Biomedical subjects
Publications and source records attributed to L Reni.
The clinical and neurophysiologic data from 65 patients taking thalidomide were reviewed. Thalidomide sensory neurotoxicity was found to be cumulative dose dependent but occurs only when the total dose is relatively high (>20 g). The risk of developing sensory neuropathy is around 10% below this threshold but increases with higher doses.
Myelofibrosis with myeloid metaplasia (MMM) is a clonal disorder involving disregulation of angiogenesis and immunomodulatory mechanisms. Thalidomide (Thal) retains antiangiogenic, immunomodulatory and cytokine regulatory properties and recently it has been used successfully in multiple myeloma. Here, we report our experience in 10 MMM patients treated with Thal. Patients with agnogenic MMM treated in an early phase of the disease obtained significant benefits from the therapy and remain transfusion-free. In contrast, all secondary MMM failed to respond. These preliminary findings confirm that Thal plays a role in MMM therapy, although the efficacy in the different phases of the disease must be further evaluated.
Changes in amplitude of the soleus H (S(H))-reflex and its neurographic correlates (P(1) and P(2) waves) after vibration of the soleus muscle have been evaluated as a function of mechanical stimulation frequency, duration of the conditioning train, and test stimulus intensity. Additional experiments aimed at assessing the nervous system mechanisms underlying the postvibration depression (PVD) have been performed. In particular, homonymous (S(HMR) or S(H)) versus heteronymous (S(HTR)) soleus response, evoked respectively by tibial nerve and femoral nerve electrical stimulation, the effectiveness of sub-H threshold tibial nerve conditioning volleys on the S(HTR), and the respective effects of a brief passive stretching of the quadriceps and soleus muscles on the recovery of both the S(HMR) and S(HTR) after vibration of the homologous muscle were investigated under suitable experimental conditions. It was found that PVD occurs in the absence of changes in amplitude of the P(1) wave and the S(HTR), is paralleled by a reduced effectiveness of tibial nerve-conditioning volleys on the S(HTR) and is shortened consistently by brief passive stretching of the homologous muscle. It follows that PVD may be the result of a long-lasting reduction of the transmitter release from Ia presynaptic terminals depending, at least in part, on a protracted postvibration Ia afferent discharge caused by spindles thixotropy. These findings may provide a better understanding of the pathophysiologic mechanisms underlying spasticity in humans.
Concurrent recordings of (i) the soleus H reflex and (ii) the underlying afferent (P1) and efferent (P2) neural volleys were performed during a protracted, moderate, isometric, voluntary contraction of the soleus (S) muscle, and the subsequent release period. Besides the expected enhancement of the H reflex, muscular contraction caused a significant reduction in the corresponding central delay (as extrapolated from variations of P1-P2 interval), while the opposite trend occurred during the release phase. Control experiments, based on (a) neural blockade below the stimulation site, (b) muscle stretching at the end of the muscular contraction, (c) changes in amplitude of homonymous and heteronymous S responses, and (d) variations in effectiveness of homonymous and heteronymous conditioning volleys on the S motoneuronal pool, showed that both voluntary contraction and the subsequent release period are associated with a reduced effectiveness of la afferents, while postsynaptic motoneuronal responsiveness is significantly modified only during the actual contraction time.
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Central delay (CD) changes in the soleus H reflex pathway, as demonstrated by variations in the time interval between afferent (P1) and efferent (P2) neurographic volleys underlying the reflex response, were assessed in a group of normal subjects, both during the steady state and after homosynaptic spatial summation of afferent impulses. The maximal range of CD changes, regardless of whether "spontaneous" or provoked, showed significant interindividual differences whose size was positively related to the Hmax/Mmax ratio, provided that the extension of the subliminal fringe was suitably normalized. Comparatively similar variations in amplitude of the reflex motoneuronal discharge under different experimental conditions can be associated with different CD changes. Indeed, "spontaneous" CD fluctuations occurring during the steady state were consistently greater than CD reductions provoked by spatial summation, the gap size being negatively related to the Hmax/Mmax ratio.
1. Central delay (CD) changes after facilitatory or inhibitory conditioning of the soleus H reflex have been investigated in a group of normal subjects as a function of the conditioning and test stimulus intensities and also as a function of the Hmax/Mmax ratio. Both facilitation and inhibition of the reflex response have been obtained by conditioning stimulation of the ipsilateral tibial nerve at suitable conditioning-test stimulus intervals. CD changes have been extrapolated from the variations of the time interval between afferent and efferent neural volleys underlying the H reflex, directly recorded from the sciatic nerve. 2. The CD was significantly decreased by facilitatory and increased by inhibitory conditioning. Facilitatory CD changes were positively related to test stimulus strength (at a given conditioning stimulus intensity) and negatively related to conditioning stimulus strength (at a given test stimulus intensity). Both trends were reversed after inhibitory conditioning. The effectiveness of facilitatory conditioning was positively related to the individual Hmax/Mmax ratio whereas a negative relationship could be observed after inhibitory conditioning. 3. Also, the "conditioning threshold" (the minimal conditioning stimulus strength affecting the reflex size) and the "maximal conditioning effect" (the conditioning stimulus intensities leading to either the saturation of the facilitatory effect or the suppression of the reflex response) were significantly related to the Hmax/Mmax ratio. 4. We suggest that temporal changes in the H reflex pathway after facilitatory or inhibitory conditioning stimuli depend both on the size of the motoneuronal pool underlying the reflex response, as determined by the test stimulus intensity, and on the individual excitability of the motoneuronal pool, as defined by the Hmax/Mmax ratio.(ABSTRACT TRUNCATED AT 250 WORDS)
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The effects of changing the stimulus presentation rate on early parietal (N20-P25) and frontal (P22-N30) somatosensory potentials (SEPs), evoked by median nerve stimulation, were investigated in 15 normal subjects. Stimuli were presented at 0.1, 0.4, 1.0, 4.0 and 10/sec. Only minor latency changes, mainly for the frontal P22 component, were observed when the stimulus rate was increased up to 10/sec: while the frontal P22-N30 complex was more rapidly and severely reduced in amplitude than the parietal N20-P25 complex. The differential effects of stimulus presentation rate on early frontal and parietal SEPs support the hypothesis of separate neural generators and suggest that the choice of the stimulation frequency may be critical for the interpretation of diagnostic SEP studies.
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The possible contribution of low threshold muscle afferents to the postsynaptic component (N13) of the cervical response evoked by electrical stimulation of the median nerve (MN) was investigated in normal subjects. Electroneurographic (ENG) and electromyographic (EMG) correlates of the reflex motoneuronal discharge (RMND) were recorded simultaneously. A. No reflex activity could be elicited by stimulation of the MN at the wrist, at least in the resting subjects, while well developed ENG (P2 efferent volley) and EMG (H reflex) monosynaptic responses occurred following stimulation of the MN at the elbow at suitable strengths. In neither case could a surface correlate of interneuronal activity evoked by muscle afferents be demonstrated. B. Recruitment curves showed that at stimulus intensities above maximal for the H reflex both P2 and H responses started to decrease until they completely disappeared, while N13 showed further enhancement. C. Subthreshold conditioning stimulation of the MN enhanced both P2 and H responses, while vibratory muscle stimuli provoked a clearcut suppression of these two responses. In contrast, N13 was completely unaffected by either manoeuvre. D. No cervical evoked activity could be detected following tendon tapping of the anterior forearm muscles in spite of the appearance of well developed cortical responses and the ENG and EMG correlates of the T reflex. E. Conditioning volleys elicited by tendon taps of the anterior forearm muscles suppressed both P2 and H responses following stimulation of the MN at the elbow without affecting the related N13 component. Conditioning supramaximal stimulation of the MN at the wrist suppressed the N13 component of the cervical response evoked by stimulation of the MN at the elbow without affecting the related reflex responses. No component chronologically related to the RMND could be recorded at the posterior neck region during suppression of N13, thus ruling out the possibility that failure to detect the RMND (as well as its interneuronal concomitants) with cervical electrodes is due to a masking effect of the N13 component. G. Conditioning tendon taps of anterior forearm muscles provoked a clearcut reduction of the primary cortical response to finger stimulation without affecting the postsynaptic component of the related cervical response. It is concluded that neither segmental (motoneuronal or interneuronal in origin) nor ascending postsynaptic impulses generated in the spinal cord by stimulation of low threshold muscle afferents contribute to N13, the latter being probably due to activation of both short and long axoned spinal neurons by cutaneous afferents.
The neurographic activity evoked either by stimulation of the tibial nerve at the popliteal fossa or by percussion of the Achilles tendon has been recorded at lumbar and thigh levels, in order to find out whether conduction time, temporal dispersion and central delay of the neural volleys underlying the monosynaptic reflex (H or T) may change as a function of stimulus intensity; under facilitatory or inhibitory experimental conditions; "spontaneously", i.e. during the steady state. The reflexly evoked ventral root discharge (VRD) decreases in latency with increasing stimulus intensity up to the maximum reflex response in the absence of changes in afferent (thigh to spine) or efferent (spine to thigh) conduction times. Reduction of the central delay was greater with mechanical than electrical stimulation, probably due to the combined effect of spatial and temporal summation under the former experimental condition. The latency of the VRD related to the maximal H response was not further modified by supramaximal stimulus strengths. The Jendrassik manoeuvre caused a significant decrease in latency of the VRD, the opposite effect being observed during calf muscle vibration. A significant relationship between amplitude and latency of single VRDs could be demonstrated during the "steady state". Our data point to the existence of a positive correlation between the size of the motoneuronal pool activated by an afferent volley and speed of transmission in the reflex pathway, both during the "steady state" and under either facilitatory or inhibitory experimental conditions, provided that the test stimulus strength does not exceed the maximum reflex response (H or T). No detectable signs of peripheral dispersion of the VRD could be demonstrated, irrespective of the stimulus employed: this suggests that the axon diameters of the motoneurones contributing to the monosynaptic reflex fall within a fairly narrow distribution.
Short-latency somatosensory evoked potentials (SEPs) were recorded from 54 patients with dementia as compared to 32 age-matched controls. SEPs were generally normal in patients with senile dementia of Alzheimer type, while patients with multi-infarct dementia showed a prolonged central conduction time, an increased latency of both N13 and N20 and a reduction of the primary cortical response amplitude. These findings suggest that recording SEPs may be useful in the differential diagnosis between degenerative dementia and multi-infarct dementia.
Cervical, parietal and prerolandic somatosensory evoked potentials (SEPs) to median nerve stimulation at the wrist were recorded with an earlobe reference in 24 patients with Huntington's disease (HD) and in 24 age-matched normal controls. Cortical responses of abnormal wave form and reduced amplitude were constantly observed in HD patients. SEP changes affected more severely the prerolandic (P22/N30) pattern, which could not be recognized in two-thirds of patients, than the parietal (N20/P27) pattern, which could be identified in all cases. The N20 latency and the central conduction time (N13-N20 interval) were significantly increased. The occurrence of abnormalities of central conduction and of a predominant involvement of the prerolandic SEP pattern suggests an impairment of impulse transmission along the somatosensory lemniscal pathway at subcortical, possibly thalamic, level in HD.
The occurrence of epileptic seizures was investigated in 141 patients with angiographically proven carotid or MCA occlusive disease. Epileptic seizures occurred some time during the clinical course of the disease in 17.3% of carotid patients and in 10.8% of MCA patients, being mainly represented by partial motor seizures. The pattern of occurrence of seizures in the natural history of cerebral arterial disease was different in the two groups. In the carotid group, epilepsy was the presenting symptom in 6.7% of patients, whereas no MCA patient had seizures prior to the appearance of a neurological deficit. Since epileptic seizures may complicate an otherwise asymptomatic carotid obstruction, angiography should be performed whenever the other standard investigations, including CT-scan, fail to reveal the cause of late-onset epilepsy.