Background/Aims: Vitamin B12 and folate deficiencies have been associated with cognitive impairment and various psychiatric symptoms but not specifically with behavioural and psychological symptoms of dementia (BPSD). A limitation of previous studies in dementia was lack of concurrent homocysteine measurement especially as it may provide a better indicator of tissue activities of these vitamins. This study was designed to clarify whether a relationship exists between plasma homocysteine concentration and BPSD.

Methods: Plasma homocysteine, serum vitamin B12 and folate were measured in 23 Alzheimer's disease (AD) patients with BPSD and 27 AD patients without BPSD as determined through the use of the Neuropsychiatric Inventory (NPI). Blood levels of measured substances were also correlated with individual NPI scores and with cumulative NPI scores for different cluster of symptoms.

Results: There was no significant difference (p = 0.956) in the mean plasma homocysteine levels between AD patients with BPSD (17.48 μmol/l) and AD patients without BPSD (17.34 μmol/l). Similarly, there was no significant difference between the two groups in the mean serum B12 (382.61 and 391.60 pg/ml, respectively) and folate (7.95 and 10.02 ng/ml, respectively). Mean levels for both vitamins were well within the laboratory reference range. Neither individual nor cluster NPI scores correlated significantly with plasma homocysteine.

Conclusion: This study shows for the first time that BPSD are not associated with hyperhomocysteinaemia in Alzheimer dementia. Although previous studies have identified homocysteine as an independent riskfactor in AD, the results reported here do not lend weight to an aetiological role for homocysteine specifically in BPSD. Copyright © 2006 S. Karger AG.

A 31-year-old single man (AB) sought neuropsychiatric consultation for treatment-resistant motor and vocal tics. He described himself expressing a total of 24 different tics, mainly facial twitches (eye blinking, raising eyebrows, mouth opening, lips licking, stereotyped grimacing) and inappropriate utterances (grunting, throat clearing, sniffing), since the age of 7. There appeared to be no family history of tic disorder. He reported occasional utterance of swear words in contextually inappropriate situations (coprolalia), and the urge to copy other people’s movements (echopraxia). Other tic-associated symptoms included self-injurious behaviours and forced touching of objects. A.B. met both DSM-IV-tr and ICD-10 criteria for Tourette syndrome, and also DSM-IV-tr criteria for attention deficit hyperactivity disorder (combined type) in childhood.

Rapid tryptophan (Trp) depletion (RTD) has been reported to cause deterioration in the quality of decision making and impaired reversal learning, while leaving attentional set shifting relatively unimpaired. These findings have been attributed to a more powerful neuromodulatory effect of reduced 5-HT on ventral prefrontal cortex (PFC) than on dorsolateral PFC. In view of the limited number of reports, the aim of this study was to independently replicate these findings using the same test paradigms. Healthy human subjects without a personal or family history of affective disorder were assessed using a computerized decision making/gambling task and the CANTAB ID/ED attentional set-shifting task under Trp-depleted (n=17; nine males and eight females) or control (n=15; seven males and eight females) conditions, in a double-blind, randomized, parallel-group design. There was no significant effect of RTD on set shifting, reversal learning, risk taking, impulsivity, or subjective mood. However, RTD significantly altered decision making such that depleted subjects chose the more likely of two possible outcomes significantly more often than controls. This is in direct contrast to the previous report that subjects chose the more likely outcome significantly less often following RTD. In the terminology of that report, our result may be interpreted as improvement in the quality of decision making following RTD. This contrast between studies highlights the variability in the cognitive effects of RTD between apparently similar groups of healthy subjects, and suggests the need for future RTD studies to control for a range of personality, family history, and genetic factors that may be associated with 5-HT function.

Rationale Alcohol impairs explicit memory, whilst leaving
implicit memory relatively intact. Less is known about its
effects on false memories.
Aim The present study examines the effects of alcohol on
explicit and implicit false memories using study list
repetition as a tool for modulating learning at encoding.
Methods Thirty-two participants were given either an
alcohol (0.6 g/kg) or placebo beverage before undergoing
an encoding phase consisting of 10 lists of nine associated
words (veridical items). Each list was associated to a word,
which was not presented at encoding (semantically associated
non-studied lure; critical item), serving as the measure
for false memory. Half of the lists were presented once, and
half were repeated three times. The next day, participants
underwent an implicit (stem completion and post hoc
awareness measurements), and an explicit (free recall) task.
Results Alcohol decreased veridical and false explicit
memory for singularly presented lists compared to placebo;
no group difference existed for repeated lists. Implicit
veridical memory was not affected by alcohol. Awareness
memory measures demonstrated in placebo participants an
increased ability with repetition in rejecting false memories.
The reverse was found in intoxicated participants who with
repetition accepted more false memories.
Conclusion Alcohol appears to decrease semantic activation
leading to a decline in false memories. Increased
learning with repetition, which increases the rejection of
false memories under placebo, is reversed under alcohol
leading to a decrease in rejection of false memories. The
latter effect of alcohol may be due to its ability to impair
monitoring processes established at encoding.

Introduction. The aim of this study was to explore social and emotional functions in patients with medial frontal damage including the anterior cingulate cortex (ACC).

Methods. Three patients with medial frontal lobe lesions primarily involving the ACC performed tasks on motivational decision making, emotional facial expression recognition, and social cognition, including theory of mind (ToM). Their performance on these tasks was compared with age and education matched healthy controls.

Results. Patient performance on the motivational decision making and social situations tasks did not differ from controls. Selective emotional facial expression recognition impairment for fear was evident in one patient with a unilateral right ACC lesion (patient 3). ToM impairment was present in only one patient with a bilateral ACC lesion (patient 2). In contrast, the two patients with unilateral right ACC lesions had intact ToM (patients 1 and 3).

Conclusions. These findings suggest that medial frontal lobe lesions primarily involving the ACC do not appear to critically disrupt motivational decision making or social situation processing. The ACC plays a role in processing particular types of emotion (fear). Bilateral ACC damage impairs ToM processing, but unilateral damage to the right ACC is not sufficient to disrupt ToM.

Empathic responses underlie our ability to share emotions and sensations with others. We investigated whether observed pupil size modulates our perception of other's emotional expressions and examined the central mechanisms modulated by incidental perception of pupil size in emotional facial expressions. We show that diminishing pupil size enhances ratings of emotional intensity and valence for sad, but not happy, angry or neutral facial expressions. This effect was associated with modulation of neural activity within cortical and subcortical regions implicated in social cognition. In an identical context, we show that the observed pupil size was mirrored by the observers' own pupil size. This empathetic contagion engaged the brainstem pupillary control nuclei (Edinger-Westphal) in proportion to individual subject's sensitivity to this effect. These findings provide evidence that perception-action mechanisms extend to non-volitional operations of the autonomic nervous system.

Automatic facial categorization along dimensions such as familiarity, gender, race, expression and age facilitates social exchange. Here we focus on familiarity and gender in order to gauge their independence. Previous experiments are equivocal as to whether these dimensions are processed independently or not (Bruce and Young, 1986; Goshen-Gottstein and Ganel, 2000). If familiarity and gender were independent then facilitation or inhibition of one should not affect future performance on the other. Famous and unfamiliar faces were presented in a series of go no-go tasks. External features were removed ensuring that both famousness and gender decisions were based on the internal features of a face. Faces were presented in paired blocks such that a gender block (e.g., go male, no-go female) was followed by a familiarity block (e.g., go famous, no-go unfamiliar) or vice versa. The first block of each pair consisted of five famous males, five famous females, five unfamiliar males, and five unfamiliar females (each presented twice) in a random order. The second block consisted of the previously seen faces from the first block (old) with an additional 20 new faces (five of each type) so that every block contained 20 go and 20 no-go stimuli. An experimental session consisted of 16 counterbalanced block pairs. Results indicate that only unfamiliar faces solicit automatic gender categorization. When observers made a no-go decision on unfamiliar faces based on familiarity they were subsequently slower to determine the gender of those faces compared to previously unseen faces. However, if they made a no-go decision on unfamiliar faces based on gender, subsequently they were faster to determine the unfamiliarity of those faces relative to previously unseen faces. This interaction was not found for famous faces. Since in the present studies familiarity and famousness were correlated, at this juncture it is not clear whether the results will hold for familiar but not famous individuals. We conclude automatic gender categorization is part and parcel of the `identity' of 44 unfamiliar faces. Familiarity results in the differentiation of identity from gender. In others words, unfamiliar individuals are automatically coded as male or female whereas Madonna is not.

In health, emotions are integrated with autonomic bodily responses. Emotional stimuli elicit changes in somatic (including autonomic) bodily states, which feedback to influence the expression of emotional feelings. In patients with spinal cord injury (SCI), this integration of emotion and bodily arousal is partially disrupted, impairing both efferent generation of sympathetic responses and afferent sensory feedback of visceral state via the spinal cord. A number of theoretical accounts of emotion predict emotional deficits in SCI patients, particularly at the level of emotional feelings, yet evidence for such a deficit is equivocal. We used functional MRI (fMRI) and a basic emotional learning paradigm to investigate the expression of emotion-related brain activity consequent upon SCI. We scanned seven SCI patients and seven healthy controls during an aversive fear conditioning task. Subjects viewed randomized presentations of four angry faces. One of the faces (CS + arm) was associated with delivery of electrical shock to the upper arm on 50% of trials. This shock was painful to all subjects. A face of the same gender acted as a safe' control stimulus (CS - arm). In both control subjects and SCI patients, painful cutaneous stimulation of the arm evoked enhanced activity within components of a central pain matrix, including dorsal anterior cingulate, right insula and medial temporal lobe. However, SCI patients differed from controls in conditioning-related brain activity. SCI patients showed a relative enhancement of activity within dorsal anterior cingulate, periaqueductal grey matter (PAG) and superior temporal gyrus. Conversely, SCI patients showed relative attenuation of activity in subgenual cingulate, ventromedial prefrontal and posterior cingulate cortices to threat of painful arm stimulation (CS + arm > CS - arm). Our findings provide evidence for differences in emotion-related brain activity in SCI patients. We suggest that the observed functional abnormalities including enhanced anterior cingulate and PAG reflect central sensitization of the pain matrix, while decreased subgenual cingulate activity may represent a substrate underlying affective vulnerability in SCI patients consequent upon perturbation of autonomic control and afferent visceral representation. Together these observations may account for motivational and affective sequelae of SCI in some individuals.

This is the first published case description of the association of Gilles de la Tourette's syndrome (GTS) and chromosome 22q11.2 deletion syndrome (22q11DS; previously referred to as CATCH-22 syndrome). The co-occurrence of GTS, 22q11DS, and their behavioral/neuropsychiatric abnormalities may be due to the common endophenotypic mechanisms shared by these disorders, rather than due to specificity for GTS. Research into this genomic region may lead to advancement in neurobehavioral/neuropsychiatric genetics, which will help us in further explicating a broader perspective of gene–brain–behavior interrelationships and of the genetic underpinnings of various developmental psychopathologies and behavioral/neuropsychiatric disorders that are common to both GTS and 22q11DS. Our report should warrant further genetic investigations of the chromosome 22q11.2 deletion site using alternative strategies to the quantitative trait loci endophenotype-based approach, which would be useful for establishing the biological and molecular underpinnings of obsessive–compulsive disorder, attention-deficit/hyperactivity disorder, and GTS.