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Biomedical subjects

A Priori

Publications and source records attributed to A Priori.

At least 37 records · Page 2Linked to original sources
PubMed2002

Movement-related modulation of neural activity in human basal ganglia and its L-DOPA dependency: recordings from deep brain stimulation electrodes in patients with Parkinson's disease.

Through electrodes implanted for deep brain stimulation in three patients (5 sides) with Parkinson's disease, we recorded the electrical activity from the human basal ganglia before, during and after voluntary contralateral finger movements, before and after L-DOPA. We analysed the movement-related spectral changes in the electroencephalographic signal from the subthalamic nucleus (STN) and from the internal globus pallidus (GPi). Before, during and after voluntary movements, signals arising from the human basal ganglia contained two main frequencies: a high beta (around 26 Hz), and a low beta (around 18 Hz). The high beta (around 26 Hz) power decreased in the STN and GPi, whereas the low beta (around 18 Hz) power decrease was consistently found only in the GPi. Both frequencies changed their power with a specific temporal modulation related to the different movement phases. L-DOPA specifically and selectively influenced the spectral power changes in these two signal bands.

Antiparkinson Agents↗
PubMed2002

Anatomo-clinical correlation of intraoperative stimulation-induced side-effects during HF-DBS of the subthalamic nucleus.

The efficacy of deep brain stimulation of the subthalamic nucleus (STN) is dependent on the accuracy of targeting. In order to reduce the number of passes and, consequently, the duration of surgery and risk of bleeding, we have set up a new method based on direct magnetic resonance imaging (MRI) localisation of the STN. This procedure allows a short duration of the neurophysiological session (one or two initial tracks). Whenever a supplementary track is needed, the stimulation-induced side effects are analysed to choose from one of the remaining holes in Ben's gun. A good knowledge of anatomical structures surrounding the STN is mandatory to relate side effects to the actual position of the track. In our series of 11 patients (22 sides, 37 tracks), the most common and reproducible side effects were those characterised by motor, sensorial, oculomotor and vegetative signs and symptoms. Moreover, the therapeutic window (distance between the current intensity needed to obtain the best clinical effect and the intensity capable to induce side effects) predicted clinical efficacy in the long-term, and contributed to the choice of which among the examined tracks had to be implanted with the chronic macroelectrode.

Electric Stimulation Therapy↗
PubMed2002

Distinctive abnormalities of motor axonal strength-duration properties in multifocal motor neuropathy and in motor neurone disease.

The strength-duration function is a classic measure of neural excitability. When studied on peripheral motor axons it reflects the intrinsic nodal membrane properties, and its time-constant (tau(SD) or chronaxie) predominantly depends on non-voltage-gated, rest Na(+) inward conductances. We assessed the strength-duration curve of ulnar motor axons in 22 nerves of healthy controls, in 18 nerves of patients with multifocal motor neuropathy with conduction blocks (MMN), and in 19 nerves of patients with motor neurone disease (MND). The compound muscle action potential (CMAP) was smaller in nerves of both groups of patients than in controls (P < 0.05). The rheobasic current (rh(50%)) [mean +/- standard deviation (SD)] was higher in patients with MMN than in controls (13.3 +/- 16.3 mA; controls 4.7 +/- 1.7 mA, P < 0.05). The tau(SD) was differentially abnormal in the nerves of the two groups of patients: it was prolonged in the nerves of patients with MND for >or=40 years (227.2 +/- 34.5 micro s; controls 190.9 +/- 51.0 micro s, P < 0.05), but it was shortened in the nerves of patients with MMN (146.5 +/- 55.4 micro s; controls 208.6 +/- 51.2 micro s, P < 0.05) who had not been treated recently with high-dose intravenous immunoglobulin (IVIg). Nerves of patients with recently treated MMN (<6 weeks) who were under the therapeutic effect of IVIg had a normal tau(SD)(.) Our results suggest that, probably due to an immuno-mediated rest Na(+) channel dysfunction, Na(+) conductances are reduced in MMN. This abnormality is a function of the time after the last IVIg treatment and involves also the axonal membrane outside the conduction block. Conversely, in MND, possibly owing to the ionic leakage of degenerating membrane, rest Na(+) conductances are increased. Measuring the strength-duration curve of the ulnar motor axons might be useful in the differential diagnosis between de novo MMN and MND.

Action Potentials↗
PubMed2002

Multifocal motor neuropathy: clinical and immunological features and response to IVIg in relation to the presence and degree of motor conduction block.

OBJECTIVE: To determine whether patients with clinically typical multifocal motor neuropathy (MMN) with or without definite or probable conduction block (CB) differ in terms of clinical presentation, immunological findings, or response to treatment with intravenous immunoglobulin (IVIg). METHODS: 23 consecutive patients were studied with the typical clinical features of MMN, consisting of a progressive multineuropathic motor impairment with minimal or no sensory loss. In 14 patients, electrophysiological studies disclosed the presence of a definite or probable CB according to the criteria proposed by the American Association of Electrodiagnostic Medicine (AAEM) in at least one motor nerve. Six patients had possible CB, defined as a degree of CB 10% less than that required by the AAEM for probable CB, while no CB was detected in three patients. RESULTS: Patients with possible CB did not differ from those with a definite or probable CB in terms of age at disease onset (mean 38.8 v 38.2 years, respectively), distribution and severity of limb weakness, clinical impairment (mean Rankin score 2.2 in both), and frequency of antiganglioside antibodies (33% v 29%). Patients with possible CB had a longer mean disease duration (9 v 5.9 years, p < 0.05) and a less frequent consistent response to IVIg (67% v 86%) than those with a definite or probable CB. Patients without a detectable CB had a similar frequency of antiganglioside antibodies (33%) but had a longer disease duration (20.3 years), greater impairment (Rankin score 2.7), and more frequent signs of axonal degeneration (41% of examined motor nerves) than patients with CB (13-15%, p < 0.005). Only one patient without detectable CB (33%) consistently improved with IVIg. CONCLUSIONS: Patients with possible CB were clinically and immunologically indistinguishable from those with definite or probable CB, albeit with a slightly less frequent response to IVIg. This finding suggests that failure to fulfil AAEM criteria for CB in patients with otherwise clinically typical MMN should not preclude this diagnosis and consequently a treatment trial with IVIg. Whether the longer duration and greater severity of the disease and more frequent axonal impairment in patients without detectable CB than in those with CB explain their lower response to IVIg remains to be established.

Adult↗
PubMed2001

Limb immobilization for the treatment of focal occupational dystonia.

BACKGROUND: Occupational focal upper-limb dystonia is characterized by involuntary muscle contractions that selectively interfere with the execution of specific motor tasks such as writing or playing a musical instrument. Occupational dystonias have a severe social impact, especially in certain professions. The available medical treatments offer little benefit. METHODS: In eight patients with idiopathic occupational focal dystonia of the upper limb, the dystonic forearm and hand were immobilized with a plastic splint for mean (+/-SD) 4.5 +/- 0.75 weeks. Before splinting (base line) and at various intervals afterwards (4, 12, and 24 weeks), the authors assessed the severity of dystonia and the patients' motor performance objectively (Arm Dystonia Disability Scale and Tubiana and Chamagne Score) and subjectively (Self-Rating Score). RESULTS: Assessment 4 weeks after splint removal, when patients had regained normal voluntary movements, showed that the severity of dystonia and the patients' performance of the impaired motor task had improved; the benefit persisted unchanged at later follow-up visits (Arm Dystonia Disability Scale: base line 20.6 +/- 30.2%; after 4 weeks 83.9 +/- 23.8%, p = 0.007; after 12 weeks 83.9 +/- 23.8%, p = 0.007; after 24 weeks 79.7 +/- 29.5%, p = 0.015. Tubiana and Chamagne Score: base line 28.6 +/- 22.7%; after 4 weeks 80.0 +/- 23.1%, p = 0.015; after 12 weeks 80.0 +/- 23.1%, p = 0.015; after 24 weeks 74.3 +/- 32.1%, p = 0.031. Self-Rating Score: base line 20.6 +/- 19.3%; after 4 weeks 63.7 +/- 25.2%, p = 0.015; after 12 weeks 66.9 +/- 28.1%, p = 0.015; after 24 weeks 70.6 +/- 31.8%, p = 0.015). At the 24-week visit the improvement disappeared in one patient, was moderate in three, and marked in four. CONCLUSIONS: Limb immobilization can be a simple, effective, safe, and inexpensive treatment for focal occupational upper-limb dystonia.

Adult↗
PubMed2001

Excitability of the human trigeminal motoneuronal pool and interactions with other brainstem reflex pathways.

We studied the properties of motoneurones and Ia-motoneuronal connections in the human trigeminal system, and their functional interactions with other brainstem reflex pathways mediated by non-muscular (Abeta) afferents. With surface EMG recordings we tested the recovery cycles of the heteronymous H-reflex in the temporalis muscle and the homonymous silent period in the masseter muscle both elicited by stimulation of the masseteric nerve at the infratemporal fossa in nine healthy subjects. In four subjects single motor-unit responses were recorded from the temporalis muscle. In six subjects we also tested the effect of the stimulus to the mental nerve on the temporalis H-reflex and, conversely, the effect of Ia input (stimulus to the masseteric nerve) on the R1 component of the blink reflex in the orbicularis oculi muscle. The recovery cycle of the H-reflex showed a suppression peaking at the 5-20 ms interval; conversely the time course of the masseteric silent period was facilitated at comparable intervals. The inhibition of the test H-reflex was inversely related to the level of background voluntary contraction. Single motor units were unable to fire consistently in response to the test stimulus at intervals shorter than 50 ms. Mental nerve stimulation strongly depressed the H-reflex. The time course of this inhibition coincided with the EMG inhibition elicited by mental nerve stimulation during voluntary contraction. The trigeminal Ia input facilitated the R1 component of the blink reflex when the supraorbital test stimulation preceded the masseteric conditioning stimulation by 2 ms. We conclude that the time course of the recovery cycle of the heteronymous H-reflex in the temporalis muscle reflects the after-hyperpolarization potential (AHP) of trigeminal motoneurones, and that the Ia trigeminal input is integrated with other brainstem reflexes.

Adult↗
PubMed2001

Somatosensory disinhibition in dystonia.

Despite the fact that somatosensory processing is inherently dependent on inhibitory functions, only excitatory aspects of the somatosensory feedback have so far been assessed in dystonic patients. We studied the recovery functions of spinal N13, brainstem P14, parietal N20, P27, and frontal N30 somatosensory evoked potentials (SEPs) after paired median nerve stimulation in 10 patients with dystonia and in 10 normal subjects. The recovery functions were assessed (conditioning stimulus: S1; test stimulus: S2) at interstimuls intervals (ISIs) of 5, 20, and 40 ms. SEPs evoked by S2 were calculated by subtracting the SEPs of the S1 only response from the SEPs of the response to the paired stimuli (S1 + S2), and their amplitudes were compared with those of the control response (S1) at each ISI considered. This ratio, (S2/S1)*100, investigates changes in the excitability of the somatosensory system. No significant difference was found in SEP amplitudes for single stimulus (S1) between dystonic patients and normal subjects. The (S2/S1)*100 ratio at the ISI of 5 ms did not significantly differ between dystonic patients and normal subjects, but at ISIs of 20 and 40 ms, this ratio was significantly higher in patients than in normals for spinal N13 and cortical N20, P27, N30 SEPs. These findings suggest that in dystonia there is an impaired inhibition at spinal and cortical levels of the somatosensory system which would lead to an abnormal sensory assistance to the ongoing motor programs, ultimately resulting in the motor abnormalities present in this disease.

Adult↗
PubMed2001

Transient improvement induced by motor fatigue in focal occupational dystonia: the handgrip test.

Muscle fatigue induced by a previous sustained contraction temporarily decreases the motor output, transiently worsening motor performance. Whether muscle fatigue alters motor performance also in dystonia-a disorder whose main pathophysiological abnormality is motor overflow-remains unknown. To assess the effects of muscle fatigue in patients with focal occupational upper limb dystonia, we studied the effect of a previous maximum fatiguing voluntary contraction on motor performance in 10 musicians with focal occupational dystonia, in 3 musicians with hand motor impairment due to non-dystonic disorders, and in 5 normal musicians. The fatiguing task consisted of grasping a spring handgrip as long as possible until the task failed. In dystonic musicians, a fatiguing contraction significantly improved motor performance. The improvement lasted less than 5 minutes and appeared only after fatigue of the affected upper limb. In contrast, in musicians with non-dystonic motor impairment, motor performance remained unchanged or worsened, and normal musician performance consistently worsened.

Adult↗
PubMed2001

Non-motor effects of deep brain stimulation of the subthalamic nucleus in Parkinson's disease: preliminary physiological results.

Although deep brain stimulation (DBS) is a clinically effective therapy for patients with advanced Parkinson's disease (PD), its physiological effects on the brain and possible actions on non-motor functional systems remain largely unknown. This study evaluated the effects of DBS of the subthalamic nucleus (STN) on neurophysiological variables and on cardiovascular physiology. Nine patients affected by PD undergoing chronic DBS of the STN have been studied. We performed electroencephalography (EEG), somatosensory (SEPs) and visual evoked potentials (VEPs), exteroceptive masseteric silent period and sympathetic skin response (SSR) studies with DBS ON and OFF. To assess the effects of stimulation on the cardiovascular system the tilt test and plasma renin activity were studied. When we turned the DBS OFF, both SEP N20 and the VEP P100 component increased significantly in amplitude whereas the SSR decreased in amplitude and increased in latency. Although plasma renin activity tended to increase with DBS OFF, its modification induced by postural changes and blood pressure values did not significantly differ with DBS ON and OFF. We conclude that DBS of the STN in PD, besides inducing a clinical improvement, induces several non-motor effects.

Afferent Pathways↗
PubMed2001

The prolonged cortical silent period in patients with Huntington's disease.

OBJECTIVES: In a group of patients with Huntington's disease and age-matched controls, we studied the cortical silent period (SP) elicited by single transcranial magnetic stimulation (TMS) pulses. METHODS: We measured the area of the pre-stimulus electromyographic (EMG) activity, the area of the motor evoked potentials (MEPs) and the duration of the SP induced by stimuli delivered at an intensity of 150% of motor threshold with a round coil placed over the vertex. We determined the cortical SP by sampling only the 5 traces containing the shortest SPs and by collecting 10 consecutive unselected traces without selecting trials. RESULTS: Patients and controls had normal EMG background areas, and MEP latencies and areas. Whereas data measured from selected trials gave a normal duration of the SP (patients, 154+/-58 ms; controls, 166+/-22 ms), data from unselected trials yielded a significantly longer SP duration in patients than in controls (356+/-251 vs. 159+/-44 ms) and also a larger variance and range. CONCLUSIONS: We conclude that in Huntington's disease, an abnormal cortical SP is best sought by collecting unselected consecutive traces. We suggest that the prolonged SP in HD originates from a dysfunction of the mechanisms controlling the restart of voluntary movement after TMS.

Adult↗
PubMed2001

Decreased EMG inhibition following electrical stimulation over muscle tendons in myopathies.

OBJECTIVE: To assess the central EMG inhibitory action of tendon afferent input in muscle diseases. METHODS: The EMG inhibition elicited by electrical stimulation over muscle tendons was tested in 13 healthy voluntary subjects and 8 patients who had a primary muscle disease with a mild force deficit. Electrical stimuli were delivered to the tendon of the extensor carpi radialis muscle at the wrist during tonic voluntary isometric contraction at 50% of the maximum EMG level. The EMG signal was recorded by surface electrodes over the extensor carpi radialis muscle. RESULTS: The prestimulus background EMG level was reduced in 7 out 8 of the patients. Both groups had the same phases of EMG modulation following tendon stimulation (TE1, TI1, TE2) and their latency and amplitude did not differ significantly. Conversely, the area of TI1 was significantly larger (i.e. the inhibition decreased) in patients ([mean+/-SD] absolute area: controls=4.1+/-1.6 mVms, patients=6.9+/-2.9 mVms, P<0.05). CONCLUSIONS: In muscle dysfunction there are serial 'upstream' changes of central inhibitory systems, probably to maximize the residual muscle power of the affected muscle.

Adolescent↗
PubMed2001

Axillary injection of botulinum A toxin in a patient with muscle cramps associated with severe axillary hyperhidrosis.

Muscle cramps may be caused by fluid and salt loss induced by diffuse or focal hyperhidrosis. Recent reports have described the efficacy of botulinum, toxin in the treatment of primary focal hyperhidrosis. Botulinum toxin inhibits sweating by blocking exocytosis of acetylcholine from presynaptic cholinergic nerve terminals. We report the case of a patient who complained of frequent muscle cramps associated with unusually severe axillary hyperhidrosis. We used botulinum toxin to treat the excessive focal sweating presuming that it would also reduce the muscle cramps. A total dose of 200 MU of botulinum A toxin (Dysport) per axilla markedly reduced sweating and cramps. The beneficial effect started four days after the injection and it was still present five months later. Treatment was repeated in the sixth month with analogous results. No side-effects were observed and no compensatory sweating occurred.

Axilla↗
PubMed2000

Postcontraction depression of reciprocal inhibition in human forearm muscles.

We tested whether a preceding muscle contraction changes reciprocal inhibition (RI) between forearm antagonists. RI was studied in 14 healthy subjects by assessing changes in the H reflex (evoked by median-nerve stimulation) in forearm flexor muscles after conditioning radial-nerve stimulation at 0- and 20-ms intervals. The maximum sizes of the M wave (M(max)) and H reflex (H(max)) were also measured. After a long-lasting maximum voluntary handgrip contraction (mean +/- SEM: 3.9 +/- 0.6 min) of ipsilateral forearm muscles, M(max) and H(max) were unchanged but RI was diminished. After contraction of the contralateral homologous muscles and after contraction elicited by ipsilateral muscle stimulation, RI remained unchanged. These results show that a preceding maximum voluntary contraction (lasting 30 s or more) reduces the activity of the spinal inhibitory interneurons mediating RI. This finding may imply the need to reinterpret results from RI studies in normal subjects and in patients with movement disorders.

Adult↗
PubMed2000

Spinal and cortical inhibition in Huntington's chorea.

In this article we studied spinal and cortical inhibitory mechanisms in patients with Huntington's disease. To evaluate spinal cord inhibitory circuitries, we assessed reciprocal inhibition between antagonist forearm muscles and the recovery cycle of the H reflex in the flexor carpi radialis. Patients showed a significant decrease in the presynaptic phase of reciprocal inhibition reaching a minimum at the conditioning-test interval of 20 msec and an abnormal facilitation of the test H reflex at the conditioning test interval of 40 to 60 msec. Throughout its time course (10-200 msec), the H reflex recovery cycle showed a more prominent facilitation in patients than in control subjects. To assess whether the observed pathophysiological abnormalities might have arisen from an abnormal motor cortical excitability, we examined the recovery cycle of the motor potentials evoked by paired transcranial magnetic stimuli. We found that the inhibitory mechanisms controlling motor cortical excitability were normal. An interpretation of the spinal cord abnormalities is that the intrinsically normal but deafferentated motor cortex in Huntington's disease partly loses its inhibitory control, thus disinhibiting spinal cord circuitry. Our findings from paired transcranial magnetic stimulation suggest that cortical motor areas are not hyperexcitable in Huntington's disease. Hence, the postulated thalamocortical overactivity in experimental models of Huntington's disease needs to be reappraised.

Adult↗
PubMed2000

Movement-related electroencephalographic reactivity in Alzheimer disease.

Event-related desynchronization/synchronization (ERD/ERS) of alpha and beta electroencephalographic (EEG) rhythms was investigated in normal subjects and mild Alzheimer Disease patients (AD), performing unilateral right finger movements (about 10 s intermovement interval). Electroencephalographic data were sampled based on 10-20 system electrode montage. Surface Laplacian estimate of the potential reduced the head-volume conductor effects and annulled electrode reference variations. Results showed that EEG reactivity (i.e., ERD/ERS) of modeled contralateral rolandic cortex and motor performance were preserved in mild to moderate AD. In contrast, modeled activity (i.e., ERD/ERS) of frontolateral, centromedial, and ipsilateral rolandic areas was abnormal. Furthermore, interrelatedness of cortical response and movement timing was abnormal in AD patients. These results would support the working hypothesis that mild to moderate AD is a global brain network disease, including processing of sensorimotor information (despite no overt movement disorder). Further investigations will ascertain the clinical relevance of these results.

Aged↗
PubMed2000

The excitability of human cortical inhibitory circuits responsible for the muscle silent period after transcranial brain stimulation.

The silent period after transcranial magnetic brain stimulation mainly reflects the activity of inhibitory circuits in the human motor cortex. To assess the excitability of the cortical inhibitory mechanisms responsible for the silent period after transcranial stimulation, we studied, in 15 healthy human subjects, the recovery cycle of the silent period evoked by transcranial and mixed nerve stimulation delivered with a paired stimulation technique. The recovery cycle is defined as the time course of the changes in the size or duration of a conditioned test response when pairs of stimuli (conditioning and test) are used at different conditioning-test intervals. The recovery cycle of the duration of the silent period in the first dorsal interosseous (FDI) muscle during maximum voluntary contraction after transcranial magnetic stimulation was studied by delivering paired magnetic shocks (a conditioning shock and a test shock) at 120% motor-threshold intensity. Conditioning-test intervals ranged from 20-550 ms. The recovery cycle of the silent period in the FDI muscle during maximum voluntary contraction after nerve stimulation was evaluated by paired, supramaximum bipolar electrical stimulation of the ulnar nerve at the wrist (conditioning-test intervals ranging from 20 to 550 ms). Electromyographic activity was recorded by a pair of surface-disk electrodes over the FDI muscle. The recovery cycle of the silent period after transcranial magnetic stimulation delivered through the large round coil showed two phases of facilitation (lengthening of the silent period), one at 20-40 ms and the other at 180-350 ms conditioning-test intervals, with an interposed phase of inhibition (shortening of the silent period) at 80-160 ms. The conditioning magnetic shock left the size of the test motor-evoked potentials statistically unchanged during maximum voluntary contraction. Paired transcranial stimulation with a figure-of-eight coil increased the duration of the test silent period only at short conditioning-test intervals. Conditioning nerve stimulation left the silent period produced by test nerve stimulation unchanged. In conclusion, after a single transcranial magnetic shock, inhibitory circuits in the human motor cortex undergo distinctive short-term changes in their excitability, probably involving different mechanisms.

Adult↗
PubMed2000

Abnormal central integration of a dual somatosensory input in dystonia. Evidence for sensory overflow.

Several observations suggest impaired central sensory integration in dystonia. We studied median and ulnar nerve somatosensory evoked potentials (SEPs) in 10 patients who had dystonia involving at least one upper limb (six had generalized, two had segmental and two had focal dystonia) and in 10 normal subjects. We compared the amplitude of spinal N13, brainstem P14, parietal N20 and P27 and frontal N30 SEPs obtained by stimulating the median and ulnar nerves simultaneously (MU), the amplitude value being obtained from the arithmetic sum of the SEPs elicited by stimulating the same nerves separately (M + U). Throughout the somatosensory system, the MU : (M + U) ratio indicates the interaction between afferent inputs from the two peripheral nerves. No significant difference was found between SEP amplitudes and latencies for individually stimulated median and ulnar nerves in dystonic patients and normal subjects, but recordings in patients yielded a significantly higher percentage ratio [MU : (M + U)x100] for spinal N13 brainstem P14 and cortical N20, P27 and N30 components. The SEP ratio of central components obtained in response to stimulation of the digital nerves of the third and fifth fingers was also higher in patients than in controls but the difference did not reach a significant level. The possible contribution of subliminal activation was ruled out by recording the ratio of SEPs in six normal subjects during voluntary contraction. This voluntary contraction did not change the ratio of SEP suppression. These findings suggest that the inhibitory integration of afferent inputs, mainly proprioceptive inputs, coming from adjacent body parts is abnormal in dystonia. This inefficient integration, which is probably due to altered surrounding inhibition, could give rise to an abnormal motor output and might therefore contribute to the motor impairment present in dystonia.

Adult↗