Biomedical subjects

A Uncini

Publications and source records attributed to A Uncini.

At least 73 records · Page 4Linked to original sources

PubMed1993

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↗

PubMed1993

Electrophysiologic correlates of peripheral nervous system maturation in infancy and childhood.

Peripheral nervous system maturation in infancy and childhood varies with age, especially during the first 2 years of life. Electrophysiologic values therefore changes significantly between different age groups within these first 2 years and are different from adult values. Normal values of motor and sensory nerve conduction, distal motor latency, F-wave latency, and evoked response amplitude of peripheral nerves commonly tested are reported in 155 healthy children in seven age groups from 1 week to 14 years. Interval changes are clearly shown, and in comparison with adult values, the whole group has significantly slower nerve conduction velocities, with reduced muscle and nerve evoked response amplitudes. These differences are important to recognize when evaluating the peripheral nervous system of children.

Adolescent↗

PubMed1992

Experimental conduction block induced by serum from a patient with anti-GM1 antibodies.

Increased titers of antibodies to GM1 ganglioside in humans are associated with lower motor neuron disease and predominantly motor neuropathy with or without conduction block. To investigate the possible mechanism of these antibodies, we injected the serum of a patient with anti-GM1 antibodies who had motor neuron disease and multifocal motor conduction block, into rat sciatic nerve. When injected with fresh human complement, the serum-induced conduction block with temporal dispersion and deposits of immunoglobulin were detected at the nodes of Ranvier. Electron microscopic studies revealed demyelination in 6.5% of the fibers. After preabsorption with GM1, the serum had no effect, suggesting that the anti-GM1 antibodies were responsible for the conduction abnormalities.

Animals↗

PubMed1992

Anti-sulfatide antibodies in neurological disease: binding to rat dorsal root ganglia neurons.

Increased titers of anti-sulfatide antibodies were detected by ELISA in 5 of 200 patients and control subjects. All 5 patients had sensory impairment; 4 had neuropathy, and one had multiple sclerosis. Of the patients with neuropathy, 2 had a clinical syndrome of small fiber sensory neuropathy with normal electrophysiological or nerve biopsy studies, 1 had a sensorimotor axonal neuropathy associated with IgM monoclonal gammopathy, and 1 had sensorimotor neuropathy with multifocal motor conduction block and anti-GM1 antibodies. The anti-sulfatide antibodies bound to the surface of unfixed rat dorsal root ganglia neurons and human neuroblastoma cells, and to fixed sections of central and peripheral myelin. No binding was detected following intraneural injection into rat sciatic nerves. Pre-absorption with sulfatide but not with galactocerebroside eliminated the tissue binding activity. These findings indicate that increased titers of anti-sulfatide antibodies are found in patients with sensory impairment but are not restricted to a particular neurological syndrome or type of neuropathy. The significance of anti-sulfatide antibodies is uncertain although sulfatide on dorsal root ganglia neurons may be a target antigen.

Aged↗

PubMed1992

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↗

PubMed1992

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↗

PubMed1992

Benign monomelic amyotrophy of lower limb: report of three cases.

Three patients with wasting confined to a single lower limb are reported. The characteristic features were: sporadic occurrence, insidious onset with slow progression and in 2 cases arrested course for at least 4 years, wasting out of proportion with disability, absence of sensory, pyramidal tract or bulbar signs. CK, motor and sensory conductions, and lumbar MRI were normal. Muscle CT showed selective loss of muscle tissue and fat replacement in posterior leg muscles. Quantitative electromyography and histologic findings revealed neurogenic features not only in the affected legs, but also in clinically uninvolved limbs. Monomelic amyotrophy of lower limb is a variant of spinal muscular atrophy with a benign course. However, as in the early stages of the disease there are no distinctive clinical or laboratory findings with other motor neuron diseases, the diagnosis of monomelic amyotrophy may be made only retrospectively after a prolonged observation.

Adult↗

PubMed1992

Multifocal motor neuropathy with conduction block: is it a distinct clinical entity?

We studied 169 patients with motor neuron disease. Seventeen showed abnormal amplitude reduction of the compound muscle action potential. Ten had focal loss of both amplitude and area across a specific segment (conduction block). Eight of the 10 had slowing of conduction across that segment. Nine were men and had prominent hand involvement. Six had probable or definite upper motor neuron signs. Five of the 10 showed immunologic abnormalities (elevated GM1 antibody titers or paraproteinemia), and eight had had symptoms for more than 4 years. Seven of the 17 patients showed loss of amplitude without corresponding loss of area and focal slowing of conduction (temporal dispersion). Five of the seven were men, five had prominent hand involvement, and five had definite or probable upper motor neuron signs. Two had immunologic abnormalities, and ony one had had symptoms for longer than 4 years. Among 152 patients with no abnormality of conduction, 64% wee men, hands were dominantly involved in 34%, upper motor neuron signs were definite or probable in 72%, and 3% had immunologic abnormalities. None had symptoms for more than 4 years. Because there were so many exceptions, we could not define a unique syndrome by criteria involving conduction block, GM1 antibodies, or lack of upper motor neuron signs. The clinical syndrome associated with multifocal conduction block seemed uniform, however, and patients with conduction block had slower progression if there were no upper motor neuron signs.

Action Potentials↗

PubMed1991

Chronic inflammatory demyelinating polyneuropathy in childhood: clinical and electrophysiological features.

Five children with chronic progressive polyneuropathy but no familial history of it showed electrophysiological evidence of demyelination with partial conduction block, temporal dispersion, and focal slowing of nerve conduction velocities in multiple nerves. These findings are indicative of an acquired demyelinating polyneuropathy that is chronic and inflammatory and differentiate this condition from most of the inherited neuropathies. It is very important to recognize this entity because of the availability of various treatments.

Child↗

PubMed1991

Silent period induced by cutaneous stimulation.

An electrical stimulus applied to a cutaneous nerve during isometric muscle contraction causes a suppression of EMG activity (silent period) followed by a rebound. The extent of inhibition is related to the stimulus intensity as the silent period is more evident when stimulation is perceived as painful. The silent period is present in different limb and cranial muscles after stimulation of the same cutaneous nerve and in the same muscle after stimulation of distant cutaneous nerves. It also occurs synchronously in antagonist muscles. Within the silent period induced after cutaneous stimulation the maximal inhibition on the opponens pollicis motor neuron pool, as tested by the motor response evoked after transcranial cortical stimulation, occurs between 50 and 70 msec. Using the double stimulus technique to study the recovery cycle, the silent period is present at interstimulus intervals as low as 100 msec, and does not habituate with trains of stimuli at frequencies up to 5 Hz. Our results suggest that motor neuron inhibition from nociceptive stimulation may be mediated by Renshaw cells directly activated by high threshold cutaneous afferents.

Adolescent↗

PubMed1991

Becker muscular dystrophy or spinal muscular atrophy?--Dystrophin studies resolve conflicting results of electromyography and muscle biopsy.

We studied a 29-year-old man with slowly progressive proximal leg weakness, calf hypertrophy, and high serum levels of creatine kinase activity. Clinically, it was not possible to identify his as a sporadic instance of Becker muscular dystrophy (BMD) or one of spinal muscular atrophy. The problem arose because electromyography and elevated creatine kinase suggested a myopathy whereas changes in the muscle biopsy resembled a neurogenic disorder. The diagnosis of BMD was made by DNA analysis which detected a deletion at Xp21 and by immunoelectrophoresis and immunohistochemical tests that identified an abnormal form of gene product, dystrophin. These studies were important for genetic counselling, identifying an X-linked disease instead of one that is autosomal recessive.

Adult↗

PubMed1991

HTLV-1-associated myeloneuropathy in an Italian.

A 58-year old man presented with slowly progressive spastic paraparesis, ataxia, absent ankle jerks, bladder disturbances, impairment of vibration sense and mental deterioration. Electrophysiological studies documented axonal sensory neuropathy, posterior column and optic nerve involvement. Serum tests for anti-HTLV-1 antibodies were negative but HTLV-1 proviral sequences were consistently demonstrated in white blood cell genomic DNA using the polymerase chain reaction technique. Western blot and polymerase chain reaction assays of sera and DNA from family members were negative for HTLV-1. The most likely cause of infection in this patient was a blood transfusion received 2 years before onset of symptoms. This is the second Italian case of HTLV-1 associated myelopathy and the fourth reported in white subjects living in Europe.

Amino Acid Sequence↗

PubMed1991

CNS involvement in chronic inflammatory demyelinating polyneuropathy: an electrophysiological and MRI study.

Eight consecutive patients with chronic inflammatory demyelinating polyneuropathy (CIDP) were investigated by visual evoked potential (VEP), brainstem auditory evoked response (BAER) and magnetic resonance imaging (MRI) to assess central nervous system (CNS) involvement. VEPs were abnormal in 6 patients and BAERs in 2. MRI showed changes suggestive of CNS demyelination in 2 cases. Our findings suggest the existence of a combined central and peripheral demyelinating syndrome and emphasize the possibility of a common pathogenetic mechanism for both.

Adult↗

PubMed1990

IgM deposits at nodes of Ranvier in a patient with amyotrophic lateral sclerosis, anti-GM1 antibodies, and multifocal motor conduction block.

We studied a patient with amyotrophic lateral sclerosis, multifocal motor conduction block, and IgM anti-GM1 antibodies. A sural nerve biopsy demonstrated deposits of IgM at nodes of Ranvier by direct immunofluorescence. The deposits were granular and located in the nodal gap between adjacent myelin internodes, and in some instances, they extended along the surface of the paranodal myelin sheath. When injected into rat sciatic nerve, the serum IgM bound to the nodes of Ranvier, and the binding activity was removed by preincubation with GM1. These observations suggest that anti-GM1 antibodies may have caused motor dysfunction by binding to the nodal and paranodal regions of peripheral nerve.

Adult↗

PubMed1990

Long-duration polyphasic motor unit potentials in myopathies: a quantitative study with pathological correlation.

In most myopathies, the duration of motor unit action potentials (MUAPs) is shorter than normal. However, polyphasic MUAPs of duration longer than 20% of the control mean, (long-duration polyphasic potentials, or LDPPs) may be seen. We therefore analyzed the incidence and meaning of LDPPs using quantitative MUAP analysis in 41 patients with different myopathies. The mean duration of all potentials was reduced in only 64% of patients because LDPPs increased the mean. When only simple potentials were considered, however, the mean duration was decreased in 95% of patients. This observation confirms the need to exclude LDPPs when calculating the mean duration of MUAPs for diagnosis. We found LDPPs most often in chronic polymyositis and in one patient with Becker Muscular Dystrophy. LDPPs are attributed to desynchronization of single-fiber potentials within the MUAP and may be due to slow conduction in regenerating muscle fibers.

Action Potentials↗

PubMed1990

Recurrent cranial nerve palsies, midbrain infarction and hydrocephalus due to megadolichobasilar artery.

A 67-year-old man presented four recurrent, alternating facial palsies, two right abducens palsies and eventually a right extrinsic third nerve palsy due to brain-stem infarction in a 37-year time-span. Neuroradiological examinations showed hydrocephalus and an elongated, tortuous, ectasic basilar artery. This patient presented in his lifetime the whole clinical spectrum of the dolichoectasic basilar artery complications.

Aged↗

PubMed1990

F response in vascular and degenerative upper motor neuron lesions.

The F response represents the recurrent discharge of a small percentage of the motoneuron pool activated antidromically by any single impulse delivered to the nerve. We studied F waves from median nerve stimulation in 22 controls, in 30 patients with spasticity after cerebrovascular accident (CVA), and in 4 patients with familial spastic paraplegia (FSP). The following parameters were analyzed: median nerve conduction velocity, median nerve M response amplitude (M), average amplitude of 16 F responses (F16); persistence of F response (Fp) defined as the percentage of measurable responses to 16 stimuli, average amplitude of F response expressed as percentage of maximal M amplitude: (F16/M%). Results showed that Fp, F16 and F16/M% values were significantly increased on the spastic side of CVA patients and in FSP. Our findings indicate that after upper motor neuron lesions (whatever etiology and course) a change in the frequency of recurrent discharge and/or in the total number of lower motor neurons capable of backfiring occurs. Therefore, F response reflects the hyperexcitability state of the lower motor neurons in spasticity.

Adolescent↗

PubMed1990

Orthodromic median and ulnar fourth digit sensory conductions in mild carpal tunnel syndrome.

Because the fourth digit (D4) has a dual innervation, median and ulnar D4 sensory conduction velocity (SCV) comparison may be useful in diagnosing the carpal tunnel syndrome (CTS). We studied 50 control hands and 41 hands with recent onset symptoms and signs of CTS but normal median distal motor latency and normal SCV from the second digit (D2). In CTS, D4 SCV was significantly slower than D2 SCV and D4 median and ulnar sensory conduction difference was abnormal in 38 hands (92%). In 36 CTS hands (87%), but in no control hand, a double peak potential could be recorded over the median after D4 stimulation providing an immediate visual confirmation of the diagnosis of CTS. Comparing median and ulnar D4 SCV is a very sensitive method to detect early or mild CTS and should be used whenever conventional electrodiagnostic studies are normal or borderline.

Adolescent↗