Ferdinando Sartucci

Sex differences in face gender recognition in humans

Human faces are ecologically-salient stimuli. Face sex is particularly relevant for human interactions and face gender recognition is an extremely efficient cognitive process that is acquired early during childhood. To measure the minimum information required for correct gender classification, we have used a pixelation filter and reduced frontal pictures (28,672 pixels) of male and female faces to 7168, 1792, 448 and 112 pixels. We then addressed the following questions: Is gender recognition of male and female faces equally efficient? Are male and female subjects equally efficient at recognising face gender? We found a striking difference in categorisation of male and female faces. Categorisation of female faces reduced to 1792 pixels is at chance level whereas categorisation of male faces is above chance even for 112 pixel images. In addition, the same difference in the efficiency of categorisation of male and female faces was detected using a Gaussian noise filter. A clear sex difference in the efficiency of face gender categorisation was detected as well. Female subject were more efficient in recognising female faces. These results indicate that recognition of male and female faces are different cognitive processes and that in general females are more efficient in this cognitive task.

Normative data for onset VEPs to red-green and blue-yellow chromatic contrast

OBJECTIVE To better characterize the properties of chromatic VEPs to onset-offset of red-green and blue-yellow equiluminant patterns, and establish normative values for a set of stimuli able to elicit robust and reliable responses, suitable for the clinical application. METHODS Chromatic VEPs have been recorded (Oz lead) from 28 normal subjects (age range 20-53 years) in response to monocular presentation of both red-green and blue-yellow equiluminant sinusoidal gratings. Stimuli were generated by a Cambridge VSG/2 card and displayed on a Barco CCID monitor (14x14 deg field size). Spatial frequency, chromaticity, contrast and onset-offset duration were varied. RESULTS For both red-green and blue-yellow equiluminant stimuli, robust responses have been obtained with gratings of 2 c/deg, presented in onset (300 ms) offset (700 ms) mode, at contrasts ranging from 90 to 6%. In all observers, the VEP waveform consisted mainly of a negative wave at stimulus onset, with a latency rapidly increasing with decreasing contrast. For both red-green and blue-yellow stimuli, the VEP contrast threshold coincided with the psychophysical threshold. CONCLUSIONS The results complement previous studies aimed at characterizing the properties of chromatic VEPs. In addition, normative data are provided for a set of stimulus characteristics suitable for the clinical routine.

Changes in pattern electroretinograms to equiluminant red-green and blue-yellow gratings in patients with early Parkinson's disease

Summary In Parkinson’s disease (PD), the luminance pattern electroretinogram (PERG) is reported to be abnormal, indicating dysfunction of retinal ganglion cells (RGCs). To determine the vulnerability of different subpopulations of RGCs in PD patients, the authors recorded the PERG to stimuli of chromatic (red-green [R-G] and blue-yellow [B-Y]) and achromatic (yellow-black [Y-Bk]) contrast, known to emphasize the contribution of parvocellular, koniocellular, and magnocellular RGCs, respectively. Subjects were early PD patients (n = 12; mean age, 60.1 ± 8.3 years; range, 46 to 74 years) not undergoing treatment with levodopa and age-sex-matched controls (n = 12). Pattern electroretinograms were recorded monocularly in response to equiluminant R-G, B-Y, and Y-Bk horizontal gratings of 0.3 c/deg and 90% contrast, reversed at 1Hz, and presented at a viewing distance of 24 cm (59.2 × 59 degree field). In PD patients, the PERG amplitude was significantly reduced (by 40 to 50% on average) for both chromatic and luminance stimuli. Pattern electroretinogram latency was significantly delayed (by about 15 ms) for B-Y stimuli only. Data indicate that, in addition to achromatic PERGs, chromatic PERGs are altered in PD before levodopa therapy. Overall, chromatic PERGs to B-Y equiluminant stimuli exhibited the largest changes. Data are consistent with previous findings in PD, showing that visual evoked potentials (VEP) to B-Y chromatic stimuli are more delayed than VEPs to R-G and achromatic stimuli. The results suggest that the koniocellular subpopulation of RGCs may be particularly vulnerable in early stages of Parkinson’s disease.

Vestibular-evoked myogenic potentials: A method to assess vestibulo-spinal conduction in multiple sclerosis patients

Vestibular-evoked myogenic potentials (VEMPs), elicited by acoustic stimulation, have been proposed in the assessment of the vestibulo-cervical reflex pathways. The procedure has been previously validated in several otovestibular disorders. The aim of this study was to investigate patients affected by multiple sclerosis (MS) in the attempt to clarify the underlying physiopathogenetic mechanisms and the clinical utility of VEMPs in detecting vestibulospinal involvement in this disease. VEMPs were obtained according to the technique described by Colebatch and Halmagyi [Neurology 42 (1992) 1635]. We averaged the surface tonic electromyogram from right and left sternocleidomastoid muscle, after bilateral click stimulation (click duration 0.1 ms, repetition rate 3 Hz, intensity 140 dBSPL, 256 stimuli, repeated at least twice). In all cases, we obtained the biphasic, initially positive, p13-n23 wave pattern. P13 peak latency was bilaterally or unilaterally delayed in 8 out of 15 patients (mean delay: 2.2 ms; p < 0.01 on right and <0.05 on left side) and peak-to-peak amplitude significantly reduced (mean amplitude loss: 130 microV; p < 0.01 on right and <0.05 on left side). Their overall diagnostic yield resulted in 60%. In conclusion, the present findings prove that VEMPs are delayed in p13 component and altered in amplitude in MS patients. We hypothesise that these changes might be the result of a conduction impairment in vestibulo-spinal fibres, producing a morphologic alteration of the myogenic responses.

Changes in pain perception and pain-related somatosensory evoked potentials in humans produced by exposure to oscillating magnetic fields

Nociception has been reported to be influenced by exposure to magnetic fields (MFs). The aim of this study was to investigate the effects of 2 h exposure to weak, oscillating MFs on pain perception thresholds and on pain-related somatosensory evoked potentials (SEPs). In 11 healthy volunteers, pain perception thresholds and pain-related SEPs were assessed by intracutaneous electrical stimulation. After sham treatment, pain thresholds significantly increased, whereas after MFs a slight non-significant decrease in thresholds was found. After both treatments pain-related SEP amplitude was reduced, but this decrease was more evident and statistically significant only after MF exposure. The increase found in thresholds after sham exposure may be due to stress-induced analgesia (SIA) and the contrasting behaviour recorded after MF exposure might indicate a suppression of SIA. The significant reduction in pain-related SEP amplitude observed after MF exposure provides the first evidence that human SEPs are influenced by MFs.

Botulinum neurotoxin E (BoNT/E) reduces CA1 neuron loss and granule cell dispersion, with no effects on chronic seizures, in a mouse model of temporal lobe epilepsy.

Mesial temporal lobe epilepsy (MTLE) is often the result of an early insult that induces a reorganization in hippocampal circuitry leading, after a latent period, to chronic epilepsy. Hippocampal rearrangements during the latent phase include neuronal loss, axonal and dendritic plasticity, neurogenesis, and cell repositioning, but the role of these changes in epilepsy development is unclear. Here we have tested whether administration of the synaptic blocker botulinum neurotoxin E (BoNT/E) interferes with development of spontaneous seizures and histopathological changes following an episode of status epilepticus (SE). SE was induced by unilateral intrahippocampal injection of kainic acid in mice and BoNT/E was delivered to the same hippocampus 3 h later. We found that treatment with BoNT/E prolonged the duration of the latent period but did not block the occurrence of spontaneous seizures. At the histopathological level, BoNT/E reduced loss of CA1 pyramidal neurons and dispersion of dentate granule cells. Downregulation of reelin expression along the hippocampal fissure was also suppressed by BoNT/E treatment. Our findings indicate that administration of BoNT/E after SE inhibits specific morphological changes in hippocampal circuitry but not the development of spontaneous seizures. This indicates a dissociation between certain anatomical modifications and establishment of chronic epilepsy in MTLE.

Brain structural damage in spinocerebellar ataxia type 2. A voxel-based morphometry study

Voxel‐based morphometry (VBM) enables an unbiased in‐vivo whole‐brain quantitative analysis of differences in gray matter (GM), white matter (WM) and cerebro‐spinal fluid (CSF) volumes. We assessed with VBM 20 spinocerebellar ataxia Type 2 (SCA2) patients with mild or moderate cerebellar deficit and 20 age and sex‐matched healthy controls. SCA2 patients showed a significant (P < 0.05 corrected for multiple comparison) symmetric loss of GM in the cerebellar vermis and hemispheres sparing lobules I,II, Crus II,VII, and X, and of the WM in the peridentate region, middle cerebellar peduncles, dorsal pons, and cerebral peduncles. The CSF volume was increased in the posterior cranial fossa. No GM, WM or CSF volume changes were observed in the supratentorial compartment. A mild (P < 0.05, >0.01) correlation was observed between the GM and WM loss and severity of the neurological deficit. In SCA2 patients with mild to moderate cerebellar deficit, GM and WM volume loss and CSF volume increase are confined to the posterior cranial fossa.

N70 and P100 can be independently affected in multiple sclerosis

We have studied the relationship between N70 and P100 of the pattern visual evoked potential in 98 patients with multiple sclerosis and in 59 controls. In patients with multiple sclerosis, P100 was either absent or had prolonged latency in 121 eyes (61.7%), while N70 was absent or prolonged in 97 eyes (49.5%). The total number of eyes with either N70 and/or P100 abnormalities was 137 (69.9%). Eighty eyes (40.8%) had abnormal latency of both P100 and N70, while 41 eyes showed P100 delays without corresponding N70 changes. Seventeen eyes had abnormal N70, but normal P100 latency. N70 and P100 appear to be more often absent in the definite rather than in the possible multiple sclerosis group. These data show that N70 and P100 can be independently affected in patients with MS.

Chromatic pattern-reversal electroretinograms (ChPERGs) are spared in multiple system atrophy compared with Parkinson’s disease

Idiopathic Parkinson’s disease (IPD) patients have abnormal visual evoked potentials (VEPs) and pattern electroretinograms (PERGs), attributed to dopaminergic transmission deficiency in visual pathway, probably the retina. VEP abnormalities are not reported in multiple system atrophy (MSA). The aim of this study was to investigate and compare chromatic (Ch) red-green (R-G) and blue-yellow (B-Y), and luminance yellow-black (Y-Bk) PERGs in patients with MSA and IPD. We investigated 6 MSA patients (mean age: 62±7.4 years) not undergoing any pharmacological treatment, as well as 12 early IPD patients (mean age: 60.1±8.3 years) and 12 age-matched normal observers. ChPERGs were recorded monocularly in response to full-field equiluminant R-G, B-Y and Y-Bk horizontal gratings. In MSA only responses to R-G stimuli showed minimal insignificant changes (slight but not significant amplitude reduction without any significant latency delay); no significant abnormality was detected for B-Y and luminance Y-Bk stimuli. By contrast, in IPD all responses were reduced in amplitude and delayed in latency, above all for B-Y stimuli. Present data indicate that both chromatic and achromatic PERGs are virtually unaffected in MSA, whereas in early IPD they are clearly impaired, suggesting different pathogenic retinal mechanisms and a useful simple tool for distinguishing MSA from IPD.

Transcutaneous spinal direct current stimulation modulates human corticospinal system excitability

This study aimed to assess the effects of thoracic anodal and cathodal transcutaneous spinal direct current stimulation (tsDCS) on upper and lower limb corticospinal excitability. Although there have been studies assessing how thoracic tsDCS influences the spinal ascending tract and reflexes, none has assessed the effects of this technique over upper and lower limb corticomotor neuronal connections. In 14 healthy subjects we recorded motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) from abductor hallucis (AH) and hand abductor digiti minimi (ADM) muscles before (baseline) and at different time points (0 and 30 min) after anodal or cathodal tsDCS (2.5 mA, 20 min, T9-T11 level). In 8 of the 14 subjects we also tested the soleus H reflex and the F waves from AH and ADM before and after tsDCS. Both anodal and cathodal tsDCS left the upper limb MEPs and F wave unchanged. Conversely, while leaving lower limb H reflex unchanged, they oppositely affected lower limb MEPs: whereas anodal tsDCS increased resting motor threshold [(mean ± SE) 107.33 ± 3.3% increase immediately after tsDCS and 108.37 ± 3.2% increase 30 min after tsDCS compared with baseline] and had no effects on MEP area and latency, cathodal tsDCS increased MEP area (139.71 ± 12.9% increase immediately after tsDCS and 132.74 ± 22.0% increase 30 min after tsDCS compared with baseline) without affecting resting motor threshold and MEP latency. Our results show that tsDCS induces polarity-specific changes in corticospinal excitability that last for >30 min after tsDCS offset and selectively affect responses in lower limb muscles innervated by lumbar and sacral motor neurons.