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Biomedical subjects

D Gambi

Publications and source records attributed to D Gambi.

At least 37 records · Page 2Linked to original sources

Long time echo STIR sequence magnetic resonance imaging of optic nerves in optic neuritis.

Magnetic resonance images of optic nerves were obtained in 20 patients with acute optic neuritis (ON), and assessed by means of clinical, visual field and visual evoked potential evaluations; the imaging was repeated 1 year later. The results of the conventional Short Tau Inversion Recovery (STIR) sequence obtained using short time echo (STE-STIR: 22 msec) were compared with those of the long time echo sequence (LTE-STIR: 80 msec). The conventional STE-STIR sequence revealed lesions in 57.2% cases of acute ON and in 42.9% of the optic nerves affected by previous ON; the LTE-STIR sequence was diagnostic in 95.2% of acute ON cases and in 85% of patients with previous ON. The calculated length of the optic nerve lesions was significantly longer in the images obtained using the LTE-STIR sequence than in those obtained using conventional STE-STIR sequences.

Adult↗

Are VEP abnormalities in optic neuritis (ON) dependent on plaque size? A reappraisal of the physiopathology of ON based on improved MRI and multiple-lead recordings.

Twenty patients with optic neuritis (ON) described in the previous study [23] underwent serial VEP recordings (using multiple electrode arrays) for two years. The VEPs could be correlated with the lesions revealed by MRI, Visual Field tests and other clinical findings. On the basis of their scalp distribution, they were classified as "really delayed" VEPs and "pseudo-delayed" VEPs. Real delays could be recorded at the onset of ON or shortly afterwards, and their appearance indicated the recovery of visual function and a good prognosis. Pseudo-delays indicated an alteration in the visual field and, unless a breakthrough of normal or delayed components appeared in the first three months, following acute ON, indicate a poor prognosis for the recovery of visual function. The pseudo-delayed VEPs were mainly observed in patients with longer lesions revealed by means of LTE-STIR MRI [23]; there was no correlation between VEP latency and the length of plaques. Our findings contradict previous theories on the timing of conduction alterations in ON and multiple sclerosis.

Adult↗

Differential electrophysiological features of neuropathies associated with 17p11.2 deletion and duplication.

UNLABELLED: Hereditary neuropathy with liability to pressure palsies (HNPP) and hereditary motor-sensory neuropathy type IA (HMSN IA) are quite distinct clinical entities recently associated to deletion and duplication, respectively, of the 17p11.2 segment including the gene for peripheral myelin protein 22 (PMP-22). We studied the electrophysiological features of 48 HNPP and 62 HMSN IA motor nerves. Conduction velocities (CV) and compound muscle action potential amplitudes were significantly reduced and distal latencies prolonged in HMSN IA compared to HNPP. CV was uniformly slowed in HMSN IA nerves whereas in HNPP it was focally slowed in 80% of ulnar and 12% of peroneal nerves at usual compression sites. Conduction block was present in 6% of HNPP nerves but in none of HMSN IA. IN CONCLUSION: (1) HMSN IA with 17p11.2 duplication presents marked, diffuse, and uniform slowing; (2) HNPP with 17p11.2 deletion presents focal electrophysiological abnormalities possibly correlated with the presence of tomaculae; and (3) under- and overexpression of PMP-22 in concurrence with environmental factors might be responsible for the distinctive features of HNPP and HMSN IA.

Action Potentials↗

Interferon effects on interleukin-10 secretion. Mononuclear cell response to interleukin-10 is normal in multiple sclerosis patients.

The mechanism of action of recombinant interferon beta 1b (rIFN beta 1b/IFN beta-1b), the approved therapy for multiple sclerosis (MS), is still unclear. Here we present evidence that part of the therapeutic effects of rIFN beta 1b in MS might result from the induction of the secretion of interleukin (IL)-10, a cytokine previously designated cytokine synthesis inhibitory factor (CSIF). We observed that rIFN beta 1b stimulated significant IL-10 secretion by monocytes from MS patients after brief incubation (18 h), whereas rIFN gamma, an inducer of MS exacerbations, was unable to stimulate IL-10 production in similar conditions. To determine the role of IL-10 as CSIF in the disease, we have also investigated its effects on TNF alpha and IL-6 secretion by peripheral blood mononuclear cells from MS patients. Recombinant human IL-10 significantly inhibited tumor necrosis factor alpha and IL-6 secretion induced by rIFN gamma, lipopolysaccharide (LPS), and rIFN gamma + LPS in MS patients and in control subjects. The induction of IL-10 secretion by rIFN beta 1b and the IL-10 inhibitory activity on pro-inflammatory cytokine secretion induced by rIFN gamma in MS make this cytokine a potential candidate to treat the disease.

Cells, Cultured↗

Hereditary motor and sensory neuropathy with calf hypertrophy is associated with 17p11.2 duplication.

The demyelinating type of hereditary motor and sensory neuropathy (HMSN I) is characterized by progressive weakness and atrophy of leg muscles. Six patients (age, 25-79 yr) belonging to three generations had calf hypertrophy (6 of 6), foot drop or difficulty with heel walking (4 of 6), pes cavus (3 of 6), absent or depressed tendon jerks in the lower limbs (4 of 6), and mild distal sensory loss (3 of 6). No other family member had leg atrophy. Motor conduction velocities ranged from 20 to 40 m/sec. Sural nerve biopsy showed loss of large myelinated fibers, numerous onion bulbs, and segmental demyelination and remyelination. Computed tomographic scans of leg muscles and histological and morphometric findings in gastrocnemius revealed true muscular hypertrophy. Southern blot and fluorescence in situ hybridization documented the duplication of the entire 17p11.2 segment associated with classical HMSN IA. The pathogenesis of muscle hypertrophy in our cases is unclear. Chronic leg muscle weakness and long-standing partial denervation might cause calf enlargement by a combination of compensatory "work-induced" and "stretch-induced" fiber hypertrophy. Alternatively, that all the affected family members presented calf hypertrophy might suggest the action of a genetic factor associated with the duplication at 17p11.2.

Adult↗

Hand dystonia secondary to cervical demyelinating lesion.

Dystonia is generally considered a disease of basal ganglia. We report two patients with definite MS who acutely developed hand dystonia and athetoid movements. In both patients: 1) dystonia was electrophysiologically demonstrated by lack of reciprocal inhibition between antagonistic forearm muscles; 2) SEP from median nerve stimulation showed delayed cervical N13 and absent frontal and parietal components; 3) the long latency response after stimulation of median nerve of the affected hand was absent or delayed; 4) MRI showed lesions in the posterolateral cervical spine but no involvement of basal ganglia and thalami. We think that, in these cases, dystonia and athetoid movements could be ascribed respectively to the involvement of descending pathways regulating reciprocal inhibition of motoneurons and to the involvement of large diameter afferents due to the demyelinating lesion at the cervical level.

Adult↗

Sensitivity of three median-to-ulnar comparative tests in diagnosis of mild carpal tunnel syndrome.

We studied 193 hands of 113 patients referred for typical carpal tunnel syndrome (CTS). Ninety-five (49%) hands had normal median distal motor latency (< or = 4.2 ms) and normal or borderline sensory conduction velocity from digit 2 stimulation (> or = 45 m/s). In these cases we performed three median to ulnar comparative tests: (1) difference between median and ulnar distal motor latencies recorded from the second lumbrical and interossei muscles (2L-INT); (2) difference between median and ulnar sensory latencies from digit 4 stimulation (D4M-D4U); and (3) difference between median and ulnar mixed nerve latencies from palmar stimulation (PM-PU). The 2L-INT difference was > or = 0.6 ms in 10% of hands. PM-PU and D4M-D4U were > or = 0.5 ms in 56% and 77% of hands, respectively. The greater sensitivity of D4M-D4U might be explained by the funicular topography and consequent greater susceptibility to compression of the cutaneous fibers from the third interspace which, at the distal carpal tunnel, are clumped superficially in the anteroulnar portion of the median nerve just beneath the transverse ligament.

Action Potentials↗

Early MRI findings in Creutzfeldt-Jakob disease.

We describe the MRI changes preceding the onset of myoclonus in two patients whose post-mortem examination confirmed the diagnosis of Creutzfeldt-Jakob disease (CJD). MRI showed changes in the striatum early in the course of CJD (2-6 months after the onset of apathy, interpreted as depression, and 1-2 months before the onset of further clinical symptoms). Only in one patient did electroencephalography record the typical triphasic sharp-waves, 1 month after MRI.

Brain↗

Acute hemispheric stroke: correlation between three-dimensional transcranial Doppler, MR-angiography, CT and clinical findings.

We examined 50 ischemic stroke patients and 67 controls free of vascular disease, intra- or extracranial. We assessed all subjects clinically by neurological examination (quantified on the Canadian Neurological Scale or CNS), by three-dimensional transcranial Doppler sonography (TCD-3D) and by computed tomography (CT) within 24 h of the acute event, repeating CT 15 days later. 15 patients also underwent magnetic resonance angiography (MRA) and digital subtraction angiography (DSA). We used the following Doppler parameters: interhemispheric asymmetry index (AI), mean flow velocity (mV) and pulsatility index (PI) for the middle cerebral artery (MCA). The difference between patients and controls on analysis of the variance (ANOVA) in respect of AI was significant: F = 50.8, p < 0.0001. The CNS-AI correlation was equally valid: r = -0.56, p < 0.001. The CNS-CT correlation proved to be highly significant: r = -0.72, p < 0.0001. TCD-3D allowed quantitative evaluation of the hemodynamic changes and of the collateral blood supply and proved to be a sound method for the investigation of ischemic stroke, correlating well with the clinical findings, MRA and lesion size on CT.

Acute Disease↗

Sensitivity and specificity of diagnostic criteria for conduction block in chronic inflammatory demyelinating polyneuropathy.

Detection of conduction block (CB) has important clinical implications because it suggests segmental demyelination potentially reversible following treatment. There are no universally accepted criteria to define CB. We tested the sensitivity of two diagnostic criteria of partial motor CB in patients with chronic inflammatory demyelinating polyneuropathy (CIDP) and hereditary motor-sensory neuropathy type I (HMSN I) which are thought to be the prototypes of segmental and uniform demyelination respectively. Criterion I requires > 20% drop in negative peak amplitude and area and < 15% change in duration between proximal and distal compound muscle action potentials (CMAPs). Criterion II requires > 50% drop in negative peak amplitude and area of proximal CMAP independently from temporal dispersion. Twenty-eight percent of CIDP nerves and 65% of CIDP patients had CB according to criterion I. However, 29% of nerves and 61% of patients with HMSN I also fulfilled the same criterion. Thirty-four percent of CIDP nerves and 78% of CIDP patients and none of HMSN I patients fulfilled criterion II. Criterion II has the same sensitivity as criterion I, but seems to be highly specific in diagnosis of the segmental demyelination characteristic of CIDP. Therefore this criterion should be employed, as the diagnostic tool of CB, in chronic neuropathies presenting high stimulation threshold and coexisting axonal loss.

Action Potentials↗

Topical naphazoline in treatment of myopathic ptosis.

We instilled naphazoline Hcl (0.1%), an imidazole derivative with preferential alpha-2 activity, in 17 eyes of 12 patients with myopathic ptosis due to involvement of the levator palpebrae superioris, in the attempt to selectively stimulate Müller's smooth muscle. Naphazoline significantly widened the palpebral fissure with little change in pupillary diameter and no significant change in ocular pressure, visual acuity and near point determination. However, a reduction of the effect, probably due to tachyphylaxis, was noticed when using naphazoline regularly several times a day for few weeks. In conclusion naphazoline has powerful cosmetical and functional effects in mild to moderate myopathic ptosis above all if taken occasionally.

Administration, Topical↗

[Acute carbamazepine poisoning treated with plasmapheresis. Description of a clinical case].

A case of severe Carbamazepine poisoning initially misdiagnosed is reported. Treatment consisted in plasmapheresis (3.5 liters exchanged) repeated for 3 consecutive days, in conjunction with activated charcoal and advanced life support. It was obtained a rapid decay in Carbamazepine plasmatic level (with rebound phenomenon only after first treatment day) and a contemporary improvement in clinical conditions. The patient was discharged without complications after 6 days stay in ICU. Taking pharmacokinetic characteristics into account, it is suggested that plasmapheresis may be useful in this kind of poisoning.

Acute Disease↗

Memory and naive CD4+ lymphocytes in multiple sclerosis.

Helper-inducer (CD29+CD4+) and suppressor-inducer (CD45RACD4+) T-cells have been recently renamed as memory and naive T-cells, respectively. We measured cells expressing these phenotypes in peripheral blood of 46 definite multiple sclerosis (MS) patients [32 relapsing-remitting (RR-MS), 14 secondary progressive (P-MS)] and controls. CD25+ (interleukin-2-receptor-positive) cells were also evaluated in the same groups of patients. RR-MS patients showed increased levels of CD29+CD4+ and CD25+ cells compared with controls. This finding was more evident in RR-MS patients during the attack than during the stable phase of the disease. In P-MS patients we found a reduction of CD45+CD4+ cells compared with either RR-MS patients or control subjects. Our results show that RR-MS and P-MS are characterized by two different T-cell subpopulations. This finding supports the hypothesis that during the evolution from RR-MS and P-MS changes occur in the immunological status of the patients.

Adult↗

Sympathetic skin response in hemispheric lesions.

We recorded the sympathetic skin response (SSR) from electrical nerve stimulation in 16 patients with cerebrovascular accident (CVA). Location and nature of the lesion were documented by computerized tomography (CT). Median (pre-rolandic and parietal) somatosensory evoked potentials (SEP) were also recorded. SSR was absent bilaterally in eight hemiplegics after stimulation of the plegic side and present bilaterally after stimulation of the normal side in the first weeks after CVA. Parietal and pre-rolandic SEPs were absent in the affected hemispheres. SSR was present bilaterally after stimulation of each side in the remaining CVA cases with reduced amplitude SEPs. Absence of the electrically evoked SSR in hemispheric lesions may be due to involvement of central afferent pathways or temporary suppression of suprasegmental excitatory influences.

Aged↗

Inhibition of interleukin-1 (alpha and beta), interleukin-2 secretion and surface expression of interleukin-2 receptor (IL-2R) by a novel cytokine interleukin-1 receptor antagonist (IL-1ra).

IL-1 is a mediator of the acute inflammatory response and plays a key role in influencing growth and differentiation of immunocompetent lymphocytes. It can enhance transcription and secretion of the T-cell growth factor interleukin-2 (IL-2) and can stimulate the expression of membrane receptors for IL-2. However, the regulation and control of IL-1 activities are poorly understood. Recently an IL-1 inhibitor, interleukin-1 receptor antagonist (IL-1ra), has been described and cloned. This protein is a monokine originally found in the urine of febrile patients and in supernatants of human monocytes adhering to an IgG-coated surface, with an approximate molecular weight of 17 kDa, which is similar to IL-1 beta but having no IL-1-like activity and antagonizing IL-1 by binding to its cell surface receptor. These studies have examined some biological properties of hrIL-1ra, such as its effects on the secretion of IL-1 alpha or IL-1 beta and IL-2, the surface expression of IL-2R and DNA synthesis by peripheral blood mononuclear cells (PBMC). PBMC from normal volunteers were separated and used at a concentration of 2.5 x 10(6) cells/ml. The cells were pretreated for 2 h with hrIL-1ra (0.025-250 ng/ml), treated with LPS (10 ng/ml), and IL-1 alpha and IL-1 beta secretion were determined by an ELISA method. In addition the influence of hrIL-1ra (25 ng/ml) on IL-2 generation was determined. In another set of experiments, flow cytometric analysis with an anti-CD25 monoclonal antibody was determined on PHA-stimulated PBMC pretreated with hrIL-1ra (2 h) and cultured for 48 h. The inhibition by hrIL-1ra of IL-2R expression was dose-dependent and when hrIL-1ra was used at 250 ng/ml the IL-2R was completely abolished. Lymphocyte DNA synthesis calculated from the net uptake of [3H]-thymidine (3H-TdR) was also inhibited by hrIL-1ra (0.025-25 ng/ml). In this report we found that hrIL-1ra inhibits, in a dose-dependent manner, the secretion of IL-1 alpha, IL-1 beta, IL-2, the surface expression of IL-2R and 3H-TdR incorporation in PBMC in vitro. These data suggest a new biological activity of hrIL-1ra and further extend the immunomodulatory potential and significance of this new cytokine. The action of IL-1ra on modulating the synthesis of IL-1 may be of paramount importance in the regulation of these effects.

Concanavalin A↗

Compressive bilateral peroneal neuropathy: serial electrophysiologic studies and pathophysiological remarks.

A case of bilateral common peroneal neuropathy following prolonged squatting is reported. Serial peroneal conduction velocities with analysis of compound muscle action potential (CMAP) amplitude, area and duration performed at Days 1, 2, 5, 7, 14, 21, 37, 80 showed conduction block localized at the fibular head which lasted 14 days and paralleled clinical conditions. Axonal loss coexisted as indicated by amplitude reduction of CMAP from peroneal nerve stimulation at the ankle which reached the lowest values at Day 7. Excessive temporal dispersion, as indicated by abnormal increased duration of the CMAP from stimulation above the fibular head, was never detected. Conduction velocity in the segment across the fibular head was reduced as long as conduction block was present, due to preferential block of large diameter, fast conducting, fibers. The rapid resolution of conduction block and the absence of temporal dispersion suggest that compressive conduction block is not necessarily due to demyelination. Mechanical factors or ischemic-metabolic mechanisms might play a role.

Adult↗