Possible utility of bilateral simultaneous TCD.
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Blood Flow Velocity↗
Biomedical subjects
I Prohovnik
Publications and source records attributed to I Prohovnik.
Management of cerebral vasospasm in the 1990s.
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Animals↗
Dementia associated with bilateral carotid occlusions: neuropsychological and haemodynamic course after extracranial to intracranial bypass surgery.
A 55 year old man with bilateral internal carotid and unilateral vertebral artery occlusions presented subacutely with profound behavioural and cognitive changes featuring frontal lobe deficits. Neuropsychological testing showed severe cognitive impairment compatible with dementia. Anatomical imaging showed only a small right superior frontal infarction. Cerebral blood flow was severely reduced, with profound hypofrontality and limited hypercapnic reactivity, and cerebral metabolism was reduced primarily in the medial frontal lobes. After right sided extracranial to intracranial cerebral bypass surgery, both flow and metabolism improved, as did behavioural and neuropsychological deficits. Perfusion insufficiency from bilateral carotid occlusions, with secondarily reduced metabolism in the frontal zones bilaterally, may be an unusual cause of a reversible frontal dementia syndrome.
Arterial Occlusive Diseases↗
Cortical perfusion and gray matter weight in frontal lobe dementia.
To evaluate the pathophysiology of frontal lobe dementia (FLD), the authors compared regional cerebral blood flow (rCBF) in matched groups of FLD, probable Alzheimer's disease (AD), and major depression patients and normal control subjects (n = 7 each). The planar xenon-133 technique allowed full quantification of cortical perfusion and estimates of the relative weight of gray matter (wg). FLD patients showed lower blood flow and wg in the frontal cortex than the other groups. Mean cortical perfusion was correlated with cortical wg in the FLD group only. These findings 1) suggest that matched reductions of frontal gray matter weight and perfusion occur in FLD and 2) support the use of rCBF in distinguishing FLD from AD and severe depression.
Aged↗
Rapidly progressive frontal-type dementia associated with Lyme disease.
The authors report a case of fatal neuropsychiatric Lyme disease (LD) that was expressed clinically by progressive frontal lobe dementia and pathologically by severe subcortical degeneration. Antibiotic treatment resulted in transient improvement, but the patient relapsed after the antibiotics were discontinued. LD must be considered even in cases with purely psychiatric presentation, and prolonged antibiotic therapy may be necessary.
Aged↗
Increased cerebral blood flow during m-CPP exacerbation of obsessive-compulsive disorder.
The partial serotonin agonist m-chlorophenyl-piperazine (m-CPP) has been reported to increase obsessive-compulsive symptoms in some patients with obsessive-compulsive disorder (OCD). The authors investigated the underlying physiological mechanisms of this variable exacerbation by imaging regional cerebral blood flow with the planar xenon-133 method after administration of oral m-CPP (0.5 mg/kg). Seven patients who responded to m-CPP with symptomatic exacerbation had a marked increase in global cortical perfusion (18.1%), in contrast to the remaining 7 nonresponders to m-CPP, who showed no change. These results suggest that m-CPP exacerbation of OCD symptoms is associated with increased cortical blood flow.
Administration, Oral↗
Relationship between lifetime occupation and parietal flow: implications for a reserve against Alzheimer's disease pathology.
We previously reported an inverse relation between parietal cerebral blood flow and years of education in Alzheimer's disease (AD) patients matched for clinical severity. This suggested that the clinical manifestation of advancing AD pathology is delayed in patients with higher educational attainment. Other aspects of life experience may also provide a reserve against the clinical expression of AD. To test this hypothesis, we classified the primary life-time occupations of 51 AD patients using the Dictionary of Occupational Titles, published by the US Department of Labor, and derived six factor scores describing intellectual, interpersonal, and physical job demands. Regional cerebral blood flow was measured using the xenon-133 inhalation method. After controlling for age, clinical dementia severity, and education, there was less relative perfusion in the parietal region in subjects whose occupations were associated with higher interpersonal skills and physical demands factor scores. We conclude that independent of education, aspects of occupational experience may provide a reserve that delays the clinical manifestation of AD.
Administration, Inhalation↗
Intellectual decline predicts the parietal perfusion deficit in Alzheimer's disease.
UNLABELLED: The pathophysiology of Alzheimer's disease may be reflected more in an individual's decline from premorbid levels of functioning than in current measures of absolute severity. To test this hypothesis, we computed an index of intellectual decline for individual patients and examined its relationship to Alzheimer's disease-related functional brain abnormalities. METHODS: We studied 27 patients with Alzheimer's disease diagnosed by ADRDA-NINCDS criteria. We used patient demographics and published formulas to construct estimates of premorbid Wechsler Adult Intelligence Scale (WAIS-R) IQs for each subject in the sample and used a current IQ assessment to estimate the decline in IQ that occurred during the disease for each subject. Cortical perfusion was quantified by the planar 133Xe regional cerebral blood flow (rCBF) technique. The characteristic abnormality in parietal cortex was expressed by the parietal index (PI). RESULTS: Over the estimated disease duration of 3.8 +/- 2.2 yr, the full-scaled IQ declined by an estimated 28.0 +/- 15.5 points. The current PI was in turn well correlated with the IQ decline (r = 0.66; p < 0.001). This association was linear and stronger than those with other, more common measures of current severity. A multiple stepwise regression analysis suggested that IQ decline alone accounted for the variance in PI related to clinical deterioration. Actual images showed a mild blood flow deficit in patients with the smallest estimated IQ declines but deep and extensive lesions in patients with large declines. CONCLUSION: These results suggest that the decline from the premorbid baseline, rather than current level of functioning, best predicts the extent of brain damage reflected in the rCBF abnormality, a finding independent of demographic variance.
Age of Onset↗
Radiation exposure to human trachea from xenon-133 procedures.
UNLABELLED: The general dosimetry of 133Xe for human studies is well documented, but the resultant radiation exposure to tracheal tissue is poorly known. This organ is of central relevance because the tracer is primarily eliminated through exhalation. METHODS: We report actual 133Xe concentrations in respiratory air during measurement of regional cerebral blood flow (rCBF), when the tracer is administered both by inhalation and intravenous injection. Data were collected from 102 patients, with equal gender representation and an age range of 18-82 yr. Most of the patients had subarachnoid hemorrhage or Alzheimer's disease or were normal control subjects. Average administered doses were 18 +/- 4 mCi by inhalation and 15 +/- 3 intravenously. RESULTS: We found average respiratory concentrations of about 1.80 mCi/liter during a 1-min inhalation and 0.74 mCi/liter following intravenous injection of standard doses. These activities drop rapidly: average respiratory concentrations during the second minute are 0.70 mCi/liter for inhalation and 0.19 mCi/liter for intravenous injection and reach negligible levels thereafter. We calculate that the tracheal absorbed dose from 133Xe procedures is approximately 28 mrad following inhalation and about 11 mrad following intravenous injection. These values reflect the full 11-min exposure, but most of the activity is only present initially. CONCLUSION: These values will agree with previous estimates and indicate an excellent safety margin.
Administration, Inhalation↗
Strategic infarcts in vascular dementia. A clinical and brain imaging experience.
The mechanisms of dementia resulting from small deep infarctions are incompletely understood. The thesis underlying the concept of "multi-infarct dementia" is that multiple lesions have a synergistic effect on mental functions, resulting in dementia irrespective of specific location or volume. In this report, we summarize our experience with six patients reported previously along with additional patients examined subsequently, whose clinical features and brain imaging findings allow an alternative formulation for dementia resulting from lacunar stroke. The six initial patients presented with an abrupt change in behavior after acute infarction involving the inferior genu of the internal capsule documented by computed tomography (CT) and magnetic resonance imaging (MRI). The acute syndrome featured fluctuating alertness, inattention, memory loss, apathy, abulia, and psychomotor retardation suggesting frontal lobe dysfunction. Contralateral hemiparesis and dysarthria were generally mild, except when the infarct extended into the posterior limb. Neuropsychological testing in five patients with left-sided infarcts revealed severe verbal memory loss. Additional cognitive deficits consistent with dementia were evident in four patients. A right-sided infarct caused transient impairment in visuospatial memory. Functional brain imaging in three patients using 133xenon regional cerebral blood flow (rCBF) and single photon emission computed tomography (SPECT) showed focal reduction in hemispheric perfusion most prominent in the ipsilateral inferior and medial frontal cortex. Perfusion was also defective in the medial and laterial temporal cortex. Important pathways of the limbic system traverse the inferior capsule in the region of the genu. Corticothalamic and thalamocortical fibers form the thalamic peduncles which detach from the internal capsule and enter the thalamus at its rostral and caudal poles and along its dorsal surface. The anterior thalamic peduncle, conveys reciprocal connections between the dorsomedial nucleus and the cingulate gyrus, as well as the prefrontal and orbitofrontal cortex. The inferior thalamic peduncle carries fibers which connect the thalamus with orbitofrontal, insular, and temporal cortex, as well as the amygdala via the ansa peduncularis to the ventral amygdalofugal pathway. Thus, damage to one or both white-matter tracts may occur with infarctions in the region of the inferior genu, causing striking frontal behavioral effects and memory loss in our patients associated with functional deactivation of the ipsilateral frontal and temporal cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
Cerebral Infarction↗
Regional cerebral blood flow in mood disorders, III. Treatment and clinical response.
BACKGROUND: Global and regional deficits in cerebral blood flow and glucose metabolism have been reported in major depression, but there is limited information on the effects of somatic treatment and clinical recovery on these abnormalities. METHODS: We assessed cortical blood flow with the xenon 133 technique in depressed patients prior to a course of electroconvulsive therapy (ECT), 30 minutes before and 50 minutes after a single treatment, and during the week following ECT. Acute (preictal and postictal) effects of a single treatment also were studied in manic patients. RESULTS: In the depressed and manic groups, larger blood flow reductions in the acute period, both globally and in particular patterns of brain regions, were associated with a superior clinical outcome following the treatment course. In depressed patients, similar patterns were observed for the blood flow changes over a full treatment course. Blood flow reductions in anterior cortical regions were strongly associated with a positive clinical response in both depression and mania. CONCLUSIONS: The findings indicated that cerebral blood flow abnormalities in major depression were not reversed by successful treatment with ECT. Rather, particularly in responders, ECT resulted in additional perfusion reductions. The therapeutic properties of ECT are related to reduced functional brain activity in specific neural regions.
Adult↗
WAIS-R subtest profile and cortical perfusion in Alzheimer's disease.
WAIS-R profiles were investigated in 28 Alzheimer's disease (AD) and 21 healthy elderly subjects. The Fuld subtest profile, previously reported to have potential as a diagnostic marker for AD, was observed in 35.7% of our AD patients and 4.8% of the controls. We compared AD patients with the Fuld profile (ADF+) to a group of patients without the profile (ADF-) with similar demographics and dementia severity and demographically matched normals using regional Cerebral Blood Flow. Both AD groups showed reduced blood flow in the parietotemporal cortex compared to normals, but the ADF+ patients had greater flow reductions than the ADF- group. Examination of WAIS-R performance indicated that the ADF+ group had lower scores than the ADF- patients on the Digit Symbol and Block Design subtests, and further, that these two subtests were associated with the parietotemporal perfusion deficit in our AD sample. Our findings do not support the use of the Fuld profile as a diagnostic marker for AD, but do provide physiological evidence for behavioral heterogeneity among AD patients based on WAIS-R subtest performance.
Aged↗
Middle cerebral artery velocity changes during transfusion in sickle cell anemia.
BACKGROUND AND PURPOSE: Sickle cell disease is associated with cerebral hyperemia, which is therapeutically reduced by transfusion; however, the process of transfusion-induced cerebral perfusion changes has heretofore not been observed. METHODS: We document the acute changes of intracranial arterial velocity in 10 patients (7 with strokes, 3 without) undergoing transfusion therapy using transcranial Doppler ultrasonography. Middle cerebral artery velocities were bilaterally measured every 30 minutes for the duration of transfusion (4 to 5 hours). Regional cerebral blood flow was quantified in 5 of these patients before the transfusion and 24 hours later by the 133Xe technique. RESULTS: Velocities in stroke-associated vessels (64.33 +/- 18.65 cm/s; n = 6) were significantly lower than in uninfarcted territories (99.54 +/- 27.39 cm/s; n = 13), and both types of vessels showed a robust reduction of blood flow velocities during transfusion. The rates of reduction were not significantly different as a function of prior stroke but did correlate with pretransfusion velocities and with the rise in hematocrit (multiple r = .887, P < .001). These reductions occurred rapidly within the first 3 hours of transfusion. Velocities attained at the end of transfusion were maintained in the hour after transfusion and the next day. CONCLUSIONS: We conclude that transfusion induces rapid changes in cerebral hemodynamics that are related to pretransfusion velocities and a rise in hematocrit. Transcranial Doppler provides a safe, simple, and noninvasive technique of monitoring these changes and may provide a means of making therapeutic decisions regarding transfusion therapy in patients with sickle cell anemia.
Adolescent↗
Effects of total hemoglobin and hemoglobin S concentration on cerebral blood flow during transfusion therapy to prevent stroke in sickle cell disease.
BACKGROUND: The standard treatment of stroke in sickle cell disease is chronic transfusion to maintain the fraction of abnormal hemoglobin (hemoglobin S [HbS]) below 20%. Risks associated with such transfusion can be reduced by allowing higher HbS levels, but the physiological consequences of this modification are unknown. Cerebral blood flow is elevated in sickle cell disease proportionate to the degree of anemia and is reduced by transfusion. We tested the effects of various HbS levels on cerebral blood flow during the course of transfusion therapy. CASE DESCRIPTIONS: We monitored cerebral blood flow (by the 133Xe inhalation method) in three patients whose chronic transfusion program was changed from a traditional regimen (HbS < 20%) to a moderate one, allowing HbS to rise to 45% to 50% between treatments. As expected, cerebral blood flow was higher with lower hemoglobin and higher HbS concentration. However, the HbS fraction appeared to exert a separate influence on the hyperemia, independent of total hemoglobin concentration. Furthermore, cerebral blood flow was higher during the modified regimen, despite equivalent anemia. CONCLUSIONS: These results suggest caution in adapting the modified transfusion regimen. Although HbS concentrations of 50% did not cause any frank neurological sequelae, the possible consequences of the associated hyperemia over time are unknown. We conclude that larger clinical and physiological studies of moderate transfusion regimens (allowing higher concentration of HbS) are necessary before it can become standard therapy.
Adolescent↗
Cerebral hyperemia in MELAS.
BACKGROUND: The pathophysiology of stroke-like episodes in MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) is uncertain. CASE DESCRIPTION: We studied a 24-year-old man with MELAS who had fluent aphasia and right hemianopia. Magnetic resonance imaging and computed tomography showed a large infarction in the parietal, temporal, and occipital lobes. We performed serial planar 133Xe regional cerebral blood flow studies and single-photon emission computed tomography. Fifteen and 26 days after the stroke-like episode, there was generalized hyperperfusion, highest in infarcted areas. Four and 8 months after the stroke-like episode, the brain was still hyperemic, with highest flow in noninfarcted tissue. Reactivity to CO2 was less than normal within the infarct at 26 days but improved thereafter. In the noninfarcted region, vasomotor reactivity was impared at 4 months, when resting flows were at their peak. CONCLUSIONS: We observed generalized cerebral hyperemia and fluctuating CO2 reactivity in MELAS, possibly a consequence of local lactic acid production. In addition, this case suggests that nonquantitative functional imaging may be misleading in MELAS.
Adult↗
Evidence for adaptive autoregulatory displacement in hypotensive cortical territories adjacent to arteriovenous malformations. Columbia University AVM Study Project.
We hypothesized that chronic hypotension in normal vascular territories fed by arteriovenous malformation pedicles may reset the lower limit of autoregulation and allow flow to remain constant over a lower pressure range. We studied the effect of increasing systemic mean arterial pressure (SMAP) with phenylephrine on cerebral blood flow using a novel technique. Fourteen patients undergoing 15 procedures were studied before endovascular embolization of arteriovenous malformations under neuroleptic conscious sedation. Mean pressures were transduced via a 1.5-F intracranial microcatheter, which was passed under fluoroscopic guidance into the target feeding artery. The microcatheter was positioned (unwedged) at a point that was relatively hypotensive to systemic pressure but that irrigated normal cortex on angiography; feeding mean arterial pressure (FMAP) and SMAP were recorded. A bolus of 133Xe in saline was injected into the microcatheter, and washout was recorded for 3 minutes by a scintillation detector placed over the vascular territory of the injected pedicle. SMAP was then increased approximately 25 mm Hg by phenylephrine infusion, a second bolus was given, and washout was recorded. After exclusion of the shunt spike, initial slope was calculated. The SMAP (mean +/- standard error) increased from 65 +/- 3 to 89 +/- 2 mm Hg (P < 0.0001), and FMAP increased from 46 +/- 3 to 63 +/- 3 mm Hg (P < 0.0001); cerebral blood flow did not change (40 +/- 2 to 40 +/- 2 ml/100 g per min, P = 0.9199). Dividing the cases on the basis of the baseline FMAP into a "severe" hypotensive group (FMAP = 38 +/- 2; n = 7) and a "moderate" hypotensive group (FMAP = 54 +/- 3; n = 8), cerebral blood flow did not change in either group during phenylephrine challenge. Chronic hypotension does not necessarily result in "vasomotor paralysis" with loss of the ability to vasoconstrict to acute increases in perfusion pressure. Instead, it appears to displace adaptively the lower limit of autoregulation in affected vascular territories by a shift of the autoregulatory curve to the left, conceptually analogous to the adaptive displacement seen with chronic hypertension and its treatment.
Adolescent↗
Acquired immunodeficiency syndrome and the developing nervous system.
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AIDS Dementia Complex↗
Physical properties and quantification of the ECT stimulus: I. Basic principles.
The physical properties of the electroconvulsive therapy (ECT) stimulus markedly affect both efficacy and side effects. We review basic principles in characterizing these physical properties and in quantifying the ECT stimulus. The topics discussed include the application of Ohm's law, alternative composite units of ECT dosage (energy and charge), the use of constant-current, constant-voltage, and constant-energy principles in ECT devices, the nature of current shunting in ECT and the determinants of impedance, the relations between impedance and seizure threshold, the seizure-eliciting efficiency of alternative stimulus waveforms and of stimulus parameter configurations, and the role of reactive components (capacitance and inductance) in the ECT circuit. New findings are also presented regarding several of these issues.
Electric Impedance↗