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Biomedical subjects

M Inghilleri

Publications and source records attributed to M Inghilleri.

At least 55 records · Page 3Linked to original sources
PubMed1997

Urodynamic and neurophysiological evaluation in Parkinson's disease and multiple system atrophy.

AIMS: To determine whether Parkinson's disease and multiple system atrophy each has a distinct pattern of micturition abnormalities and whether a urodynamic evaluation could be useful in the differential diagnosis between the two diseases. METHODS: Sixty two patients (30 with Parkinson's disease and 32 with multiple system atrophy) underwent a complete urodynamic evaluation and neurophysiological testing. RESULTS: Of the parkinsonian patients 36.6% had normal micturition findings with normal bladder sensitivity; 26.7% had delayed or incomplete pelvic floor relaxation; 26.7% had hyperreflexia with vesicosphincteric synergy; and 10% had hyperreflexia with vesicosphincteric synergy associated with incomplete pelvic floor relaxation. Parkinsonian patients with a normal urodynamic pattern had significantly less severe disease and a shorter duration of disease in years than those who had abnormal patterns. Patients with hyperreflexia had significantly higher severity of disease. All the patients with multiple system atrophy had hyperreflexia with synergy. Two urodynamic patterns were identified: hyperreflexia with vesicosphincteric synergy (90.6% of patients), and hyperreflexia with vesicosphincteric synergy and incomplete pelvic floor relaxation (in 9.4%). Hyperreflexia with synergy correlated neither with the severity nor with the duration of disease. Sphincter EMG analysis showed that all the parkinsonian patients had normal sphincter EMG whereas 24 of the 32 patients with multiple system atrophy had neurogenic signs. CONCLUSIONS: Urodynamic evaluation and sphincter EMG are both useful tests in the differential diagnosis between Parkinson's disease and multiple system atrophy. Urodynamic findings may be abnormal before patients with multiple system atrophy reach an advanced stage of the disease. Recordings of EMGs from perineal muscles become abnormal as the disease progresses in multiple system atrophy but not in Parkinson's disease.

Aged↗
PubMed1996

Effects of diazepam, baclofen and thiopental on the silent period evoked by transcranial magnetic stimulation in humans.

The cortical silent period evoked by magnetic transcranial stimulation and the peripheral silent period were studied in healthy subjects after intravenous injection of diazepam, baclofen or thiopental. None of the drugs tested changed the peripheral silent period. But, unexpectedly, diazepam significantly shortened the cortical silent period, the inhibitory effect lasting about 30 min. In experiments using paired transcranial stimuli, the conditioning shock inhibited the test response to a similar extent with and without diazepam. Although baclofen did not change the cortical silent period, it reduced the size of the H reflex in the forearm muscles. Thiopental also left the duration of the cortical silent period unchanged. These findings show that the cortical silent period can be modified pharmacologically. Diazepam possibly shortens the silent period by modulating GABA A receptors at a subcortical site.

Adult↗
PubMed1996

Cortical inhibition in Parkinson's disease. A study with paired magnetic stimulation.

The activity of motor cortical inhibitory circuits was studied with paired transcranial magnetic stimuli in 16 patients with Parkinson's disease 'off' therapy, five patients 'off' and 'on' therapy, and 11 normal subjects. Paired stimuli were delivered at short (3-20 ms) as well as long (100-250 ms) intervals during slight voluntary contraction. The intensity of the conditioning stimulus was subthreshold (80%) at short, and suprathreshold (150%) at long intervals. In addition, the silent period following a single magnetic shock given at 150% of threshold was measured. With short interstimulus intervals, no significant difference between patients and normal subjects could be detected. With long interstimulus intervals, the test response was significantly more inhibited in patients than in normal subjects. Although the cortical silent period was found to be slightly shorter, the recovery of motor evoked potentials was incomplete in patients with Parkinson's disease. This alteration could be partially reverted in dopaminergic therapy. In conclusion, the responsiveness of motor cortices to suprathreshold magnetic stimuli delivered after the end of the silent period is impaired in patients with Parkinson's disease, possibly due to prolonged activity in intracortical inhibitory circuits. The positive effect of L-dopa suggests that dopaminergic modulation of cortical activity, most probably at basal ganglia level, is involved in the pathogenesis of this phenomenon.

Adult↗
PubMed1995

Thrombosis of cerebral veins dural sinuses after paratyphi.

A 20 year old woman was admitted to our Department 15 days after the onset of typhoid fever treated with chloramphenicol. The patient showed intracranial hypertension with generalized seizures, slight right hemiparesis and a left VI cranial nerve deficit with diplopia. Magnetic Resonance Imaging (MRI) showed occlusion of the superior longitudinal, right transverse, right sigmoid sinus combined with a single hemorrhagic infarct in the left occipito-parietal area. Serum tests were positive for Salmonella Paratyphi A and B. The results of cerebrospinal fluid (CSF) examination were normal and blood cultures were negative. Clinical data, laboratory and MRI examinations indicate that the neurological signs are the result of aseptic cerebral sinus thrombosis; the physiopathologic mechanisms of the case are discussed.

Adult↗
PubMed1995

The effect of hyperventilation on motor cortical inhibition in humans: a study of the electromyographic silent period evoked by transcranial brain stimulation.

We studied the effects of hyperventilation under control of the end-tidal PCO2, on the electromyographic silent period evoked by transcranial magnetic brain stimulation and by peripheral nerve stimulation. We also studied the effects of hyperventilation on the threshold, latency and amplitude of motor potentials. Hyperventilation significantly reduced the duration of the cortical silent period, but did not affect the length of the peripheral silent period. Neither did it alter the latency, amplitude or threshold of the motor potentials. These findings suggest that hyperventilation selectively depresses motor cortical inhibition in humans.

Adult↗
PubMed1995

Inhibition of hand muscle motoneurones by peripheral nerve stimulation in the relaxed human subject. Antidromic versus orthodromic input.

In active muscle, a supramaximal conditioning stimulus to peripheral nerve produces a classic silent period in the EMG. The present experiments examined the effect of this type of conditioning stimulus on motoneurone excitability in relaxed muscle. EMG responses evoked by transcranial magnetic stimulation of the brain were recorded from the first dorsal interosseus muscle (FDI) in 10 healthy subjects and 5 patients with sensory neuropathy. These responses (motor evoked potentials) were conditioned by supramaximal peripheral nerve stimuli given 0-150 msec beforehand. In the normal subjects, the classic silent period in the FDI lasted about 100 msec. The same conditioning stimulus only abolished motor evoked potentials when the conditioning-test interval was so short that the antidromic peripheral nerve volley collided with the orthodromic volley set up by magnetic brain stimulation. At longer conditioning-test intervals, although remarkably inhibited (65% mean suppression between 10 and 40 msec), the test motor potential was never completely abolished and gradually recovered by 100 msec. Inhibition of cortically evoked motor potentials did not depend upon activity set up by the conditioning stimulus in peripheral nerve sensory fibres. The patients with complete peripheral sensory neuropathy had the same extent and time-course of inhibition as the normal subjects. We conclude that in relaxed subjects the inhibitory effect of peripheral conditioning results almost exclusively from the motoneuronal inhibitory mechanisms consequent to antidromic invasion.

Adult↗
PubMed1994

Electromyographic silent period after transcranial brain stimulation in Huntington's disease.

The silent period evoked by transcranial (TCS) and nerve stimulation was studied in the hand muscles in 13 patients with Huntington's disease and in 11 normal subjects. The duration of the silent period after TCS was longer in patients and correlated significantly with the severity of chorea; in contrast, the duration of the silent period after nerve stimulation was similar in patients and controls. The prolongation of the cortical silent period suggests that the duration of the silent period is a functional correlate reflecting basal ganglia influence over the motor cortex.

Adult↗
PubMed1994

Effects of transcranial magnetic stimulation on single and sequential arm movements.

We studied in humans the effects of transcranial stimulation of cortical motor areas on the execution of single and sequential rapid arm movements. In a reaction time paradigm with an auditory "go" signal, stimulation given after an auditory tone and before the start of movements delayed the onset but did not affect the subsequent performance of single or sequential movements; high intensities of cortical stimulation determined a long-lasting inhibition of movements. Cortical stimulation given during the execution of a sequential movement temporarily interrupted the movements. Reaction time was not prolonged and movements were not inhibited when cortical stimulation was delivered before the auditory tone and the start of movement. Neither electrical stimulation of the corticospinal tracts at the cervico medullary junction nor magnetic stimulation of the cervical roots delayed the onset or interrupted the execution of movements. Transcranial stimulation affects the performance of both single and sequential movements, through cortical mechanisms that interfere with the transfer of the motor program from other cortical structures to the motor cortex.

Adult↗
PubMed1994

Motor cortical inhibition and the dopaminergic system. Pharmacological changes in the silent period after transcranial brain stimulation in normal subjects, patients with Parkinson's disease and drug-induced parkinsonism.

The silent period after contralateral and ipsilateral transcranial magnetic brain stimulation was studied in patients with Parkinson's disease before and after dopaminergic and anticholinergic therapy; in normal subjects before and after L-dopa administration and in patients with drug-induced parkinsonism. In patients and normal subjects the silent period was also studied after peripheral nerve stimulation. The silent period after transcranial cortical stimulation was shorter in Parkinson's disease patients than in normal subjects. In patients with Parkinson's disease L-dopa prolonged the silent period after transcranial brain stimulation and after ipsilateral cortical stimulation. Biperiden prolonged the silent period after transcranial brain stimulation. In normal subjects, L-dopa produced similar but smaller changes. In the patients with drug-induced parkinsonism the silent period after transcranial magnetic stimulation was shorter than normal subjects. The peripheral silent period was similar in normal subjects and in patients and did not change after drug administration. In conclusion cortical silent period is abnormal in patients with Parkinson's disease and drug-induced parkinsonism. Dopaminergic drugs modulate the duration of the cortical silent periods in patients and in normal subjects, through mechanisms acting mainly at basal ganglia and possibly also directly at cortical level.

Adult↗
PubMed1994

Pathophysiology of hemimasticatory spasm.

Two patients aged 21 and 50 years presented with facial hemiatrophy and unilateral spasms of the masticatory muscles. Masticatory muscle biopsy showed normal findings in both patients and facial skin biopsy specimens only showed atrophy, although morphoea (localised facial scleroderma) had been diagnosed nine years previously in the second patient. The involuntary movements consisted of brief twitches and prolonged contractions clinically and electromyographically similar to those of hemifacial spasm and cramps. The jaw jerk and the silent periods were absent in the affected muscles. Direct stimulation of the muscle nerve and transcranial stimulation of the trigeminal root demonstrated slowing of conduction and after-activity due to autoexcitation. Observations in other reported cases and these two patients suggest that hemimasticatory spasm is produced by ectopic activity secondary to focal demyelination of the trigeminal motor nerve fibres. The proposed cause of the neuropathy is focal damage to the masticatory nerves caused by compression, possibly resulting from the deep tissue changes that occur in facial hemiatrophy.

Adolescent↗
PubMed1994

Transcranial electrical stimulation in patients with apallic syndrome.

Muscle responses (MEPs) to transcranial electrical stimulation were studied in 7 patients with apallic syndrome. All the patients showed clinical signs of upper motor neurone impairment in the upper and lower limbs. MEPs were absent or markedly delayed in 4 of the 7 patients. Since patients with apallic syndrome show only minimal voluntary movement, transcranial stimulation is the only way to demonstrate abnormalities of fast corticospinal axons in these patients. Even though these patients often look similar clinically, with tetraplegia and decorticate or decerebrate posture, only some cases showed dysfunction of fast corticospinal neurons.

Adolescent↗
PubMed1993

Silent period evoked by transcranial stimulation of the human cortex and cervicomedullary junction.

1. The silent period evoked in the first dorsal interosseous (FDI) muscle after electrical and magnetic transcranial stimulation (TCS), electrical stimulation of the cervicomedullary junction and ulnar nerve stimulation was studied in ten healthy subjects. 2. With maximum-intensity shocks, the average duration of the silent period was 200 ms after electrical TCS, 300 ms after magnetic TCS, 43 ms after stimulation at the cervicomedullary junction and 100 ms after peripheral nerve stimulation. 3. The duration of the silent period, the amplitude of the motor-evoked potential, and the twitch force produced in the muscle were compared at increasing intensities of magnetic TCS. When the stimulus strength was increased from 30 to 70% of the stimulator output, the duration of the silent period lengthened as the amplitude of the motor potential and force of the muscle twitch increased. At 70 to 100% of the output, the amplitude of the motor potential and force of the muscle twitch saturated, whereas the duration of the silent period continued to increase. 4. Proximal arm muscle twitches induced by direct electrical stimulation of the biceps and extensor wrist muscles produced no inhibition of voluntary activity in the contracting FDI muscle. 5. The level of background activation had no effect on the duration of the silent period recorded in the FDI muscle after magnetic TCS. 6. Corticomotoneurone excitability after TCS was studied by means of a single magnetic conditioning shock and a test stimulus consisting either of one single magnetic shock or single and double electrical shocks (interstimulus interval 1.8 ms) in the relaxed muscle. A conditioning magnetic shock completely suppressed the response evoked by a second magnetic shock, reduced the size of the response evoked by a single electrical shock but did not affect the response evoked by double electrical shocks. Inhibition of the test magnetic shock was also present during muscle contraction. 7. Our findings indicate that the first 50 ms of the silent period after TCS are produced mainly by spinal mechanisms such as after-hyperpolarization and recurrent inhibition of the spinal motoneurones. If descending inhibitory fibres contribute, their contribution is small. Changes in proprioceptive input probably have a minor influence. From 50 ms onwards the silent period is produced mainly by cortical inhibitory mechanisms.

Adult↗
PubMed1991

Effects of electric and magnetic transcranial stimulation on long latency reflexes.

The interaction of transcranial electric and magnetic brain stimulation with electrically elicited short- and long latency reflexes (LLR) of hand and forearm flexor muscles has been investigated in normal subjects. In the first paradigm, the motor potential evoked in thenar muscles by transcranial stimulation was conditioned by median nerve stimulation at various conditioning-test intervals. At short intervals (electric: 5-12.5 ms, magnetic: 0-7.5 ms) facilitation occurred that corresponded to the H-reflex and at longer intervals (electric: 25-40 ms, magnetic: 22.5-35 ms) there was a facilitation corresponding to the LLR. Electric and magnetic stimulation resulted in a similar degree of facilitation. A second paradigm investigated the facilitation of the forearm flexor H-reflex by a cutaneo-muscular LLR elicited by radial superficial nerve stimulation and transcranial stimulation used separately or together. When electric and magnetic brain stimulation were compared, magnetic brain stimulation was followed by significant extrafacilitation but electric stimulation was not. This result favours an interaction between the afferent volley eliciting the LLR and transcranial magnetic stimulation most likely at supraspinal level.

Adult↗
PubMed1991

Corticobulbar and corticospinal projections to neck muscle motoneurons in man. A functional study with magnetic and electric transcranial brain stimulation.

The cortical projections to neck muscle motoneurons were studied in normal subjects by electrical and magnetic transcranial brain stimulation. After magnetic stimulation with a large coil, motor evoked potentials were present in about 20% of relaxed and 100% of contracting neck muscles. The latency of these responses was short: about 7 ms in the sternomastoid and splenius and 9 ms in the trapezius muscles. Subtraction of the M-wave latency after stimulation of the accessory nerve at the skull base resulted in a central latency of about 4.5 ms. We suggest that rapid cortical projections connect with neck muscle motoneurons mono or disynaptically. The latency difference between the responses after electrical and magnetic stimulation was smaller in neck than in limb muscles but similar to that seen in masticatory muscles. A small magnetic coil was used to study the pattern of functional lateralization of cortical projections to neck muscle motoneurons; the projections for the sternomastoid and splenius are bilateral but predominantly contralateral, whereas those for the trapezius are exclusively contralateral.

Adult↗
PubMed1991

Electrical and magnetic transcranial stimulation in patients with corticospinal damage due to stroke or motor neurone disease.

Twenty patients with hemiplegia and 13 patients with motor neurone disease were studied with electrical and magnetic transcranial stimulation. Motor evoked potentials were recorded from the biceps, thenar and tibialis anterior muscles. In both groups of patients magnetic stimulation with a Novametrix stimulator revealed fewer abnormalities than electrical stimulation with a Digitimer D180 stimulator. In patients with hemiplegia, motor evoked potentials after electrical stimulation were absent in 70% of muscles, delayed in 22% and normal in 8%; after magnetic stimulation, they were absent in 53% of muscles, delayed in 28% and normal in 19%. In patients with motor neurone disease, motor evoked potentials after electrical stimulation were absent in 62% of muscles, delayed in 10%, and normal in 29%; after magnetic stimulation, they were absent in 45% of muscles, delayed in 15%, and normal in 40%. The reason why magnetic stimulation reveals fewer abnormalities than electrical stimulation could be that magnetic stimulation repetitively discharges the pyramidal cells and, because of temporal summation mechanisms, produces more powerful excitatory potentials at the lower motoneurone synapse.

Adult↗
PubMed1991

Multiple firing of motoneurones is produced by cortical stimulation but not by direct activation of descending motor tracts.

In the present report we have tested whether stimulation of the motor descending tracts at the brain-stem level could set up repetitive motor unit discharges in a similar manner to that described for motor cortical stimulation. We have seen that a large descending motor volley, evoked by brain-stem stimulation, cannot produce repetitive firing of motor units. Repetitive motoneurone firing is therefore produced by multiple excitatory volleys set up by single cortical shocks.

Brain Stem↗