Movement analysis in early infancy: Towards a motion biomarker of age.

BACKGROUND: Early motor development is characterized by progressive changes in general movements paralleled by a gradual organization of the four limbs' repertoire towards the midline, as shown by computerised movement analysis. AIMS: Our aim was to test the performance of quantitative computerised kinematic indexes as predictors of post-term age in an independent cohort of typically developing subjects at fidgety age, tested cross-sectionally. SUBJECTS: We selected twelve low risk term infants, who were video recorded between 9 and 20 weeks (fidgety age) during one spontaneous movements session. STUDY DESIGN: We correlated post-term age with I)indexes of coordination including interlimb correlation of velocity and position, II)indexes of distance, including interlimb and limb-to- ground, both expressed as linear distance and as probability of midline limbs position III)indexes of global movement quality by calculating Hjorth's activity, mobility and complexity parameters. All indexes were calculated for both upper and lower limbs. RESULTS: Significant positive correlations were found between post-term age and indexes of distance, and probability of occurrence of upper-limb antigravity patterns, and with both indexes of global movement quality. By combining linear and non-linear parameters related to the upper limb kinematics, we determined individual post-term age with a mean error of <1 week (5.2 days). No correlations were found between age and indexes of coordination. CONCLUSIONS: Quantitative computerised analysis of upper-limb movements is a promising predictor of post-term age in typically developing subjects at fidgety age.

The term diplegia should be enhanced. Part II: contribution to validation of the new rehabilitation oriented classification.

Recent proposals of classification for cerebral palsy (CP), mainly revised for epidemiological purposes, suggest to abandon the use of the term diplegia. Conversely, in this paper data are presented to support the proposal to maintain the distinction between spastic tetraplegia and diplegia, and to subdivide this latter according to four main clinical patterns of walking observable in these children. This proposal of classification was validated by testing a group of 467 subjects with CP, of whom 213 with diplegia and 115 with tetraplegia, consecutively admitted between January 2005 and December 2006 to two national reference centers for this disability. The results were compared with findings obtained by other methods of classifying gross and fine motor function and associated disorders. The subjects with tetraplegia strongly differ from those of diplegia, both for motor functions and for other disabilities. The four main walking patterns of spastic diplegia were easily recognizable and observers were able to assign most of the subjects to one form of the classification. Significant correlations between walking forms of diplegia and distribution of Gross Motor Function Classification System (GMFCS) levels were found. Some of the forms significantly differ also for fine motor and mental disability. These findings suggest that in clinical practice the category of diplegia not only can be kept as a separate form of CP, but it may be enhanced, through the identification of different subcategories of children, divided according to their walking patterns.

[Clinical characteristics, familial distribution and preliminary genetic data in 9 different families with "Brugada's syndrome"]. / Caratteristiche cliniche, distribuzione familiare e preliminari dati genetici in nove diverse famiglie con "sindrome di Brugada".

Clinical electrocardiographic evaluation and complete non-invasive assessment including nuclear magnetic resonance (NMR) are reported for 7 subjects with cardiac arrest (CA), 6 due to ventricular fibrillation (VF) and 1 to ventricular tachycardia (VT). Two more subjects, one with and one without a family history of non-resuscitated sudden death (NRSD), were included. All 9 subjects showed the typical pattern of the Brugada's syndrome (BS), characterized by incomplete right bundle branch block, ST T elevation in V1 V3. We globally evaluated 64 subjects belonging to the 9 families examined, 5 of whom were identified in Bologna, 3 in Florence and one in Parma. BS is characterized in the experience described in the present paper by a family distribution of the ECG pattern in different members. Furthermore, a family distribution of NRSD, even at a young age, was observed. Electrocardiographic features were consistent with variable degrees and aspects of the intraventricular conduction delay (ICD) and of the ST T elevation pattern. NMR has been performed so far in 23 out of 64 members examined by echo, and was normal in 17/23, with only 6 showing pathological aspects such as mild dilatation of the right ventricle, reduced thickness of the right free wall, isolated dilatation of the right ventricular infundibulum and other minor pathological aspects. Preliminary genetic screening (GS), performed on 20 members of three families, was negative for the typical genetic patterns of right ventricular dysplasia (ARVD). In six families, GS is still ongoing. Genetic screening of sodium channel pathology is in progress in the same families. In conclusion, BS has been documented in the present paper as a hereditary syndrome, both for clinical and ECG aspects, associated with CA due to VF, which required an AICD implantation, at least in symptomatic subjects. There may exist a CONGENITAL form of BS due to pathology of sodium channels, without a demonstrable structural heart disease and an ACQUIRED form of BS secondary to an initial ARVD. From the clinical point of view, a complete evaluation, including serial ECG, pharmacological testing and programmed electrical stimulation of other subjects in the families, may be important in preventing sudden death, mainly in symptomatic subjects who always require an implantable cardioverter defibrillator.

Cerebral visual impairment in preterm infants with periventricular leukomalacia.

Neonatal brain lesions are the main cause of cerebral visual impairment in infancy, i.e., of a visual deficit caused by damage to posterior visual pathways. Visual outcome of preterm infants with periventricular leukomalacia (PVL) was investigated in 14 subjects affected by severe cystic PVL, another 34 with moderate PVL (prolonged periventricular echodensities), and 18 control preterm infants. All cases with significant ocular abnormalities (such as retinopathy of prematurity state III or upwards, optic nerve atrophy, or major refraction problems) were excluded. Visual acuity, visual field, eye alignment, fixation and following, optokinetic nystagmus, and visual threat were tested at 1 year of corrected age. A high incidence of cerebral visual impairment, consisting mainly of low visual acuity, severe oculomotor disorders, and reduced visual field, was found in infants with severe PVL. Visual defects were less frequent and less severe in the moderate PVL group, and very rare in the control group. The results of neuroimaging, and especially of magnetic resonance imaging, correlated with the visual outcome and indicate lesions at the level of optic radiations as the main anatomic substrate of the visual impairment. All infants with PVL need a visual follow-up, from the first months of life, the results of which are important both for visual and motor rehabilitation of these cases and for their daily care.

Comparative efficacy of nicardipine, a new calcium antagonist, versus nifedipine in stable effort angina.

The relative efficacy of nicardipine and nifedipine was examined in a double-blind placebo-controlled randomized crossover trial. We studied 12 patients with chronic effort angina involving reproducible angina and greater than or equal to 1.5 mm of ST-segment depression on exercise treadmill test performed before and after a 1-week control period of single-blind placebo administration. Subsequently, indistinguishably prepared nicardipine 20 mg, nifedipine 10 mg, or placebo, four times a day, was administered in a randomized double-blind crossover fashion for 3 weeks (total study period 9 weeks). Exercise treadmill test was performed at the end of each 3-week period. Both nicardipine and nifedipine significantly reduced the frequency of anginal attacks and nitroglycerin consumption. Compared with placebo both drugs caused a comparable increase of the duration of exercise, of the time to angina and to the appearance of 1.5 mm ST-segment depression (P less than 0.05 placebo versus nicardipine; P less than 0.01 placebo versus nifedipine respectively). No significant side effects were observed with either drug. We conclude that nicardipine and nifedipine produce similar hemodynamic and clinical effects in patients with stable effort angina.

Comparative efficacy of nicardipine, a new calcium antagonist, versus nifedipine in effort stable angina.

The relative efficacy of nicardipine and nifedipine was examined in a double-blind randomized trial. We studied 12 patients with chronic effort angina who had reproducible chest pain and greater than or equal to 1.5 mm of ST-segment depression on treadmill exercise testing performed before and after 1-week control period of single-blind placebo administration. Subsequently over a 9-week period, nicardipine 20 mg or nifedipine 10 mg or an identical placebo four times a day, was administered in a randomized double-blind crossover fashion. Treadmill exercise testing was performed at the end of each 3-week period. Both nicardipine and nifedipine reduced the frequency of anginal attacks and trinitrate consumption. Compared with placebo both drugs caused a comparable increase of the total duration of exercise (p less than 0.05 placebo versus nicardipine; p less than 0.01 placebo versus nifedipine) and of the time to the onset of angina (p less than 0.05 placebo versus nicardipine; p less than 0.01 placebo versus nifedipine) and to the appearance of 1.5 mm ST depression (p less than 0.05 placebo versus nicardipine; p less than 0.01 placebo versus nifedipine). Moreover 4 patients no longer had angina with either drug and only 1 patient with placebo. Both drugs increased resting heart rate and reduced systolic blood pressure at resting (p less than 0.01) and submaximal exercise (p less than 0.01). Peak heart rate, systolic blood pressure and rate-pressure product were similar with placebo, nicardipine and nifedipine. No important side effects were observed with either drug. We conclude that nicardipine and nifedipine produce similar haemodynamic and clinical effects in patients with stable angina.