at later times after injection to allow for complete clearance from the blood. Alternately, imaging using labeled A beta itself may provide a means for noninvasive targeting of cerebral amyloid.

Alzheimer Disease↗
PubMed1997

Amyloid-beta protein angiopathies masquerading as Alzheimer's disease?

Current evidence from genetic and epidemiological studies supports the view that Alzheimer's disease (AD) is a heterogeneous disorder. While the disease is pathologically defined by the presence of specified lesions in form of amyloid plaques and neurofibrillary tangles within the parenchyma, other features of pathology are often either neglected or considered coincidental. Our studies suggest that cerebrovascular pathology is inherently part of the disorder, which could be an important factor in a cause or effect manner. We have recently identified subjects having died with severe amyloid beta (A beta) protein cerebral amyloid angiopathy (CAA) in the absence of a profound Alzheimer pathology. These subjects, diagnosed with dementia had a late onset disease and were found at autopsy to exhibit severe CAA but paucity of typical AD changes. Immunocytochemical studies showed numerous microvascular abnormalities as well as characteristic degeneration of the vascular smooth muscle in both surface and intracortical vessels. The pathology was also characterized by occasional intracerebral hemorrhages and multiple infarcts. Further assessment of the abnormalities and amyloid infiltrated cerebral vessels with antibodies to the carboxyl terminus of A beta indicated that the longer, more pathogenic form of A beta(1-42) was found to be highly associated with intracerebral hemorrhages. Our observations suggest that these mild AD cases with a predominantly vascular pathology are variants of AD and bear resemblance to the familial Dutch and Flemish versions of cerebral amyloidosis. We propose that AD is a group of diseases with a variable pathology analogous to the prion diseases, in which a vascular variant also exists.

Aged↗
PubMed1997

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: study of two American families with predominant dementia.

Few European families have been reported with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). We describe four patients from two independent American families. All four cases underwent comprehensive clinical, neuropsychological and pathological examination. Pathological data were correlated with clinical features. Dementia was a prominent and constant feature in all subjects. The families differed in phenotypical presentation and we analyzed possible pathological substrates that may account for the differences. Autopsy showed multiple ischemic infarcts in the white matter, abnormal vasculature with thickening and degeneration of the vessel wall. The clinical course in the first family was characterized by early dementia without stroke-like episodes; however, autopsy demonstrated strokes in the basal ganglia and thalamus. The members of the second family developed dementia later and had history of several clinically evident strokes. Pathological examination showed only widespread degeneration of the white matter. Our study of two American families with CADASIL suggests that involvement of the basal ganglia and thalamus is important for early development of dementia and clinically can present as a gradual dementia, resembling a neurodegenerative process. Selective damage of the white matter and central gray matter provides further insight to the pathogenesis of vascular dementia.

Adult↗
PubMed1997

Delirium in Alzheimer disease.

Advanced age and dementia are well-known risk factors for delirium, and most studies of delirium have concentrated on hospitalized populations. We reviewed the records of 199 community-dwelling Alzheimer disease (AD) patients and identified 43 (22%) who had had episodes of delirium during their dementing illness. These patients were matched for age, gender, and disease duration to AD patients without previous episodes of delirium. Variables examined included causes of delirium, Mini-Mental State Examination scores, Clinical Dementia Rating scores. Blessed Activities of Daily Living (ADL) scores, years of education, neuropsychological performance, and incidence of behavioral symptoms on the Brief Psychiatric Rating Scale. In six of 198 (3%) patients delirium was an initial symptom of AD. Conditions associated with onset of delirium were urinary tract infections, stressful events, surgery, medical illnesses, and medications. No significant differences were found between groups on neuropsychological testing. Patients with previous episodes of delirium had worse ADL scores and higher disease-course incidences of hallucinations and paranoid delusions, mostly occurring during the delirious episode. We conclude that delirium is common in AD, but it is an unusual initial symptom and it occurs in diverse clinical settings. Measures of behavioral symptoms and ADLs are more likely to reflect the impact of delirium on clinical status than measures of cognition or stage of dementia.

Aged↗
PubMed1997

Paroxysmal dystonic choreoathetosis linked to chromosome 2q: clinical analysis and proposed pathophysiology.

We describe clinical features of a large Polish-American kindred in which autosomal-dominant, paroxysmal dystonic choreoathetosis (PDC) was linked to a locus on chromosome 2q. Episodes of generalized dystonia and choreoathetosis involving the face and all extremities began in early childhood, lasted for 30 minutes to several hours, and occurred up to several times each week. There was no interruption of consciousness and EEGs were normal during the episodes. Paroxysmal dyskinesia occurred at rest both spontaneously and following caffeine or alcohol consumption. Neurologic examinations were normal between attacks. The cause of PDC is unknown. We deduced a model of PDC pathophysiology from analyzing neurophysiologic effects of alcohol and caffeine (which provoke attacks of PDC), the variably beneficial effects of levodopa-carbidopa, and the occurrence of dystonia and paroxysmal dyskinesia in biopterin synthesis disorders. We propose that nigrostriatal neurons in PDC patients have either marginally deficient dopamine synthesis or excessive alcohol- and caffeine-induced dopamine release; and that following alcohol- and caffeine-induced dopamine release, PDC patients experience a period of dopamine deficiency.

Athetosis↗
PubMed1996

Paroxysmal dystonic choreoathetosis: tight linkage to chromosome 2q.

Paroxysmal dystonic choreoathetosis (PDC) is characterized by attacks of involuntary movements that last up to several hours and occur at rest both spontaneously and following caffeine or alcohol consumption. We analyzed a Polish-American kindred with autosomal dominant PDC and identified tight linkage between the disorder and microsatellite markers on chromosome 2q (maximum two-point LOD score 4.77; recombination fraction 0). Our results clearly establish the existence of a locus for autosomal dominant PDC on distal chromosome 2q. The fact that three other paroxysmal neurological disorders (periodic ataxia with myokymia and hypo- and hyperkalemic periodic paralysis) are due to mutation in ion-channel genes raises the possibility that PDC is also due to an ion-channel gene mutation. It is noteworthy that a cluster of sodium-channel genes is located on distal chromosome 2q, near the PDC locus. Identifying the PDC locus on chromosome 2q will facilitate discovery of the PDC gene and enable investigators to determine whether PDC is genetically homogeneous and whether other paroxysmal movement disorders are also genetically linked to the PDC locus.

Athetosis↗
PubMed1996

Apolipoprotein E-epsilon4 alleles in cerebral amyloid angiopathy and cerebrovascular pathology associated with Alzheimer's disease.

The presence of apolipoprotein E-epsilon4 (APOE-epsilon4) allele has been implicated as a risk factor for Alzheimer's disease (AD). We examined the frequencies of APOE-epsilon4 alleles in age-matched controls and subgroups of 190 AD subjects exhibited cerebral amyloid angiopathy (CAA) and other frequently associated lesions. CAA was evident in 96% of the AD subjects, which were divided into two groups, one bearing mild or no apparent CAA and the other with moderate to severe CAA. APOE-epsilon4 allele frequency (48%) in the latter advanced CAA group was six times higher than in those who exhibited mild CAA. In the advanced CAA subjects, the occurrence of an epsilon4 allele was increased by a factor of 17 (95% confidence interval, 7.56 to 38.9). This was despite the fact that neocortical amyloid-beta plaque densities in the two groups were similar and that all of the AD subjects had met the accepted neuropathological criteria. We also observed that the degree of CAA severity was greatest in the group of subjects with the epsilon4/epsilon4 genotype. The association between CAA and APOE-epsilon4 was further implicated in two non-AD subjects among neurological controls with severe CAA. These two subjects, both homozygous for the APOE-epsilon4 allele, were primarily diagnosed as having Creutzfeldt-Jakob disease and Pick's disease in the absence of significant neocortical amyloid deposition. Allele frequency comparisons between neurological control subjects with CAA and those without likewise accorded a strong relationship between the APOE-epsilon4 allele and the presence of CAA. More remarkably, the epsilon4 allele frequency was highly associated with AD subjects exhibiting lobar or intracerebral hemorrhage, all of whom had advanced CAA. We observed that 36% of the AD subjects had concomitant cerebrovascular pathology resulting from single infarcts, multiple microinfarcts, ischemic white matter lesions, or petechial hemorrhages. Although the difference in APOE genotype distribution between subjects with and without cerebrovascular lesions did not reach statistical significance, we did note that the frequency of the epsilon4 allele was significantly higher in subjects with such pathology as compared with those without. However, we found no evidence to suggest that the acquisition of an APOE-epsilon4 allele or one of the alleles, epsilon2 or epsilon3, was a factor in the occurrence of atherosclerosis localized in the basal surface arteries. Analyses of our sample also confirm that there was a lower frequency of the APOE-epsilon2 allele in AD subjects and that the frequency of the epsilon4 allele in AD subjects with concomitant diffuse Lewy body disease was intermediate between controls and AD subjects. Our results suggest that the APOE-epsilon4 allele is a significant factor in the development of CAA in AD and reveal the possibility that APOE is an independent factor in CAA and other vascular abnormalities associated with AD.

Aged↗
PubMed1995

Differential degeneration of the cerebral microvasculature in Alzheimer's disease.

We used immunocytochemical methods to define abnormalities in the cerebral endothelium and the vascular basement membrane in patients with Alzheimer's disease (AD) and in aging control subjects. Double immunostaining with antibodies to the endothelial cell markers CD34 and CD31 revealed an absence of endothelial staining in many capillary profiles that still appeared to retain their basement membranes stained by antibodies to collagen IV. Such differential labeling, clearly suggesting capillaries with collapsed or degenerated endothelium, was frequently (> 90% of cases) evident in AD but relatively lacking in brain regions or other diseases and controls (< 30%) free of amyloid beta (A beta) deposits. We suggest that this profound vascular phenomenon is concomitant with A beta deposition and implies abnormalities in the integrity of brain microvasculature related to neuronal degeneration in AD.

Adult↗
PubMed1995

Concurrence of Alzheimer's disease, Parkinson's disease, diffuse Lewy body disease, and amyotrophic lateral sclerosis.

A 71-year-old man developed signs of progressive dementia, followed by extrapyramidal and motor neuron disease symptoms, which led to death in 6 years. Neuropathological examination revealed neuritic plaques, neurofibrillary tangles, and Lewy bodies in the substantia nigra and neocortex. Atrophy and gliosis with intraneuronal ubiquitin inclusions were present in the anterior horns of the spinal cord. Overlapping of Alzheimer's disease, Parkinson's disease, diffuse Lewy body disease and amyotrophic lateral sclerosis is rare and can increase our understanding of the process of neurodegeneration.

Aged↗
PubMed1995

Influence of extreme head rotations on brainstem auditory evoked potentials (BAEP).

The influence of extreme head rotations on BAEP was studied in 47 patients who had vertebral artery angiogram. Patients with and without unilateral hypoplasia of the vertebral artery (VA) lumen were identified and all patients were further divided into two groups: with and without hypertension. The subjects underwent a BAEP examination in three head positions: neutral position, extreme right and extreme left rotation. In the subgroup of patients with hypertension and unilateral VA hypoplasia, and following the rotation away from the non-hypoplastic vessel a statistically significant decrease in the PV wave amplitude and prolonged PV wave latency was found. Head maneuvers in subjects with normal blood pressure or in hypertensive patients with symmetrical VA did not cause significant changes in BAEP. These results document the effect of head rotation in subjects with potentially impaired collateral flow. An increase in the PV wave latency and decrease in its amplitude may reflect subtle changes in the brainstem perfusion in hypertensive patients. These changes maybe due to a reduced capacity to compensate for dynamic obstruction of VA following the head rotations.

Adult↗
PubMed1995

Temporal patterns of uncoupling between oxidative metabolism and regional cerebral blood flow demonstrated by functional magnetic resonance imaging.

RATIONALE AND OBJECTIVES: Brain activation can be detected by functional magnetic resonance imaging. Termination of stimulation can cause drop of postactivation signal below preactivation baseline; the nature of this "undershoot" remains controversial. The authors investigated postactivation signal after stimulation of the visual cortex with photic stimuli of different duration. METHODS: Activation of visual cortex in 11 healthy subjects was studied. The authors underwent short and long stimulation. The relation between activation and postactivation signal was investigated after both durations of stimulation. RESULTS: Average postactivation signal after short stimulation was -1.71 +/- 2.66% and after long stimulation 0.82 +/- 1.59% (P < or = 0.01). Significant "undershoot" was detected after short stimulation in the majority of cases, although this was typically absent after long stimulation. CONCLUSIONS: The authors propose that "undershoot" is caused by decreased oxygen content in venous blood compared with the preactivation level and may reflect increased extraction of oxygen as a result of glycolytic metabolism. The absence of "undershoot" after longer stimulation suggests a gradual shift from uncoupling between regional cerebral blood flow and oxygen consumption toward a steady state.

Adult↗
PubMed1995

Effect of collateral flow patterns on outcome of carotid occlusion.

The relationship between anatomical configuration of collateral flow and the outcome of the internal carotid artery (ICA) occlusion was analyzed. Sixty-one patients with occlusion of ICA were studied with transcranial Doppler ultrasonography. The authors monitored blood flow velocities in the middle cerebral artery (MCA) ipsilateral to the ICA occlusion during a series of carotid compressions. Blood flow through three major collateral arteries (anterior and posterior communicating arteries and ophthalmic artery) was determined as a residual flow in MCA after each compression. Twelve subjects had asymptomatic occlusion and 46 had stroke; patients with stroke were divided into mild, moderate, and severe stroke groups. Subjects with asymptomatic occlusion had a higher number of patent collateral vessels than severe stroke patients (p < or = 0.001). The same relationship was found between mild and severe stroke patients (p < or = 0.001) and between moderate and severe stroke (p < or = 0.01). Patients with watershed ischemia had a lower number of patent collateral arteries than patients with thromboembolic ischemia as revealed by CT examination (p < or = 0.02). This study demonstrates the crucial role of collateral flow in the stroke pathogenesis and stroke outcome in subjects with extracranial ICA occlusions.

Adult↗
PubMed1994

2D and 3D high resolution gradient echo functional imaging of the brain: venous contributions to signal in motor cortex studies.

Recent emphasis on high resolution gradient echo studies in functional imaging has led to the conclusion that there are likely three domains of response to the blood circulation in the brain when considering field inhomogeneity effects of the venous blood pre- and during activation. The first is a coherent effect due to large or macroscopic vessels on the order of the size of the voxel (ca 200-500 microns in most studies). These can lead to very large signal changes (up to 100%). The second is at the venule level (ca 50-200 microns) and is associated with smaller parenchymal changes (usually ca 10% or less). The third is at the capillary level and is associated with much smaller signal changes at 1.5 T and even up to 4 T. The actual signal changes depend on field strength and sequence design. In this paper, we present our experience in detecting the first two domains with 2D and 3D gradient echo imaging at 1.5 T. We find that high resolution enables visualization of the larger small veins in motor cortex studies and that, on occasion, it is possible to see the venule effects as well. We suggest a simple model to explain the large signal changes based on susceptibility changes and partial volume effects. Comparisons of the functional imaging data to this model and to MR angiographic studies are also shown as evidence of the venous sources of the susceptibility changes.

Brain↗
PubMed1994

Compressions of carotid and vertebral arteries in assessment of intracranial collateral flow: correlation between angiography and transcranial Doppler ultrasonography.

The authors examined 61 subjects with carotid angiography and 50 with vertebral angiography. Angiograms were evaluated for collateral flow through the ophthalmic, anterior communicating, and posterior communicating arteries. The authors evaluated the patency of collateral vessels directly using transcranial Doppler ultrasonography; they made indirect detection after the compression of carotid and vertebral arteries while monitoring flow velocities in the middle cerebral artery. They established criteria for the hemodynamic significance of tested collateral vessels. A combination of carotid compressions and transcranial Doppler ultrasonography detected the patency of the ophthalmic and anterior communicating arteries with a specificity and sensitivity of 1.00. Examination of the posterior communicating artery had a sensitivity of 0.97 and specificity of 0.98. Indirect evaluation of collateral vessels can not only detect their presence but also establish their hemodynamic significance with high accuracy.

Adult↗
PubMed1994

Abnormal connectivity of the visual pathways in human albinos demonstrated by susceptibility-sensitized MRI.

We studied activation of the human visual cortex (VC) using susceptibility-sensitized MRI at 1.5 Tesla. Three albinos and six healthy controls underwent a series of monocular and binocular photic flash stimulation. Monocular stimulation in albinos caused predominant contralateral activation with a small, well-delineated area in the anterior part of the VC in the ipsilateral hemisphere. This finding was consistent with a chiasmal crossing anomaly in albinism. All controls had symmetric patterns of activation during monocular stimulation. Functional MRI represents a promising method for evaluation of the visual pathways in humans.

Adolescent↗
PubMed1994

Concomitants of visual hallucinations in Alzheimer's disease.

Visual hallucinations (VH) are the most common hallucinations in Alzheimer's disease (AD), but their relationships with other behavioral symptoms and measures of cognitive performance are unclear. Using the BE-HAVE/AD, a semistructured behavioral inventory, we identified 20/160 AD patients (13%) who were currently having VH. Patients with VH performed worse on the Mini-Mental State Examination and had more behavioral symptoms than patients without VH. Symptoms particularly associated with VH included auditory hallucinations, verbal outbursts, delusions, and paranoid ideation. Principal factor analysis of the BEHAVE/AD yielded four factors accounting for 47% of the total variance. VH loaded on two factors involving symptoms of "paranoia" and "agitation/hallucinations." Our findings suggest that VH in AD patients are common, often occur in the presence of specific behavioral disturbances, and may have management implications.

Aged↗