Sympathetic skin response (SSR) in the foot after sural nerve biopsy.
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Biomedical subjects
Publications and source records attributed to D Medici.
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Chylopericardium as an isolated complication after open heart surgery is a rare event. We present here a case of late postoperative chylopericardium and comment on the clinical course, the aetiopathology and treatment.
We describe two cases of hemifacial spasm (HFS) with unusual synkinetic movements between facial muscles and respiratory activity. Patient 1 developed an idiopathic HFS. She underwent microvascular decompression surgery, followed by transitory facial nerve palsy; she recovered but later developed a facial synkinesia characterized by involuntary and forced eyelid closure on spontaneous and deep breathing; the orbicularis oculi muscle was active also when her mouth was open (the so-called Marin-Amat syndrome). Patient 2, 1 year after a peripheral facial nerve palsy (Bell's palsy), developed an HFS together with synkinetic movements between the orbicularis oculi muscle and respiration. In both cases electrophysiological studies showed pathological synkinetic electromyographic activity. An enhanced hyperexcitability of brain stem interneurons and facial motoneurons could be suggested to explain the phenomenon.
We studied an AIDS patient who suffered from numbness, paresthesias and pain in the territories of different non-contiguous cutaneous nerves at different times. A transitory partial loss of touch and pinprick sensibility was also present in the same cutaneous areas. Sensory conduction velocities and SAP amplitudes were normal. The clinical picture was consistent with the Migrant Sensory Neuritis of Wartenberg. This rare neuropathy has never previously been described in patients affected by AIDS.
A case of Holmes-Adie syndrome was studied clinically and electrophysiologically. A total loss of tendon reflexes was observed in upper and lower limbs. The main electrophysiological finding was a marked increase of the central conduction time after stimulation of peroneal and tibial nerves. Motor evoked potentials in soleus muscle after transcranial magnetic stimulation showed normal threshold and latencies. We suggest that tendon areflexia could be a consequence of a dysfunction of somatosensory large diameter afferent fibres at the spinal level.
This report describes a 26 year old woman with a Coxsackie B virus infection complicated by an acute pandysautonomic and sensory neuropathy. Electrophysiological studies suggested an axonal neuropathy. A sural nerve biopsy performed early in the disease showed axonal degeneration with a virtual absence of unmyelinated fibres and moderate loss of myelinated fibres, mainly affecting the small fibres; this differs from previous reports. An immune-mediated or direct virus action might explain the pathogenesis of this unusual evolution of a viral infection.
The clinical involvement of the facial nerve is a rare finding among the initial symptoms of acoustic neurinomas. However, compression of the facial nerve is a common intraoperative finding. Blink reflex was recorded in 20 patients affected by cerebellar-pontine angle tumor confirmed at surgery. Recordings were also made of the M-response of the facial nerve from the naso-labial folds. In 6 cases jaw reflex was also recorded. In summary, these electrophysiological studies revealed a facial nerve damage in 13 and a trigeminal nerve dysfunction in 2 out of 18 clinically unaffected patients. The combined study of the 3 tests proved to be useful when the blink reflex showed an isolated R1 delay, that is, in cases in which the level of damage along the trigemino-facial reflex arc cannot be defined by the recording of the blink reflex alone.
Electromyographic responses of the masseter muscles and orbicularis oris muscles following transcranial magnetic stimulations were recorded with surface and needle electrodes. MEPs in masseter muscles (latency 6.9 +/- 0.71 ms, mean +/- SD) due to activation of controlateral cortico-nuclear connections were evoked by magnetic stimulations at 4 cm laterally to the vertex on the biauricular line. These MEPs were followed bilaterally by a silent period lasting about 20 ms and, less constantly, by a later silent period lasting up to 80 ms. The ipsilateral responses to the same stimuli presented shorter latencies and higher amplitudes and they were ascribed to direct stimulation of the trigeminal nerve, probably its intracisternal portion. Ipsilateral masseter "cortical" MEPs could be elicited only by a lower output setting (70% of the maximum output) of the stimulator. Orbicularis oris MEPs were polyphasic and dispersed with latencies ranging from 7 to 11 ms. In patients with hemispheric or capsular ischemic lesions "cortical" MEPs were absent when stimulating the affected hemisphere and present when stimulating the unaffected one. We suggest that the direct corticomotoneuronal projections for the masseter are mainly crossed.
After a brief description of the intraoperative angioplasty technique carried out together with direct revascularization through bypass with venous segments or with internal mammary (IMA) we hereby report the immediate and mid-term results obtained in 18 patients with this treatment. The simplicity of execution, having the possibility to operate on still heart and under the direct vision of the lesion the rareness of any complication, the fact that the coronary segment is open also during all checks done after 3 years from the treatment, and finally the considerable improvement in clinical symptomatology, lead the authors to consider this therapeutical succession possible in some selected cases, for which surgical operation is necessary.
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The main parameters of muscle acid-base, water and energy metabolism were studied in ten patients undergoing low-flux (1.5 l/min/m2), low-pressure (40 to 60 mmHg) hypothermic (26 degrees C) cardiopulmonary bypass (CPB) for aortocoronary grafting; absolute gas exchange and haemodynamic data were also measured throughout the entire CPB period. At the end of CPB a substantial preservation of water and energy metabolic indexes was found; a condition of extracellular metabolic acidosis was apparently sustained by muscle cell anaerobic glycolysis enhancement with a consequent increase of both muscle and plasma lactate content. Subnormal cell phosphocreatine levels as well as reduced bicarbonate buffer stores and decreased intracellular pH, were detected. Direct limiting effects of hypothermia on tissue O2 delivery and muscle oxidative metabolism as well as vasoconstriction and arteriovenous shunting associated with CPB procedures are likely to be involved in the above mentioned alterations of cell metabolism.
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Thyroid hormone serum concentrations, the thyrotropin (TSH) and prolactin (PRL) response to thyrotropin-releasing hormone (TRH) were evaluated in patients undergoing cardiopulmonary bypass (CPB) conducted in hypothermia. During CPB a marked decrease of thyroxine (T4) and triiodothyronine (T3) concentration with a concomitant increase of reverse T3 (rT3) were observed similarly to other clinical states associated with the 'low T3 syndrome'. Furthermore, in the present study elevated FT4 and FT3 concentrations were observed. In a group of patients, TRH administered during CPB at 26 degrees C elicited a markedly blunted TSH response. In these patients, PRL concentration was elevated but did not significantly increase after TRH. The increased concentrations of FT4 and FT3 were probably due to the large doses of heparin administered to these patients. Thus, the blunted response of TSH to TRH might be the consequence of the elevation of FT4 and FT3 in serum, however, other factors might play a role since also the PRL response to TRH was blocked.
In eight patients undergoing open heart surgery for elective myocardial revascularization, extra-intracellular acid-base and water metabolism parameters were studied before and after cardiopulmonary bypass procedures. All patients presented a different degree of metabolic acidosis related to plasma lactate increase. Intracellular acid-base indexes did not change significantly, though all but one patient showed an intracellular buffers consumption. Both total muscle and extracellular water increased, while intracellular water did not change. It was concluded that low flux-low pressure perfusion CPB was related to a substantial preservation of cell integrity.
The new H2-antagonist mifentidine was tested on human atrium, in comparison with cimetidine and ranitidine, for its activity against histamine-induced inotropic effect. Mifentidine was found to be 10 times more potent than ranitidine and 100 times more potent than cimetidine. The kinetics of the three compounds are typical of a competitive antagonism and the pA2 value was of 8.60, 6.35, 5.94 for mifentidine, ranitidine and cimetidine, respectively. Our data confirm previous findings in another isolated heart preparation, namely the guinea-pig papillary muscle.
Nine patients with acute myocardial infarction underwent intracoronary urokinase infusion within 3 hours after the onset of AMI, and subsequent coronary artery by pass grafting. After thrombolytic therapy 3 patients showed single-vessel disease, 2 double-vessel disease and 4 triple-vessel disease. The ventricular function was normal in 2 patients, moderately depressed in 5 and severely depressed in 2. The coronary artery by-pass grafting was performed from 6 to days after the onset of the acute myocardial infarction (average 37 days) and the average number of grafts performed per patient was 3.2. There was no operative death. The follow up period ranged from 24 to 38 months: 7 patients are in NYHA Class I and 2, symptomatic for dispnea, are in NYHA Class II. These preliminary data suggest than the coronary artery by-pass grafting after intracoronary urokinase therapy for acute myocardial infarction can be performed safely and the surgical results do not differ from those obtained with standard coronary artery by pass grafting.