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Biomedical subjects

A Berardelli

Publications and source records attributed to A Berardelli.

At least 19 recordsLinked to original sources
PubMed1999

Pathophysiology of chorea and bradykinesia in Huntington's disease.

This article reviews the neurophysiological abnormalities described in Huntington's disease. Among the typical features of choreic movements are variable and random patterns of electromyographic (EMG) activity, including cocontraction of agonist and antagonist muscles. Studies of premotor potentials show that choreic movements are not preceded by a Bereitschaftspotential, therefore demonstrating that choreic movement is involuntary. Early cortical median-nerve somatosensory-evoked potentials have reduced amplitudes and the reduction correlates with reduced glucose consumption in the caudate nucleus. Long-latency stretch reflexes evoked in the small hand muscles are depressed. These findings may reflect failed thalamocortical relay of sensory information. In Huntington's disease, the R2 response of the blink reflex has prolonged latencies, diminished amplitudes, and greater habituation than normal. These abnormalities correlate with the severity of chorea in the face. Patients with Huntington's disease perform simple voluntary movements more slowly than normal subjects and with an abnormal triphasic EMG pattern. Bradykinesia is also present during their performance of simultaneous and sequential movements. Eye movements show abnormalities similar to those seen in arm movements. In Huntington's disease, arm movement execution is associated with reduced PET activation of cortical frontal areas. Studies using transcranial magnetic stimulation show that patients with Huntington's disease have normal corticospinal conduction but some patients have a prolonged cortical silent period. Bradykinesia results from degeneration of the basal ganglia output to the supplementary motor areas concerned with the initiation and maintenance of sequential movements. The coexisting hyperkinetic and hypokinetic movement disorders in patients with Huntington's disease probably reflect the involvement of direct and indirect pathways in the basal ganglia-thalamus-cortical motor circuit.

Basal Ganglia↗
PubMed1999

Effects of repetitive cortical stimulation on the silent period evoked by magnetic stimulation.

The effects of repetitive transcranial stimulation (rTMS) on brain activity remain unknown. In healthy subjects, we studied the effects of rTMS on the duration of the cortical silent period (SP). Repetitive stimuli were delivered with a Cadwell High Speed Magnetic Stimulator and a figure-of-eight coil placed over the hand motor area. rTMS was delivered in trains of 11 or 20 stimuli at frequencies of 3 and 5 Hz and at stimulation intensities of 110 and 120% of motor threshold. The SP was recorded from the forearm muscles during a voluntary contraction (20% of maximum effort). rTMS delivered at a frequency of 3 and 5 Hz and intensities of 110 and 120% motor threshold prolonged the duration of the SP, without modifying either the size or the latency of the muscle-evoked potentials (MEP). A conditioning train of 11 stimuli at 3 Hz had no effect on the duration of the SP evoked by a single magnetic shock delivered 600 ms after the train. These findings show that rTMS increases the duration of the cortical SP, but does so only during the train of stimuli. rTMS probably changes the duration of the SP by facilitating cortical inhibitory interneurons.

Adult↗
PubMed1998

Polarization of the human motor cortex through the scalp.

Direct currents (DC) applied directly to central nervous system structures produce substantial and long-lasting effects in animal experiments. We tested the functional effects of very weak scalp DC (< 0.5 mA, 7 s) on the human motor cortex by assessing the changes in motor potentials evoked by transcranial magnetic brain stimulation. We performed four different experiments in 15 healthy volunteers. Our findings led to the conclusion that such weak (< 0.5 mA) anodal scalp DC, alternated with a cathodal DC, significantly depresses the excitability of the human motor cortex, providing evidence that a small electric field crosses the skull and influences the brain. A possible mechanism of action of scalp DC is the hyperpolarization of the superficial excitatory interneurones in the human motor cortex.

Adult↗
PubMed1998

Reciprocal inhibition in forearm muscles in patients with essential tremor.

Reciprocal inhibition of the H-reflex in the forearm flexor muscles was studied in 11 patients with essential tremor and in 10 normal controls. Whereas patients and controls had a similar first, disynaptic phase of reciprocal inhibition, patients had a significantly reduced second phase. Patients with more severe functional impairment had more pronounced abnormalities of reciprocal inhibition. Abnormalities of reciprocal inhibition may play a role in the pathophysiology of essential tremor and probably arise from defective suprasegmental control.

Electromyography↗
PubMed1998

Cortical excitability in patients with essential tremor.

We used transcranial magnetic stimulation in 10 patients with essential tremor and 8 matched healthy subjects. A round stimulating coil was placed over the vertex and electromyographic activity was recorded from the first dorsal interosseous muscle. Paired transcranial stimuli were delivered at interstimulus intervals of 3, 5, 20, 100, 150, and 200 ms. The intensity of the conditioning stimulus was 80% of motor threshold at short and 150% at long interstimulus intervals (ISIs). We also measured the silent period obtained after a single magnetic pulse delivered at 150% of motor threshold during a submaximal muscle contraction. Patients and controls had similar motor threshold and similar latencies. Paired magnetic stimuli given at short and long ISIs at rest, and during a voluntary muscle contraction, elicited similar responses in both groups. The silent period evoked by transcranial magnetic stimulation had a similar duration in patients with ET and controls. In conclusion, these findings suggest that patients with essential tremor have normal cortical motor area excitability.

Aged↗
PubMed1998

Botulinum toxin restores presynaptic inhibition of group Ia afferents in patients with essential tremor.

We studied the effect of botulinum toxin A injection on the abnormal presynaptic phase of reciprocal inhibition between forearm antagonist muscles in patients with essential tremor. Ten patients with essential tremor were investigated before and 1 month after botulinum injection. Reciprocal inhibition was studied by conditioning the H reflex in forearm flexors with a radial-nerve stimulus delivered at a range of time intervals. Botulinum toxin produced a significant functional improvement in tremor (about 20%). Before botulinum toxin injection, patients had a reduced presynaptic phase of reciprocal inhibition. After botulinum toxin this phase was significantly more pronounced. The normal early disynaptic phase of reciprocal inhibition was normal before and after botulinum treatment. Although botulinum treatment reduced the size of the H reflex and the M wave to a similar extent, it left the H/M ratio unchanged. These findings show that botulinum toxin treatment restores presynaptic inhibition between forearm antagonist muscles. The results are also consistent with botulinum toxin having a beneficial effect in patients with essential tremor. Both effects probably depend upon the toxin's concurrent action on the extrafusal and intrafusal motor end-plates, the latter resulting in decreased spindle afferent input to the spinal cord.

Adult↗
PubMed1998

Alterations of motor cortical inhibition in patients with dystonia.

Cortical inhibitory mechanisms were investigated with the technique of paired transcranial magnetic stimulation in 10 patients with dystonia of the right arm: six patients had focal, task-specific dystonia (writer's cramp) and three had segmental and one had generalized dystonia. Paired stimuli were delivered in a conditioning-test design during slight voluntary activation of the target muscle, with subthreshold conditioning stimuli at short intervals (3-20 ms) and suprathreshold conditioning stimuli at long intervals (100-250 ms). The amount of inhibition at short interstimulus intervals did not differ significantly between patients and normal subjects. With long interstimulus intervals, patients showed more inhibition of the test response, which was significant at the 150-ms interval. The cortical silent period following a single suprathreshold magnetic stimulus was slightly shorter in patients. No significant difference was detected between the affected side and the unaffected side in patients with unilateral task-specific dystonia, neither in the duration of the silent period nor in the response to paired magnetic stimuli. These results indicate that the different types of motor cortical inhibition are produced by different inhibitory circuits. We propose that the alterations observed in patients with dystonia are the result of impaired feedback from the basal ganglia to motor cortical areas, with the ultimate effect of a flattening of the excitability curve of the cortical motoneuron pool during voluntary muscle activation.

Adult↗
PubMed1998

Clinical impairment of sequential finger movements in Parkinson's disease.

A retrospective analysis was performed on the records of 33 off-therapy parkinsonian patients. We analyzed the clinical score of three sequential upper limb movements: finger tapping, hand opening and closing, and forearm pronation and supination. The records showed that nearly all patients had difficulty in performing all three motor tasks, but movement scores showed that they found the sequential finger-tapping task significantly more difficult than the other two tasks. We suggest that parkinsonian patients find individual finger movements more difficult to execute than gross hand movements because--owing to their abnormal basal ganglia output--they lack the finer cortical control and greater facilitation that the finger task demands.

Aged↗
PubMed1998

Sleep disorders in Parkinson's disease.

The nature of sleep is one of the major sources of dissatisfaction with the quality of life among patients with Parkinson's disease (PD). Difficult sleep maintenance (light and fragmented sleep) and difficulties with sleep initiation are the earliest and most frequent sleep disorders observed in these patients. Sleep disorders are also common in the normal elderly population, suggesting that normal aging may play a role in the etiology of sleep disorders in PD. Factor et al. examined the frequency of various sleep disorders in PD and compared them to those of normal elderly subjects. Sleep fragmentation and spontaneous daytime dozing occurred much more frequently in PD patients than in controls. Sleep fragmentation in PD may be due to an increased skeletal muscle activity, disturbed breathing and REM/non-REM variations of the dopaminergic receptor sensitivity. In parkinsonian patients who developed motor fluctuations (on-off phenomenon, wearing-off) during the day, other common sleep-related motor complaints including nocturnal akinesia, dystonia and painful cramps are observed. In a double-blind cross-over study, we compared the efficacy of a single dose of a chronic release formulation of levodopa/carbidopa (Sinemet CR) with that of a placebo in improving sleep-related motor disturbances in a group of 40 fluctuating PD patients. Sinemet CR significantly improved nocturnal akinesia and increased the hours of sleep in this group of patients. Initiation and maintenance of sleep are problems that may not be solved with antiparkinsonian treatment.

Aged↗
PubMed1998

Facilitation of muscle evoked responses after repetitive cortical stimulation in man.

The technique of repetitive transcranial magnetic stimulation (rTMS) allows cortical motor areas to be activated by trains of magnetic stimuli at different frequencies and intensities. In this paper, we studied long-term neurophysiological effects of rTMS delivered to the motor cortex at 5 Hz with an intensity of 120% of motor threshold. Each stimulus of the train produced muscle-evoked potentials (MEPs) in hand and forearm muscles, which gradually increased in size from the first to the last shock. After the end of the train, the response to a single-test stimulus remained enhanced for 600-900 ms. In contrast, the train had no effect on the size of the MEPs evoked by transcranial electrical stimulation, while it suppressed H-reflexes in forearm muscles for 900 ms. We conclude that rTMS of these parameters increases the excitability of the motor cortex and that this effect outlasts the train for almost 1 s. At the spinal level, rTMS may increase presynaptic inhibition of Ia afferent fibers responsible for the H-reflex.

Adult↗
PubMed1998

Peripheral nervous system involvement in a patient with large T-cell lymphoma arising from a pre-existing mycosis fungoides.

A 29-year-old man was examined for disseminated erythematous scaling patches and plaques and reddish, partially ulcerated nodules. Histological examination showed a dense, diffuse, epidermotropic infiltrate located in the entire dermis to the subcutaneous tissue, composed mainly of large pleomorphic T lymphocytes. Immunohistochemistry revealed positivity of neoplastic cells for T-cell-associated markers, negativity for CD30 antigen and for B-cell markers. Polymerase chain reaction analysis detected a clonal amplification of T-cell receptor gamma. Based on clinicopathological and molecular findings, the diagnosis of large T-cell lymphoma (LCL) arising from a pre-existing mycosis fungoides was made. Seven months after primary diagnosis, meningeal and peripheral nervous system involvement developed with no other evidence of systemic disease. Despite chemotherapy and radiation therapy, the patient died 3 months after the diagnosis of nervous system involvement. In patients with cutaneous LCL, mild neurological symptoms may precede the complete diagnostic picture by some weeks. A rapid and fatal progression characterizes the clinical course of the disease.

Adult↗
PubMed1998

Electrical stimulation over muscle tendons in humans. Evidence favouring presynaptic inhibition of Ia fibres due to the activation of group III tendon afferents.

Electrical stimulation over muscle tendons produces a transient suppression of voluntary EMG activity; its onset latency is approximately 55 ms in the forearm extensor muscles. This phenomenon has been attributed to the activation of a polysynaptic inhibitory pathway originating from Ib afferent fibres. To clarify its origin we conducted several experiments in 10 normal healthy subjects. The EMG silence after tendon stimulation appeared at relatively high stimulus intensities (> 50 mA); conditioning cutaneous stimulation left it unchanged, and the inhibition had a short recovery cycle (50 ms). Tendon stimulation still evoked EMG suppression during an ischaemic block of fast-conducting afferents. The motor potentials evoked by transcranial magnetic stimulation of the motor cortex during the EMG silence remained almost unchanged, whereas the H reflex was strongly inhibited. Hence we conclude that tendon stimulation activates slow-conducting tendon afferents, possibly group III fibres, connected not through a polysynaptic pathway originating from Ib afferents but through an oligo- or disynaptic inhibitory circuit. The EMG suppression after tendon stimulation probably represents a dysfacilitation of the alpha-motor neurons due to presynaptic inhibition of Ia fibres produced by tendon afferent input to the spinal cord.

Adult↗
PubMed1998

The pathophysiology of primary dystonia.

Co-contraction and overflow of EMG activity of inappropriate muscles are typical features of all dystonic movements whether voluntary or involuntary. Voluntary movements are slow and more variable than normal, and there is particular difficulty switching between component movements of a complex task. Reduced spinal cord and brainstem inhibition is common to many reflex studies (long-latency reflexes, cranial reflexes and reciprocal inhibition). These reflex abnormalities may contribute to the difficulties in voluntary movements but cannot be causal as they can occur outside the clinically involved territory. Clinical and neurophysiological studies have emphasized the possible role of sensory feedback in the generation of dystonic movements. Abnormalities of cortical and basal ganglia function have been described in functional imaging and neurophysiological studies of patients with dystonia and in animal models of primary dystonia. Studies of cortical function have shown reduced preparatory activity in the EEG before the onset of voluntary movements, whilst magnetic brain stimulation has revealed changes in motor cortical excitability. Functional imaging of the brain in primary dystonia has suggested reduced pallidal inhibition of the thalamus with consequent overactivity of medial and prefrontal cortical areas and underactivity of the primary motor cortex during movements. These findings are supported by preliminary neuronal recordings from the globus pallidus and the thalamus at the time of stereotaxic surgery in patients with dystonia. All this evidence suggests that primary dystonia results from a functional disturbance of the basal ganglia, particularly in the striatal control of the globus pallidus (and substantia nigra pars reticulata). This causes altered thalamic control of cortical motor planning and executive areas, and abnormal regulation of brainstem and spinal cord inhibitory interneuronal mechanisms.

Animals↗
PubMed1998

Possible risk factors for primary adult onset dystonia: a case-control investigation by the Italian Movement Disorders Study Group.

OBJECTIVES: Little is known about the aetiology of idiopathic adult onset dystonia. The Italian Movement Disorders Study Group promoted a case-control study on some hypothetical risk factors including past medical events, life events, life habits, occupational hazards, and family history of dystonia, parkinsonism, and tremor. METHODS: Cases affected by idiopathic adult onset dystonia (age at symptom onset >20 years, duration of disease >one year and <five years) were selected among consecutive outpatients attending 14 Italian centres. Control outpatients matched for age (+/-5 years), sex, and referral centre were identified among diagnostic categories thought to be unassociated with study exposures. Information was obtained by a standardised questionnaire administered by medical interviewers. Conditional logistic univariate and multivariate regression analyses were performed by a standard statistical package. RESULTS: Multivariate analysis on 202 cases and 202 age and sex matched control outpatients indicated that head or facial trauma with loss of consciousness, family history of dystonia, and family history of postural tremor independently increased the risk of developing adult onset dystonia, whereas hypertension and cigarette smoking exerted a protective effect. The findings also suggested a positive association between local body injury-for example, previous ocular diseases and neck or trunk trauma-and dystonia of the same body part. CONCLUSIONS: The results support the idea that environmental and genetic factors may both be important in the aetiology of adult onset dystonia, and suggest aetiological clues worthy of further analytical investigation.

Adult↗
PubMed1997

Cortical mechanisms mediating the inhibitory period after magnetic stimulation of the facial motor area.

We studied the silent period (SP) that interrupts voluntary electromyographic activity (EMG) in facial muscles, after transcranial magnetic stimulation (TMS), in normal subjects. High-intensity magnetic stimulation with a 12-cm round coil centered at the vertex induced a long-lasting SP (215 ms), whereas supramaximal stimulation of the facial nerve only induced a short (< 20 ms) and incomplete EMG suppression, and cutaneous stimuli had no inhibitory effect at all. Cutaneous trigeminal stimulation delivered after TMS evoked blink-like reflexes, showing that facial motoneurons were not inhibited during the SP. Simultaneous recordings from perioral muscles (large cortical representation) and from orbicularis oculi and masseter muscles (small cortical representation) showed SPs of identical duration. Focal stimuli with a figure-of-eight coil showed that positioning of the coil was critical and that the optimal scalp sites for evoking the largest motor potentials and longest SPs coincided. Low-intensity stimulation occasionally elicited short SPs without a preceding motor potential. We conclude that the SP induced in facial muscles by TMS results from the excitation of cortical inhibitory interneurons surrounding the upper motoneurons.

Adult↗
PubMed1997

Performance of sequential arm movements with and without advance knowledge of motor pathways in Parkinson's disease.

Patients with Parkinson's disease are slower than normal subjects in executing sequential arm movements, and their bradykinesia worsens as the execution of motor sequences progresses. In parkinsonian and normal subjects, we studied the execution of two types of fast sequential arm movements. The subjects had to perform a motor sequence following with their arm a path marked by six targets on a screen. In one experimental condition, they performed the motor sequence without advance knowledge of its path and executed each submovement in response to the consecutive appearance of the targets on the screen (unknown motor sequences). In the other condition, all the targets appeared simultaneously on the screen before the subject moved, and the subject internally determined when to execute each submovement (known motor sequences). Patients were slower than normal subjects in executing both sequences. Patients and normal subjects were faster in executing known than unknown sequences, but the patients' percentage of total movement time diminished less. During the unknown condition, both groups tended to lengthen submovement duration whereas, during the known condition, both groups tended to correct this trend. Patients performed submovements during both sequences with longer acceleration phases. The submovement symmetry ratio of the velocity profile changed according to the direction of movement (up or down). We conclude that these findings depend mainly on the model of movement execution. They also suggest that patients with Parkinson's disease have more difficulty in executing internally determined than externally triggered sequential movements.

Adult↗
PubMed1997

Guidelines for the therapeutic use of botulinum toxin in movement disorders. Italian Study Group for Movement Disorders, Italian Society of Neurology.

Since its introduction in the early '80s the use of botulinum toxin has improved the quality of life of the patients affected by movement disorders. Toxin's neuromuscular blocking action allows a symptomatic treatment of those clinical conditions characterised by excessive muscular activity. Although the dosages used are safe and the side-effects are reversible, a correct use of botulinum toxin depends on the knowledge of its clinical pharmacology and of the anatomy of the body segments to be injected. In addition, the treatment of more complex conditions, i.e. laringeal dystonia, imposes an inter-disciplinary approach and specialised injection techniques. In this review, the Italian Study Group on Movement Disorders presents the consensus guidelines for the therapeutic use of botulinum toxin in movement disorders. The main toxin types, their use and administration modalities, and the training guidelines will be presented.

Botulinum Toxins↗