Abstract: People with Parkinson's disease (PD) often have a posture characterized by lateral trunk flexion poorly responsive to antiparkinsonian drugs. To examine the effects of a rehabilitation programme (daily individual 90-minute-sessions, 5-days-a-week for 4-consecutive weeks) on lateral trunk flexion and mobility, 22 PD patients with mild to severe lateral trunk flexion, and 22 PD patients without trunk flexion were studied. Patients were evaluated using the Unified Parkinson's Disease Rating Scale motor subscale (UPDRS-III) score, and the kinematic behavior of the trunk was recorded by means of an optoelectronic system to determine: a) trunk flexion, inclination and rotation values in the erect standing posture; b) ranges of trunk flexion and inclination during trunk movements. After the treatment, significant decreases in trunk flexion [24 degrees (4) vs. 14 degrees (3), P < 0.001] and inclination in the static condition [23 degrees (5) vs. 12 degrees (4), P < 0.001)] were observed, both of which were maintained at the 6-month follow up. During the trunk flexion task, a significantly increased range of trunk flexion [64 degrees (15) vs. 83 degrees (15), P < 0.001] was observed; similarly, during the lateral bending task, the range of trunk inclination was found to be significantly increased, both toward the side of the trunk deviation [29 degrees (8) vs. 42 degrees (13), P < 0.01] and toward the contralateral side [14 degrees (6) vs 29 degrees (11), P < 0.01]. No further significant changes were observed at the 6-month follow-up. Trunk flexion and inclination values in the upright standing posture correlated slightly with the UPDRS-III score. Our findings show that significant improvements in axial posture and trunk mobility can be obtained through the 4-week rehabilitation programme described, with a parallel improvement in clinical status.
Abstract: We investigated changes in visual cortex excitability by analyzing visual evoked potential (VEP) habituation in healthy subjects during tonic pain evoked by the cold-pressor test (CPT). We tested VEP amplitude habituation (slope of the linear regression line for N1-P1 amplitude from the 1st to 6th block of 100 sweeps) in 19 healthy volunteers during 4 experimental conditions: baseline; no-pain (hand held in warm water, 25 degrees C); pain (hand held in cold water, 2-4 degrees C); and the after-effects of tonic pain. During baseline and no-pain sessions, VEPs habituated normally across the 6 consecutive blocks (mean slope -.28 and -.18%), whereas during pain and its after-effects they failed to decrease (0%, and -.11%). Tonic pain induced by the CPT abolishes normal VEP habituation and the lack of habituation persists after the CPT is stopped. Tonic pain probably abolishes VEP habituation by acting on brainstem neural structures which modulate thalamo-cortical activation thereby changing visual cortex excitability. PERSPECTIVE: This study shows that tonic pain alters visual cortex excitability, a brain region unrelated to pain processing. These changes probably reflect defensive strategies against pain. Extending the study from healthy volunteers to patients with migraine between attacks would offer the opportunity to investigate visual cortical excitability under conditions when baseline habituation is absent.
Abstract: In patients with migraine, the various sensory stimulation modalities, including visual stimuli, invariably fail to elicit the normal response habituation. Whether this lack of habituation depends on abnormal activity in the sub-cortical structures responsible for processing incoming information as well as nociception and antinociception or on abnormal cortical excitability per se remains debateable. To find out whether inducing tonic pain in the hand by cold pressure test (CPT) alters the lack of visual-evoked potential (VEP) habituation in migraineurs without aura studied between attacks we recorded VEPs in 19 healthy subjects and in 12 migraine patients during four experimental conditions: baseline; no-pain (hand held in warm water, 25 degrees C); pain (hand held in cold water, 2-4 degrees C); and after-effects. We measured P100 amplitudes from six blocks of 100 sweeps, and assessed habituation from amplitude changes between the six sequential blocks. In healthy subjects, the CPT decreased block 1 VEP amplitude and abolished the normal VEP habituation (amplitude decrease to repeated stimulation) in patients with migraine studied between attacks; it left block 1 VEP amplitude and abnormal VEP habituation unchanged. These findings suggest that the interictal cortical dysfunction induced by migraine prevents the cortical changes induced by tonic painful stimulation both during pain and after pain ends. Because such cortical changes presumably reflect plasticity mechanisms in the stimulated cortex, our study suggests altered plasticity of sensory cortices in migraine. Whether this abnormality reflects abnormal functional activity in the subcortical structures subserving tonic pain activation remains conjectural.
Abstract: OBJECTIVE: Electrical stimulation of the supraorbital trigeminal nerve branch induces trigeminocervical reflex responses (TCRs) in the neck muscles. The purpose of this study was to elicit more nociceptive TCR responses through preferential activation of the nociceptive afferents with a concentric surface electrode. METHODS: We recorded TCRs in 10 healthy subjects using both a standard (sTCR) and a nociceptive (nTCR) concentric surface electrode. We compared the baseline parameters, stimulus intensity/response, recovery, and habituation curves recorded for the two types of electrode, and assessed the effects of local anaesthesia. RESULTS: Compared with the sTCRs, nTCRs showed a significantly longer latency of the late reflex component, as well as lower pain and higher reflex thresholds. They also showed a different recovery cycle and stimulus intensity/response curve, but similar habituation rate. Local anaesthesia attenuated by 85% the late reflex response to stimulation by the concentric electrode, and by only 15% the response to standard electrode stimulation. CONCLUSIONS: The differences observed stimulating with these two electrode types may be due to their different activation of the afferent fibres. SIGNIFICANCE: If this study were extended to patients affected by primary headaches, TCR monitoring could emerge as a sensitive tool for detecting changes in nociceptive transmission at the level of trigeminocervical complex.
Abstract: Hyperventilation is often associated with stress, an established trigger factor for migraine. Between attacks, migraine is associated with a deficit in habituation to visual-evoked potentials (VEP) that worsens just before the attack. Hyperventilation slows electroencephalographic (EEG) activity and decreases the functional response in the occipital cortex during visual stimulation. The neural mechanisms underlying deficient-evoked potential habituation in migraineurs remain unclear. To find out whether hyperventilation alters VEP habituation, we recorded VEPs before and after experimentally induced hyperventilation lasting 3 min in 18 healthy subjects and 18 migraine patients between attacks. We measured VEP P100 amplitudes in six sequential blocks of 100 sweeps and habituation as the change in amplitude over the six blocks. In healthy subjects, hyperventilation decreased VEP amplitude in block 1 and abolished the normal VEP habituation. In migraine patients, hyperventilation further decreased the already low block 1 amplitude and worsened the interictal habituation deficit. Hyperventilation worsens the habituation deficit in migraineurs possibly by increasing dysrhythmia in the brainstem-thalamo-cortical network.
Abstract: A lesion of the median nerve may occur as a consequence of a compression by a haematoma or for a direct damage of the axons caused by a needle insertion. To date, no investigation reported a very selective lesion of the median nerve at the elbow, with the suffering limited only to the fibres for the first digit. A 53 year-old left-handed violinist underwent an arterial blood gas drawing. The patient complained immediately of an electrical shock impression going down the arm, followed by pin sensation into the first finger. A tingling sensation associated with numbness in the first fingertip and difficulty in the index-thumb pinch became progressively evident. The ENG-EMG findings showed an impairment mainly of the sensory fibres innervating the first digit and a drop of the motor action potential amplitude when the nerve was stimulated at the elbow. We reported a very partial lesion of the left median nerve at the elbow in a violinist who had a selective involvement of the fibres for his first digit. Even minimal lesions of the median nerve may impair severely the quality of life of patients.
Abstract: BACKGROUND: It has been proposed that the patent foramen ovale (PFO) may be associated with migraine, in particular migraine with aura. However, it is not clear whether paradoxical embolism triggers crises of headache. Cerebral embolization is provoked in subjects with PFO through contrast echocardiography, a safe method to diagnose the presence of foramen ovale pervium. METHODS: Twenty-four men practicing diving, an activity characterized by increased prevalence of PFO and migraine, underwent trans-thoracic echocardiography with contrast solution, composed of saline and air mixture and checked for the occurrence of migraine in the following 24 hours. RESULTS: A PFO (five of minimal size, i.e. visible only during Valsalva, one of small and two of medium size) was detected in 8/24 divers (33%). No one reported headache over the 24 hours after the procedure. DISCUSSION: Our preliminary data suggest that cerebral micro-embolism, provoked by contrast echocardiography, does not systematically trigger migraine crises when a minimal-to-medium sized patent foramen ovale is present.
