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A low plasma arginine vasopressin (AVP) responsiveness to hypertonic saline infusion has been described in bulimic women. At present, it is unknown whether this phenomenon is peculiar for the osmotic regulation of AVP secretion or whether it represents an aspect of a more general disorder of AVP secretion in bulimia nervosa. In order to answer these questions, in the present study the AVP responses to metoclopramide (MCP) (20 mg in an i.v. bolus) and insulin (0.15 IU/kg)-induced hypoglycemia were tested in normal weight bulimic women and in weight- and age-matched normal women. Basal AVP concentrations were similar in normal and bulimic women. In the normal controls, plasma AVP levels rose 2.6 times after MCP and 2.2 times in response to hypoglycemia. Both AVP increments were significantly lower in bulimic patients. In this group, plasma AVP levels rose 2 times after MCP and 1.8 times in response to hypoglycemia. When data of the MCP and insulin tolerance test were combined, regression analyses showed a significant positive correlation between AVP peak responses to MCP and hypoglycemia in the bulimic group. These data show an impaired AVP response to different releasing stimuli in bulimia, suggesting that a more general disorder than a simple change in the sensitivity to osmotic stimulation affects the AVP secretory system in bulimic patients. It is likely that bulimic subjects are affected by a neuroendocrine alteration in the control of AVP secretion, whose mechanisms are still unknown.

In order to test possible changes in the stimulating effect of intravenously-infused substance P (SP) on ACTH/cortisol and GH secretion in Parkinson's disease, 10 male parkinsonian patients and 10 age-matched normal controls were infused intravenously for 60 min with SP (1.0 or 1.5 pmol/kg-1/min-1 SP) or normal saline. The circulating levels of ACTH, cortisol and GH were measured during and for 20 min after SP or saline infusion. No untoward side effects or changes in blood pressure were observed during SP infusion in any subjects. In basal conditions and during saline infusion, plasma ACTH and cortisol levels were similar in normal and parkinsonian patients. During SP infusions, ACTH/cortisol concentrations in normal controls rose significantly vs baseline and saline test in a dose-dependent fashion. In contrast, at both SP infused amounts, parkinsonian patients showed ACTH/cortisol levels similar to those observed in the saline test. All subjects showed similar basal concentrations of GH. GH levels rose significantly in the normal controls when the higher dose of SP was infused, but they were not modified by the infusion of the lower dose of SP or saline. At both tested amounts of SP and during saline infusion, GH levels remained unchanged in the parkinsonian subjects. In agreement with previous observations in the literature showing SP abnormalities in the parkinsonian brain, these data fail to show significant effects of plasma SP on the ACTH/cortisol and GH secretory systems in Parkinson's disease.

Several lines of evidence suggest impaired right hemisphere function in depression. In order to further investigate this phenomenon, simple reaction times (RTs) to lateralized visual stimuli were studied in patients with mild unipolar depression, in patients with chronic anxiety, and in medical patients free of psychiatric symptoms. The results showed a marked slowing of RTs to left visual field (right hemisphere) stimuli in depressed patients. Anxious patients showed a trend toward an opposite asymmetry, with slower responses to right field (left hemisphere) stimuli. In the nonpsychiatric group no visual field differences were present. The results are discussed in light of two alternative interpretations: depression may engage the right hemisphere's mechanisms, interfering with its functioning at a premotor level, or it may influence the regulation of performance by arousal and vigilance mechanisms lateralized to the right hemisphere, possibly operating at an earlier sensory stage.

The Fuld formula and the linear discriminant function applied to WAIS subtest scores were tested for their ability to identify Alzheimer's disease and senile dementia of the Alzheimer type in a group of 101 demented subjects. The sensitivity and specificity of Fuld's formula for Alzheimer dementia against other dementias were 44.2% and 73.8% respectively; when compared with an age-matched normal control group specificity was 91.4%. When the linear discriminant function was applied only WAIS subtest scores in "similarities and digit span" and "object assembly" significantly differentiated Alzheimer from other dementias (sensitivity 61.5% and specificity 63.3%). Specificity increased to 97.1% when the function was applied to discriminate Alzheimer from normal controls. Discriminant analysis applied to other WAIS subtests for the two demented groups revealed "picture completion" as significantly differentiating the groups but it did not contribute to diagnostic accuracy. WAIS scores are of limited value in the differential diagnosis of dementias.

In order to establish whether the inhibitory control exerted by endogenous opioid peptides on ACTH/cortisol secretion changes in patients affected by Parkinson's disease, ten parkinsonian male subjects and eight age matched normal controls were tested with naloxone (4 mg an i.v. bolus plus 10 mg infused in two hours). In a different occasion all subjects were tested with normal saline. Experiments started at 09.00 h. Plasma ACTH and cortisol concentrations showed a slight physiological decline during saline test in both groups. In the normal controls and in the parkinsonian patients both ACTH and cortisol levels were significantly higher after naloxone administration than during saline test. However, both naloxone induced ACTH and cortisol responses were significantly higher in normal than in parkinsonian subjects. In agreement with the well-known opioid deficiency characterizing the parkinsonian brain, these data show a reduced opioid inhibitory control of ACTH/cortisol secretion in patients with Parkinson's disease.

In order to evaluate whether the stimulating effect of GABA on growth hormone (GH) secretion changes in patients affected by Parkinson's disease, ten male parkinsonian patients and ten age matched normal controls were tested with the GABA derivative and GABAergic agent Baclofen (10 mg in a single oral administration at 09.00 h) (experimental test). In a different occasion, normal men and parkinsonian patients were tested with a placebo (control test). Basal GH levels were similar in normal controls and parkinsonian patients and remained unmodified during the control test. Plasma GH levels rose three times within 120 min after the administration of baclofen in the normal subjects. In contrast, plasma GH concentrations remained unmodified after baclofen treatment in the parkinsonian patients. In agreement with previous reports in the literature showing alterations of GABAergic neurotransmission in the parkinsonian brain, these data show a reduced GABAergic control of GH secretion in patients with Parkinson's disease.

The Authors, considering the insufficiency of data in this condition, have studied the memory functions in patients who, in the follow up after an episode of TGA, did not show any clinical sign. A selective loss of a short-term "verbal" memory, without any psychometric alteration, is found out. The meaning of those observations is discussed with regard to the possible further differentiation of TGA syndrome in acute and chronic phases.

The case of a right-handed man with pure alexia without hemianopia due to intraparenchymal haematoma is reported. Ct scan and nuclear magnetic resonance showed a lesion in the lateral temporo-occipital area confirming the assumption that the anatomic pathways responsible for reading run close to the lateral temporo-occipital or inferior temporal gyrus.

Sixteen patients, who had suffered only one episode of transient global amnesia and showed no clinically evident abnormalities in their follow-up, were examined with psychometric and memory tests. Deficits in verbal long-term memory and in verbal IQ were found. These observations seem to demonstrate that in transient global amnesia patients regarded as being 'normal' in their follow-up there is no complete recovery and the sequelae seem to conform to a definite pattern. Problems of nosology and localization are discussed.

Twenty-one patients showing memory deficits were submitted to neuropsychological battery, before and after treatment with Deanol. No significant effect has been found. Arguments suggesting further investigation are discussed.

Three cases of complicated migraine are reported. A few days after neurological accidents, one patient showed an angiographic evidence of diffuse cerebral vasospasm. This finding possibly bears out vasomotor hypothesis of migraine.

The Authors report the case of a 32-years-old woman taking oral contraceptives for twelve years, who developed multi-infarct dementia and motor-sensory signs as a consequence of repeated cerebrovascular episodes associated with migraine-like attacks. Neuroradiological findings suggested vascular pathologic changes. Mechanisms of cerebro-vascular diseases related to oral contraception are discussed, especially emphasizing the possibility of intrinsic vascular lesions caused by exogenous steroid stimulation. Epidemiologic and pathophysiological relationship between migraine, stroke and oral contraception are also pointed out.

The authors report two cases of motor apraxia, agraphia and tactile anomia on the left side, associated with bilateral constructive apraxia. These cases are discussed in relation to their unusual etiology and in relation to possible pathogenetic hypothesis other than classical Liepmann's scheme.

A case of permanent global amnesia resulting from a bilateral hippocampal lesion is reported, remarkable for its typical clinical picture and prolonged period of observation with repeated neuropsychological testing. No tendency toward spontaneous recovery was noted, even though extra-mnesic cognitive functions remained undamaged. No differences were observed between this amnesic syndrome and the neuropsychological picture during an acute episode of transient global amnesia.

Simple reaction times to visual stimuli were studied in 8 patients affected by depression and in 8 normal subjects. Regardless of the hand used, the condition of depression produced a specific lengthening of the responses to stimuli located in the left visual field. It is concluded that the right hemisphere plays a major role in modulation of negative emotional behaviour.