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Biomedical subjects

P Caffarra

Publications and source records attributed to P Caffarra.

At least 19 recordsLinked to original sources
PubMed2003

A normative study of a shorter version of Raven's progressive matrices 1938.

A shorter four-set (A, B, C, D) version of Raven's progressive matrices 1938 (PM38) has gained increasing use in neuropsychological assessment. No normative data spanning across a wide age range are, however, available. This study collected norms for the shorter version of PM38, established an inferential cut-off value and derived equivalent scores in a sample of 248 individuals from 20 to 89 years of age, evenly distributed across sex, age and education levels. Results showed significant effects of age and education but no effect of sex on performance. These normative data will complement existing norms for other tests, will increase the wealth of neuropsychological tools for which normative data are available for the Italian population, and may be useful in the early detection of individuals at risk of developing dementia.

Adult↗
PubMed2002

Rey-Osterrieth complex figure: normative values in an Italian population sample.

The Rey-Osterrieth complex figure test (ROCF) is a neuropsychological test extensively used in clinical practice to investigate visuospatial constructional functions, visuographic memory and some aspects of planning and executive function. The aim of the present study was to collect normative values in an Italian normal population sample (n=280) for the direct copying and delayed (10 min) reproduction of the ROCF. Multiple regression analysis revealed significant effects of age and education on performance of both copying tasks, whereas sex appeared to affect only performance on the delayed copying task. Inferential cut-offs have been determined and equivalent scores computed. The availability of equivalent scores for the ROCF will prove useful in clinical assessment since it allows the comparison of a subject's performance on the ROCF with that on other neuropsychological tests for which normative values collected with similar methods are already available for the Italian population.

Adult↗
PubMed2000

Muscarinic cholinergic mediation of the GH response to gamma-hydroxybutyric acid: neuroendocrine evidence in normal and parkinsonian subjects.

We have recently reported that parkinsonian patients show a significant GH response to gamma-hydroxybutyric acid (GHB), but not to gamma-aminobutyric acid (GABA)-ergic drug administration. In order to establish whether muscarinic cholinergic receptors mediate the GH secretion induced by GHB, normal men and parkinsonian patients were tested with GHB both in the absence and in the presence of the anticholinergic agent, pirenzepine. Both normal controls and parkinsonian patients showed a significant serum GH rise in response to GHB (25 mg/kg body weight p.o.) even though a slightly, but significantly lower response was observed in parkinsonian patients. Pretreatment with pirenzepine (100 mg p.o. 2 h before GHB) completely suppressed the GHB-induced GH release in both normal controls and parkinsonian patients. These data indicate that a cholinergic mechanism mediates the GH response to GHB in normal men. In addition the data indicate that this pathway is preserved in the parkinsonian brain.

Aged↗
PubMed1999

Neural basis of endogenous and exogenous spatial orienting. A functional MRI study.

Whole-brain functional magnetic resonance imaging (MRI) was used to examine the neural substrates of internally (endogenous) and externally (exogenous) induced covert shifts of attention. Thirteen normal subjects performed three orienting conditions: endogenous (location of peripheral target predicted by a central arrow 80% of the time), exogenous (peripheral target preceded by noninformative central cue). Behavioral results indicated faster reaction times (RTs) for valid than for invalid trials for the endogenous condition but slower RTs for valid than for invalid trials for the exogenous condition (inhibition of return). The spatial extent and intensity of activation was greatest for the endogenous condition, consistent with the hypothesis that endogenous orienting is more effortful (less automatic) than exogenous orienting. Overall, we did not observe distinctly separable neural systems associated with the endogenous and exogenous orienting conditions. Both exogenous and endogenous orienting, but not the control condition, activated bilateral parietal and dorsal premotor regions, including the frontal eye fields. These results suggest a specific role for these regions in preparatory responding to peripheral stimuli. The right dorsolateral prefrontal cortex (BA 46) was activated selectively by the endogenous condition. This finding suggests that voluntary, but not reflexive, shifts of attention engage working memory systems.

Adult↗
PubMed1998

Cognitive dysfunction and impaired organization of complex motility in degenerative parkinsonian syndromes.

BACKGROUND: A frontostriatal pattern of cognitive decline, consisting of a frontal lobe-like syndrome without genuine cortical defects such as amnesia, apraxia, aphasia, or agnosia, is well established in basal ganglial diseases. Recent pathological investigations, however, have again noted cortical damage in progressive supranuclear palsy (PSP), suggesting that cortical defects could be present. OBJECTIVES: To delineate the pattern of cognitive impairment and to detect higher-order motor impairments (including ideomotor apraxia) in parkinsonian syndromes. PATIENTS AND METHODS: We assessed ideomotor apraxia, and simple and sequential tapping in patients with Parkinson disease, multiple system atrophy, and PSP with similar disease severity, age range, and education. We also administered a comprehensive battery of neuropsychological tests to examine general intelligence, memory, executive functions, attention, and visuospatial orientation. The results were compared between groups and with a matched normal control group. RESULTS: Sequential tapping and the imitation of sequences of gestures were impaired in all patient groups, with patients with PSP performing worse than the other groups. Based on ideomotor apraxia scores and a qualitative analysis of errors, 3 patients with PSP and 2 with multiple system atrophy were considered apraxic. General intelligence and executive functions were compromised in all patient groups. The impairment of patients with PSP was more pervasive than that of the other groups, and included compromise of visuospatial functions, attention, and memory. Discriminant analysis of all cognitive and motor tests showed that the tapping and ideomotor apraxia tests best identified the patients vs control subjects. CONCLUSIONS: The presence of cortical as well as subcortical damage in patients with PSP and those with multiple system atrophy is indicated by the presence of pervasive cognitive and motor disturbances in the former, substantial motor disorganization in the latter, and the finding of ideomotor apraxia in some patients with these diseases. Furthermore, the discovery that tests of motor and gesture best identified all patients vs control subjects is consistent with the existence of a common motor disorganization in these parkinsonian syndromes, in agreement with the known damage to the corticostriatal pathways in these conditions.

Aged↗
PubMed1998

Transient autobiographic amnesia: EEG and single-photon emission CT evidence of an organic etiology.

We describe a 44-year-old patient who had a transient attack of autobiographic amnesia. When assessed during the attack, her learning abilities were normal, with no sign of anterograde amnesia. In the remote memory domain, she showed a striking dissociation between a detailed knowledge of public events and famous people and a complete loss of autobiographic information. During the attack, EEG recorded bilateral frontotemporal slow waves and single-photon emission CT (SPECT) showed hypoperfusion in the right temporal and parietal lobes; no abnormalities were detected when both EEG and SPECT were repeated 1 week later. This case provides evidence for an organic etiology for the episode and supports the hypothesis that autobiographic memory is independent of other forms of retrograde memory.

Adult↗
PubMed1997

Different control mechanisms of growth hormone (GH) secretion between gamma-amino- and gamma-hydroxy-butyric acid: neuroendocrine evidence in Parkinson's disease.

The observation that baclofen stimulates growth hormone (GH) secretion in normal men, but not in parkinsonian patients led us to test the GH releasing effect of other gamma-amino-butyric acid (GABA)ergic agents with different mechanisms of action in Parkinson's disease. For this purpose 10 normal men and 10 de novo parkinsonian patients were tested with sodium valproate (800 mg PO), gamma-hydroxybutyric acid (GHB) (25 mg/kg body weight PO) and baclofen (10 mg PO). All drugs induced a significant increment in serum GH levels in the normal controls. On the other hand, GH secretion in parkinsonian patients did not change after baclofen or sodium valproate administration, whereas it showed normal responsiveness to GHB. These data suggest that the mechanism underlying the GH response to GHB is different from that (or those) mediating sodium valproate and/or baclofen action. In addition, the former, but not the latter mechanism appears to be preserved in the parkinsonian brain.

Aged↗
PubMed1997

ACTH/cortisol involvement in the serotonergic disorder affecting the parkinsonian brain.

In order to establish whether the serotonergic disorder affecting the parkinsonian brain also modifies hypothalamic-pituitary function in Parkinson's disease, 10 patients (aged 57-66 years) and 10 normal controls (aged 55-69 years) were tested with the serotonergic agonist d,l-fenfluramine (60 mg p.o.), with CRH (100 micrograms i.v.) and with placebos. Plasma ACTH/cortisol levels during tests were evaluated and compared. Both groups showed similar levels of ACTH and cortisol in basal conditions and after placebo administration. A slight physiological decline in both ACTH and cortisol levels during the placebo test was observed in normal controls and parkinsonian patients. CRH induced similar ACTH/cortisol increments in all subjects. In contrast, d,l-fenfluramine significantly increased plasma ACTH/cortisol concentrations in the normal controls, but not in the parkinsonian patients. These data show a defective serotonergic control of the pituitary-adrenal axis in Parkinson's disease.

Adrenocorticotropic Hormone↗
PubMed1997

Defective 5-HT 1-receptor-mediated neurotransmission in the control of growth hormone secretion in Parkinson's disease.

In order to gain a better insight in the serotonergic disorder affecting the parkinsonian brain, the growth hormone (GH) response to the 5-HT 1 serotonergic receptor agonist sumatriptan was tested. Sumatriptan was injected subcutaneously in 10 de novo parkinsonian patients (aged 58-69 years) and in 9 age-matched normal controls. On different occasions, subjects were also tested with GH-releasing hormone (GH-RH; 1 micrograms/kg body weight in an intravenous bolus) and L-arginine (30 g in 50 ml normal saline over 30 min), which releases GH from somatostatin inhibition, to determine whether GH secretion in response to alternate secretagogues is preserved in Parkinson's disease. In addition, a control test with the administration of normal saline instead of drug treatments was performed. Plasma GH levels were recorded over 2 h in all tests. Placebo administration did not change plasma GH levels in any subject. Similar GH responses were observed in normal controls and parkinsonian patients when GH-RH or arginine were administered. A significant GH increase was observed in normal controls after sumatriptan injection; in contrast, GH secretion was not modified by sumatriptan administration in parkinsonian patients. These data show that Parkinson's disease is associated with an impairment in the 5-HT1-receptor-mediated serotonergic transmission in the control of GH secretion, suggesting that this specific defect might alter other serotonergic-mediated mechanisms in the parkinsonian brain.

Aged↗
PubMed1997

Orienting of visual attention in Alzheimer's disease: its implication in favor of the interhemispheric balance.

Visual attention in dementia of Alzheimer's disease (AD) has not been investigated as extensively as memory or language. The aim of this research was to study the orienting of attention in patients with AD (which temporo-parietal areas are primarily affected) compared with patients with Parkinson-Dementia, Parkinson's disease, and normal controls, using the Posner paradigm. Subjects were instructed to respond by pressing a response key after the appearance of a target at the same location (valid trial) or at the opposite location (invalid trial) indicated by a central cue (arrow). According to the experimental procedure developed by Posner, it has been hypothesized that parietal lobes are involved in "disengagement operation" (when attention has to move from one location to another in the controlateral field). Results showed no differences between AD and the other groups and between left and right hemifield. In conclusion, the authors did not find any sign of difficulty with disengagement, and results are discussed in terms of Kinsbourne's interpretation of a balance between hemispheres.

Aged↗
PubMed1997

Randomised, double-blind, placebo-controlled study of pivagabine in neurasthenia.

One hundred and eighteen patients with neurasthenia, as defined by ICD 10 (International Classification of Diseases), participated in a randomised, double-blind, placebo-controlled trial of pivagabine (4-[(2,2-dimethyl-1-oxopropyl)amino]butanoic acid, CAS 69542-93-4, Tonerg). Pivagabine 1800 mg/d was administered orally for four weeks. At the end of the trial, active medication was significantly superior to placebo on the Clinical Global Impression (CGI) improvement of illness scale. In addition, pivagabine treatment reduced the physical and mental fatigability of patients, and increased their sense of well-being.

Adolescent↗
PubMed1995

Effect of substance P on basal and thyrotropin-releasing hormone-stimulated thyrotropin release in humans.

To test the possible effects of intravenous administration of substance P (SP) on basal and thyrotropin-releasing hormone (TRH)-stimulated thyrotropin (TSH) release, SP was infused alone (0.5 or 1.5 pmol/kg-1/min-1 for 60 minutes) or after TRH (20 or 400 micrograms in an intravenous bolus) in 21 normal male subjects (aged 26 to 36 years) and in 18 normal women (aged 25 to 32 years). Women were studied during follicular (day 6 to 8) and luteal (day 21 to 23) phases of following regular menstrual cycles. In addition, plasma cortisol levels during SP infusion were measured. In agreement with previous findings, significant increments in plasma cortisol levels were observed in men and women when the higher (1.5 pmol/kg-1/min-1) but not the lower (0.5 pmol/kg-1/min-1) amount of SP was administered. In contrast, in both men and women basal and TRH (20 or 400 mg)-induced TSH releases were not modified by SP at any tested amount. Results in the follicular and luteal phase were similar. These data suggest that in normal men and women plasma SP is not involved in the control of TSH release, at least not outside the blood-brain barrier.

Adult↗
PubMed1995

Low-dose ovine corticotropin-releasing hormone stimulation test in diabetes mellitus with or without neuropathy.

The function of the hypothalamic-pituitary-adrenal (HPA) axis was evaluated in insulin-dependent diabetics without (group I, n = 10) or with (group II, n = 10) established symptomatic neuropathy and in age- and weight-matched normal controls (n = 11). Since the corticotropin (ACTH)/cortisol response to the minimal-effective dose of corticotropin-releasing hormone ([CRH] 0.03 microgram/kg body weight) represents a useful tool for HPA axis examination, all subjects were tested with the low-dose ovine CRH stimulation test. Experiments started at 8:30 AM, when CRH was injected after two basal blood samples were withdrawn, and lasted 2 hours. Basal serum levels of ACTH were similar in the three groups. Administration of CRH induced a small but significant increase in ACTH levels in all subjects; however, the CRH-induced ACTH increase was significantly higher in normal controls than in diabetic groups I and II. Furthermore, a significantly lower ACTH response was observed in group II than in group I. In contrast, basal and CRH-induced cortisol levels were significantly higher in diabetics than in normal controls. Comparisons between diabetic groups showed that both basal and stimulated cortisol secretion was significantly higher in group II than in group I. When peak ACTH responses to CRH and basal cortisol levels were combined, a significant negative correlation was found (r = .545, P < .02). These data show that even uncomplicated diabetes mellitus is associated with adrenal hyperfunction. Such an alteration is more pronounced in the presence of neuropathy.

Adrenocorticotropic Hormone↗
PubMed1994

Lack of seasonal variation in abnormal TSH secretion in patients with seasonal affective disorder.

The circadian variations in thyroid-stimulating hormone (TSH) secretion, with particular attention to the nocturnal serum TSH surge and the TSH response to thyrotropin releasing hormone (TRH), were measured in seven patients with seasonal affective disorder (SAD) and in eight normal controls. Both patients with SAD and normal controls were tested in fall/winter, when patients were suffering depressive symptoms, and in spring/summer, when patients were euthymic. The TRH tests were performed in the morning. In all tests, the mean peak TSH response to TRH was significantly lower in the patients with SAD than in the normal controls. No significant differences were observed in either group between spring/summer and fall/winter tests. At both periods, patients with SAD showed normal TSH levels in the morning, but did not experience a nocturnal TSH surge. In this group, morning and night TSH levels were similar. In contrast, normal controls showed significantly higher TSH levels at night than in the morning. Serum-free thyroid hormone levels were in the normal range in all subjects. Morning and night serum cortisol levels and 24-hour urinary cortisol concentrations were similar in all subjects. These data show that the secretion of TSH is impaired in SAD, regardless of the phase of the psychiatric disease. The low TSH response to TRH in the presence of normal serum thyroid hormone levels and the lack of the TSH nocturnal surge suggest that patients with SAD might be affected by mild central hypothyroidism.

Adult↗
PubMed1994

Restoration of ACTH/cortisol and LH responses to naloxone by chronic dopaminergic treatment in Parkinson's disease.

Naloxone is unable to stimulate ACTH/cortisol secretion in patients with de novo Parkinson's disease, suggesting a reduced endogenous opioid control of the hypothalamic-pituitary-adrenal axis in parkinsonian patients. In the present study we examined whether Parkinson's disease also impairs the secretion of LH, which is under the inhibitory control of different opioid peptides than ACTH/cortisol. In addition, we examined whether a chronic dopaminergic therapy for at least one year with levodopa (450 mg/day) plus benserazide (112.5 mg/day) in 3 divided oral doses/day of Madopar modifies the ACTH/cortisol and/or the LH response to naloxone (4 mg as an i.v. bolus plus 10 mg infused in 2 hours). Ten parkinsonian patients (aged 52-62 years) and 8 normal controls (50-60 years) were tested with naloxone and in a different occasion with normal saline. The parkinsonian patients were tested both before and after dopaminergic treatment. Tests started at 09.00 h and lasted 2.5 hours. Basal ACTH/cortisol and LH levels were similar in all groups. During saline tests, ACTH/cortisol levels showed a slight physiological decline in all groups, whereas LH levels remained constant. Naloxone administration significantly increased the plasma levels of ACTH/cortisol and LH in the normal controls, but not in the parkinsonian patients before the dopaminergic treatment. In contrast, dopaminergic therapy restored significant ACTH/cortisol and LH responses to naloxone in parkinsonian patients. In fact, after levodopa plus benserazide, naloxone-induced ACTH, cortisol and LH increments in parkinsonian patients were significantly higher than before therapy and were indistinguishable from those observed in the normal controls. These data suggest that in men Parkinson's-related dopaminergic alterations may underlie the defective endogenous opioid control of ACTH/cortisol and LH secretion.

Adrenocorticotropic Hormone↗
PubMed1994

Differing patterns of psychiatric impairment in Alzheimer and demented parkinsonian patients.

Psychiatric symptoms were investigated and compared in 95 patients with Alzheimer type dementia (DAT) and in 39 patients with Parkinson's disease with dementia (PD-D). The diagnosis of the dementia and psychiatric disorders was based on DSM III R criteria; dementia stage was assessed using the Clinical Dementia Rating Scale (CDR). PD-D were significantly older than DAT patients. Delirium was more frequent in the advanced stages of both PD-D and DAT, being mainly of the hypoactive type in PD-D and the hyperactive type in DAT. Delusions and hallucinations predominated in the early CDR stages of both illnesses and did not differ between groups; the same was true for depression. The results revealed different psychopathological profiles in DAT and PD-D patients.

Aged↗