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Biomedical subjects

J Kuikka

Publications and source records attributed to J Kuikka.

At least 37 records · Page 2Linked to original sources
PubMed1997

Frontal dysfunction blocks the therapeutic effect of THA on attention in Alzheimer's disease.

We evaluated the effect of a single dose of a cholinesterase inhibitor, tetrahydroaminoacridine (THA; 25 and 50 mg, orally), on attention in patients with Alzheimer's disease (AD). THA 50 mg improved performance in attentional measures (Trail Making Test, Big/Little Circle, Simple and Choice Reaction Time) in nine of 28 patients with AD. We analysed retention of 99mTc-labelled ethylene dicysteinate (ECD) in the cortical areas using single photon emission computed tomography. Those patients who benefited from THA treatment had bilaterally higher frontal and prefrontal ECD retention values. We suggest that THA may improve attention in patients with AD, but a severe frontal dysfunction may block the therapeutic effect of THA.

Aged↗
PubMed1997

Dopamine reuptake site densities in patients with social phobia.

OBJECTIVE: It has been suggested that social phobia is associated with dysfunction of the noradrenergic and dopaminergic systems, but there are no published anatomic data on the monoaminergic abnormalities found in the brains of phobic patients. The authors studied the density of dopamine reuptake sites in patients with social phobia. METHOD: The study included 11 patients with social phobia and 28 healthy comparison subjects, 11 of whom were age- and gender-matched to the patients for the analyses. Measurement of the density of dopamine reuptake sites was performed by using a 123I-labeled cocaine analogue, [123I]beta-CIT, with single photon emission computed tomography (SPECT). RESULTS: Blind quantitative analysis revealed that striatal dopamine reuptake site densities were markedly lower in the patients with social phobia than in the age- and gender-matched comparison subjects. CONCLUSIONS: The results indicate that social phobia may be associated with a dysfunction of the striatal dopaminergic system.

Adult↗
PubMed1996

Sympathetic reinnervation after acute myocardial infarction.

Myocardial infarction produces sympathetic denervation of the necrotic myocardium and noninfarcted myocardium apical to the injury. Proof of sympathetic reinnervation after myocardial infarction has, however, remained elusive. In this study, we investigated whether cardiac sympathetic reinnervation occurs in men recovering from myocardial infarction. I-123 metaiodobenzylguanidine (MIBG), I-123 paraphenylpentadecanoic acid, and Tc-99m sestamibi scintigraphic imaging were conducted in 13 men 3 and 12 months after a first myocardial infarction to determine the extent of denervated myocardium, the size of the infarct, and the size of the myocardium with reduced perfusion, respectively. A defect was determined as regional uptake of < or = 30% of the maximal myocardial activity. The size of the MIBG defect was not significantly different between 3 and 12 months after infarction (17 +/- 8% and 18 +/- 8% of left ventricular mass, respectively). There was also no significant change in the extent of viable but denervated myocardium at 3 and 12 months (average 9 +/- 6% and 10 +/- 5%, respectively). MIBG activity of the infarct zone (expressed as a percentage of MIBG activity of the myocardium with normal perfusion) did not change (17 +/- 13% and 20 +/- 16%), whereas MIBG activity of the periinfarct zone increased during follow-up (32 +/- 11% and 41 +/- 14%, p < 0.01). This was associated with an increase in periinfarct I-123 paraphenylpentadecanoic acid activity (40 +/- 11% and 48 +/- 9%, p < 0.05), but not Tc-99m sestamibi activity (48 +/- 10% and 48 +/- 11%). In conclusion, we did not observe sympathetic reinnervation in the infarct zone between 3 and 12 months after myocardial infarction. However, MIBG activity of the periinfarct zone increased, suggesting partial reinnervation, and this was associated with a recovery of myocardial metabolic activity of the periinfarct zone.

3-Iodobenzylguanidine↗
PubMed1996

Measurement of myocardial accumulation of 123I-metaiodobenzylguanidine for studying cardiac autonomic neuropathy in diabetes mellitus.

The association of myocardial 123I-metaiodobenzylguanidine (MIBG) accumulation and autonomic neuropathy, as well as factors known to affect autonomic nervous function, were studied in a group of 12 diabetic patients representing different degrees of autonomic failure. The early myocardial uptake phase of 123I-MIBG was measured by calculating the peak net influx rate for the first 30 min after the 123I-MIBG injection and by single photon emission computed tomography (SPECT) imaging 1 h after the injection. The retainment of 123I-MIBG in the myocardium was measured using SPECT imaging 6 h after the injection, and myocardial uptake and the myocardium/liver uptake ratio were calculated. The 6-h myocardium/liver uptake ratio of 123I-MIBG was significantly (p < 0.05) lower in the diabetic patients with clinically evident autonomic neuropathy compared with those without autonomic neuropathy. Greater body mass index was associated with lower peak net influx rate and 1-h myocardial uptake of 123I-MIBG, and greater diastolic blood pressure was associated with lower 1-h myocardial uptake of 123I-MIBG, whether or not the patients had diabetic autonomic neuropathy. In conclusion, reduction in the 6-h myocardium/liver uptake ratio of 123I-MIBG is related to diabetic autonomic neuropathy. Because the early 123I-MIBG accumulation in myocardium is reduced in diabetic patients with greater body mass index and diastolic blood pressure, irrespective of autonomic neuropathy, our results encourage the use of the late myocardial accumulation of 123I-MIBG for studying sympathetic neuropathy in the diabetic heart.

3-Iodobenzylguanidine↗
PubMed1996

SPECT and MRI analysis in Alzheimer's disease: relation to apolipoprotein E epsilon 4 allele.

OBJECTIVES: The epsilon 4 allele of apolipoprotein E (ApoE) is a risk factor for late onset Alzheimer's disease. ApoE is present in senile plaques, neurofibrillary tangles, and cerebrovascular amyloid, and it is implicated in synaptogenesis. The effect of ApoE polymorphism on the volumes of hippocampus, amygdala, and frontal lobe was studied. The hypothesis was that the patients with Alzheimer's disease carrying the epsilon 4 allele have more pronounced atrophy. The relation of ApoE and cerebral blood flow on cortical areas was also assessed. METHODS: Fifty eight patients with Alzheimer's disease at the early stage of the disease and 34 control subjects were studied. Patients with Alzheimer's disease were divided into subgroups according to the number of the epsilon 4 alleles. Volumes were measured by MRI and regional cerebral blood flow ratios referred to the cerebellum were examined by 99mTc-HMPAO SPECT. ApoE genotypes were determined by digestion of ApoE polymerase chain reaction products with the restriction enzyme Hha1. RESULTS: patients with Alzheimer's disease had smaller volumes of hippocampi and amygdala compared with control subjects, and the patients with Alzheimer's disease homozygous for the epsilon 4 allele had the most prominent volume loss in the medial temporal lobe structures. The frontal lobe volumes did not differ significantly. All patients with Alzheimer's disease had bilateral temporoparietal hypoperfusion and the subgroups with one or no epsilon 4 alleles also had frontal hypoperfusion compared with control subjects. The occipital perfusion ratios tended to decrease with increasing number of epsilon 4 alleles. CONCLUSIONS: Patients with Alzheimer's disease homozygous for the epsilon 4 allele seem to have severe damage in the medial temporal lobe structures early in the disease process and differ from the patients with Alzheimer's disease with one or no epsilon 4 alleles.

Age of Onset↗
PubMed1995

Tetrahydroaminoacridine modulates technetium-99m labelled ethylene dicysteinate retention in Alzheimer's disease measured with single photon emission computed tomography imaging.

The present study investigated if acute treatment with tetrahydroaminoacridine (THA) (25 or 75 mg, p.o.) affects technetium-99m labelled ethylene dicysteinate (ECD) retention abnormalities in patients with mild to moderate Alzheimer's disease (AD; mean age 69 years). THA (75 mg) increased temporal, prefrontal and occipital ECD retention (normalized to cerebellum) in mildly demented AD patients, but 25 mg of THA had no effect on ECD retention. After 75 mg THA, prefrontal and temporal ECD retention correlated with improved executive and memory functioning, respectively. THA (25 or 75 mg) had no measurable effect on ECD retention of moderately demented patients.

Aged↗
PubMed1995

Regional cerebral blood flow measured by 99mTc-HMPAO SPECT differs in subgroups of Alzheimer's disease.

Alzheimer's disease (AD) is a heterogeneous entity. Identifying AD subtypes might have impact in patients' response to different treatment strategies. We designed a study to examine regional cerebral blood flow (rCBF) in AD subtypes. To identify AD subtypes, we performed a cluster analysis including performance on memory, language, visuospatial, praxic, and executive functions. The rCBF measured by 99mTc-HMPAO SPECT was referred to the cerebellum. We examined 35 patients fulfilling the NINCDS-ADRDA criteria of probable AD and 13 age and sex-matched healthy cognitively intact controls. AD patients were at the early stage of the disease, their mean Mini-Mental Status (MMS) score (S.D.) was 22.5 (3.6). The cluster analysis revealed two AD subgroups: AD1 (N = 12) and AD2 (N = 23). The subgroups did not differ in age, sex, or global clinical severity as assessed by MMS and Brief Cognitive Rating Scale (BCRS). Both subgroups had equally impaired memory. The AD2 group was inferior to the AD1 group on verbal, visuospatial, praxic, and executive functions. The AD1 group showed reduced rCBF ratios in the temporal and parietal cortices and the amygdala compared to controls. The AD2 group differed from controls in the rCBF ratios of frontal, temporal, parietal, occipital, basal ganglia, and amygdaloid regions bilateral and from AD1 in the rCBF ratios of frontal and temporal cortices. In AD patients, the rCBF ratios did not correlate with MMS or BCRS scores. In contrast, several significant correlations were found between decreases rCBF ratios and impairment of memory and other cognitive functions. In conclusion, a cluster analysis on neuropsychological test performance identified two AD subgroups that differed on the neuropsychological profile and on the rCBF in spite of similar global clinical severity.

Aged↗
PubMed1995

Altered striatal dopamine re-uptake site densities in habitually violent and non-violent alcoholics.

Animal studies suggest that development of substance dependence is associated with dopaminergic activity in striatum and the limbic system. Several genetic studies indicate that allele A1 is associated with both D2 receptor density and alcoholism, although these findings have remained controversial. We studied striatal dopamine (DA) re-uptake site densities in 48 subjects (19 healthy controls, 19 habitually impulsive violent alcoholics, and 10 non-violent alcoholics) with single photon emission computed tomography (SPECT) using iodine-123-labelled 2 beta-carbomethoxy-3 beta(4-iodophenyl)tropane, (beta-CIT) as a tracer. Blind quantitative analysis revealed that the striatal DA transporter density was markedly lower in non-violent alcoholics than in healthy controls (P < 0.001), while violent alcoholics had slightly higher DA transporter densities than controls (P < 0.10). The results indicate that both types of alcoholics have alterations in striatal dopaminergic system, though these occur in opposite directions.

Adult↗
PubMed1995

Myocardial sympathetic nervous dysfunction detected with iodine-123-MIBG is associated with low heart rate variability after myocardial infarction.

UNLABELLED: The association between myocardial sympathetic innervation and heart rate variability after myocardial infarction was studied in a group of 12 men (aged 30-65 yr) 3 mo after their first myocardial infarction. METHODS: Viable myocardium was imaged using 123I-phenylpentadecanoic acid (pPPA). Functioning myocardial sympathetic nervous tissue was imaged using [123I]-metaiodobenzylguanidine (MIBG). Heart rate variability was measured as the ratio of maximum-to-minimum RR intervals in ECG during deep breathing. RESULTS: The patients were divided into normal (n = 6) and low (n = 6) heart rate variability groups. Myocardial infarction size (pPPA defect) was comparable in the normal and low heart rate variability groups. Even the MIBG defect size was not significantly different in the normal and low groups, the portion of viable myocardium with impaired sympathetic innervation (MIBG defect minus pPPA defect) was significantly greater in the low heart rate variability group than in the normal group. CONCLUSION: The extent of viable myocardium with disturbed sympathetic innervation was greater in patients with low heart rate variability as compared to those with normal heart rate variability 3 mo after myocardial infarction.

3-Iodobenzylguanidine↗
PubMed1994

Extent of cardiac autonomic denervation in relation to angina on exercise test in patients with recent acute myocardial infarction.

According to the current concept, anginal pain results from stimulation of sympathetic nerves within the heart. In this study, we evaluated the role of cardiac adrenergic denervation in exercise-induced angina pectoris in 15 men with recent acute myocardial infarction. Before discharge from the hospital, the patients were subjected to a symptom-limited exercise test. Three months after the infarction, cardiac scintigraphic studies using I-123 metaiodobenzylguanidine (MIBG), I-123 paraphenylpentadecanoic acid (pPPA), and Tc-99m sestamibi (MIBI) were performed in order to determine the extent of denervated myocardium, the size of infarction, and myocardium with reduced perfusion, respectively. MIBG defect (17.2 +/- 7.6% of left ventricular mass) (defect defined as an activity distribution < or = 30% of the maximal myocardial activity) was larger than pPPA defect (8.3 +/- 8.8%, p < 0.001) in all patients, which indicates that the area of myocardial necrosis was surrounded by viable myocardium with sympathetic denervation. The extent of viable but denervated myocardium was significantly greater in patients who developed angina pectoris than in patients without angina pectoris during the early exercise test (13.3 +/- 4.4% vs 5.0 +/- 2.4%, p < 0.001). In addition, patients with silent ischemia tended to have smaller areas of viable but denervated myocardium than patients with painful ischemia (5.7 +/- 3.8% vs 13.8 +/- 5.1%, p = 0.07). Thus, contrary to expectations, the extent of viable but denervated myocardium seems to be associated with increased pain sensitivity in patients with recent myocardial infarction.

Adrenergic Fibers↗
PubMed1994

Increase in cerebral blood flow of right prefrontal cortex in man during orgasm.

The functional anatomy of human emotional responses has remained poorly understood, mainly because invasive experiments in humans are unacceptable due to ethical reasons. The new functional imaging techniques such as positron emission tomography and single photon emission computed tomography have made it possible to study the neurophysiology of living humans noninvasively. We studied the regional cerebral blood flow with semi-quantitative 99mTc-HMPAO single photon emission computed tomography in eight healthy right-handed heterosexual males during organism. The results showed decrease of cerebral blood flow during orgasm in all other cortical areas except in right prefrontal cortex, where the cerebral blood flow increased significantly (P < 0.005).

Adult↗
PubMed1994

Acute ethanol-induced changes in cerebral blood flow.

Using high-resolution single photon emission computed tomography, the authors studied changes in cerebral blood flow (CBF) in six healthy men after the men rapidly consumed intoxicating amounts of ethanol. When the subjects were given intravenous placebo before ethanol intake, regional CBF was significantly increased over baseline in the right prefrontal cortex, but no significant change in CBF was observed when the subjects received intravenous naloxone before ethanol intake. The results indicate that euphoria occurring during acute ethanol intake is associated with activation of the right prefrontal cortex and mediated through the endogenous opioid system.

Alcohol Drinking↗
PubMed1992

Analysis of left ventricular function from gated first-pass and multiple gated equilibrium acquisitions.

99mTechnetium-sestamibi is a new myocardial perfusion imaging agent that offers significant physical advantages over 201thallium for myocardial perfusion imaging. One of these advantages is that it can be used in the assessment of ventricular function by means of first-pass radionuclide angiography (FPRNA), acquired during the injection of the tracer. In this study we compared gated list mode first-pass acquisition with 99mTc-sestamibi (FP-MIBI) to multiple gated equilibrium radionuclide ventriculography (MUGA) with 99mTc-labelled red blood cells for the determination of global left ventricular ejection fraction (LVEF). The study population consisted of 20 patients (mean age 54 years) who were submitted to stress-rest perfusion imaging. Resting FPRNA was performed using 99mTc-sestamibi and the reference data were acquired within a week with the MUGA technique. A linear correlation between FP LVEF and MUGA LVEF gave an r = 0.974 (p < 0.01). Diastolic and systolic timing and velocity parameters had lower correlations between these two methods. We conclude that global LVEF can be precisely measured with 99mTc-sestamibi when compared to usually employed MUGA technique with 99mTc-labelled red blood cells.

Cardiac Output↗
PubMed1992

Noninvasive detection of cardiac sympathetic nervous dysfunction in diabetic patients using [123I]metaiodobenzylguanidine.

The association between clinical autonomic dysfunction and myocardial MIBG accumulation was investigated. The study groups comprised 6 male diabetic patients with autonomic neuropathy (ANP+ group), 6 male diabetic patients without autonomic neuropathy (ANP-group), and 6 male nondiabetic control subjects. The mean age was comparable in all groups, and the subjects had no evidence of coronary heart disease. Reduced heart-rate variation in a deep-breathing test was used as a criterion for autonomic neuropathy. Immediately after injection, the peak net influx rate of MIBG to myocardium was significantly (P less than 0.05) reduced in both diabetic groups. At 6 hr after MIBG injection, the MIBG uptake of the myocardium was significantly (P less than 0.05) smaller in the ANP+ group than in the control group. In the ANP- group, the MIBG uptake of the myocardium was between that of the ANP+ group and that of the control group. Our data show that reduced myocardial MIBG accumulation is associated with autonomic dysfunction in diabetic patients, but it can occur to a lesser extent also in diabetic patients without apparent autonomic neuropathy. The measurement of the myocardial MIBG accumulation is a promising new method to detect cardiac sympathetic nervous dysfunction in diabetic patients.

3-Iodobenzylguanidine↗