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Biomedical subjects

C Vasilescu

Publications and source records attributed to C Vasilescu.

At least 37 records · Page 2Linked to original sources

Delayed neuropathy after organophosphorus insecticide (Dipterex) poisoning: a clinical, electrophysiological and nerve biopsy study.

Clinical, electrophysiological and histological findings in four patients accidentally poisoned with the organophosphorus insecticide Dipterex are reported. Three to five weeks after insecticide ingestion signs of a distal sensorimotor (preponderantly motor) neuropathy occurred. The patients complained of paraesthesia in the lower limbs, and two of them of very disagreeable pricking sensation in the soles of the feet, responsive to carbamazepine. They showed distal weakness mainly of the legs, footdrop , difficult gait and muscle hypotonia. Ankle jerk was abolished while other tendon reflexes persisted. Two months or even later after poisoning, knee jerks in all the patients were very brisk and more and less accompanied by other pyramidal signs (patellar clonus, abolishment of abdominal cutaneous reflexes, Babinski's sign). Clinical, electrophysiological and nerve biopsy data revealed a "dying-back" neuropathy in our patients. Distal muscle fatigue was confirmed by failure of neuromuscular transmission on repetitive nerve stimulation.

Adult↗

Sensorimotor neuropathy in a patient with Marinesco-Sjögren syndrome.

A case of Marinesco-Sjögren syndrome, displaying the characteristic signs (ataxia, congenital cataract and mental retardation) is presented. Electrophysiological examination pointed to the presence of a sensorimotor peripheral neuropathy with an underlying mixed process of segmental demyelination and axonal degeneration (probably secondary). The sural nerve and gastrocnemius biopsy confirmed these data, showing that in this case the segmental demyelination process was accompanied by axonal degeneration.

Ataxia↗

Peripheral neuropathy with a syndrome of continuous motor unit activity.

A chronic alcoholic who had also been submitted to partial gastrectomy developed a syndrome of continuous motor unit activity responsive to phenytoin therapy. There were signs of minimal distal sensorimotor polyneuropathy. Symptoms of the syndrome of continuous motor unit activity were fasciculation, muscle stiffness, myokymia, impaired muscular relaxation and percussion myotonia. Electromyography at rest showed fasciculation, doublets, triplets, multiplets, trains of repetitive discharges and myotonic discharges. Trousseau's and Chvostek's signs were absent. No abnormality of serum potassium, calcium, magnesium, creatine kinase, alkaline phosphatase, arterial blood gases and pH were demonstrated, but the serum Vitamin B12 level was reduced. The electrophysiological findings and muscle biopsy were compatible with a mixed sensorimotor polyneuropathy. Tests of neuromuscular transmission showed a significant decrement in the amplitude of the evoked muscle action potential in the abductor digiti minimi on repetitive nerve stimulation. These findings suggest that hyperexcitability and hyperactivity of the peripheral motor axons underlie the syndrome of continuous motor unit activity in the present case.

Alcoholism↗

Electromyographic activity of neck muscles in patients affected by retrocollis under the influence of stimulation and coagulation of the prestitial nucleus of the midbrain.

In 2 patients with retrocollis, the positive effects obtained by stereotactic high frequency coagulation of the prestitial nucleus on the tonic activity of the neck muscle were studied electromyographically and clinically. Before the stereotactic therapy, electromyographic recordings at rest were recorded from the musculi splenii. During stimulation of the prestitial nucleus at frequencies of 8, 25 and 50 Hz, the EMG activity at rest diminished in frequency and amplitude and ultimately disappeared. Passage from the EMG recordings at rest to electrical silence took place, in one case, though a rhythmic activity of potentials grouped at 11/s. After coagulation of the prestitial nucleus, the involuntary contractions of neck muscles disappeared and electrical silence occurred. On reexamination 1 month later, the positive results were still present.

Electric Stimulation↗

Clinical and electrophysiological studies of carbon disulphide polyneuropathy.

A clinical and electrophological study was performed on 30 patients with chronic carbon disulphide poisoning. Although the measurements of motor conduction velocity and of terminal latency were within the normal range in the subclinical stage, estimation of nerve excitability threshold showed distal motor hypoexcitability, thus proving a very effective means for the early detection of carbon disulphide polyneuropathy. The distal muscle fatigue found in 35% of patients was confirmed by the decrement (more than 10%) in the amplitude of muscle evoked potentials in the abductor digiti minimi muscle in response to repetitive stimulation of the ulnar nerve. Association of the above findings with the significant electrophysiological changes, viz., decrease in the amplitude of sensory evoked potentials on stimulation of the digital fibres, mild slowing of sensory conduction velocity in the peripheral nerves, and decrease in the amplitude of evoked potentials in the distal muscles, suggest that the carbon disulphide polyneuropathy would be underlain by a primary distal axonopathy.

Adult↗

Clinical and electrophysiological study of neuropathy after organophosphorus compounds poisoning.

Clinical and electrophysiological examinations were performed on 12 patients with toxic neuropathy following accidental ingestion of alcohol polluted by triorthocresyl phosphate (TOCP). Concurrent PNS and CNS lesions were found in all patients. Two to three months after ingestion, five of them showed prevalent signs of mixed, sensorimotor polyneuropathy, especially motor and distal, and the electrophysiological data pointed to the mixed process of axonal degeneration and secondary demyelination. In two of these five patients in whom examinations were repeated 13 years after TOCP ingestion, there was a marked clinical and electrophysiological improvement of signs of PNS lesions. Improvement of signs of CNS lesions was very poor even after 13 years. Signs of CNS lesions prevailed in the remaining seven patients. The clinical picture resembled that in amyotrophic lateral sclerosis and the electrophysiological data suggested a neuronal and axonal degeneration. Apart from the 12 cases of TOCP neuropathy, we also studied two cases of poisoning with organophosphorus insecticides, Dipterex and Divipan, in which a pure motor form of neuropathy was found.

Adult↗

Smoking and risk factors in deep vein thrombosis.

The incidence of deep vein thrombosis (DVT) as diagnosed by the 125I fibrinogen test (125IFT) was determined in a series of 300 newly admitted medical and 201 surgical patients. 6 medical patients died before 125IFT screening could be completed. The incidence of DVT was 14% in medical patients and 18% in surgical patients. Increasing age, a malignant condition and a past history of thromboembolism all increased the risk of DVT. Increasing levels of cigarette smoking were found to be associated with a reduced incidence of DVT. Although statistical significance was achieved at only the 10% level for this finding it is in agreement with the results from studies on patients with myocardial infarction. The protective effect of cigarrette smoking was observed at all ages, and in both medical and surgical patients.

Adult↗

Electroneurographic evidence of polyneuropathy in chronic liver disease.

An electroneurographic study performed on the peripheral nerves of 25 patients with severe cirrhosis following viral hepatitis showed slight slowing (P greater than 0.05) of motor conduction velocity (CV) and significant diminution (P less than 0.001) of sensory CV and mixed sensorimotor-evoked potentials, associated with a significant decrease in the amplitude of sensory evoked potentials. The slowing was about equal in the distal (digital) and in the proximal segments of the same nerve. A mixed axonal degeneration and segmental demyelination is presumed to explain these findings. The CV measurements proved helpful for an early diagnosis of hepatic polyneuropathy showing subjective symptoms in the subclinical stage.

Chronic Disease↗

Sensory and motor coduction in chronic carbon disulphide poisoning.

The greater decrease of conduction velocity in sensory than in motor fibres of the peroneal, median and ulnar nerves (particularly in the digital segments) found in patients with chronic carbon disulphide poisoning, permitted the diagnosis of polyneuropathy to be made in the subclinical stage, even while the conduction in motor fibres was still within normal limits. A process of axonal degeneration is presumed to underlie occurrence of neuropathy consequent to carbon disulphide poisoning.

Carbon Disulfide↗

Electromyographic investigations in torticollis.

In 13 patients with torticollis, the electromyographic (EMG) activity in the neck muscles at rest was investigated before, during and after stimulation of the H1 bundle (in horizontal torticollis) and inner part of oral ventral nucleus (in the rotatory form), as well as after coagulation. Three EMG types of torticollis-spasmodic, myoclonic and mixed - could be differentiated. During the 8-, 25- and 50-Hz stimulations, a diminution in the amplitude and frequency of muscle potentials, followed by electric silence, was most often obtained; in general, the electric silence was preceded by a rhythmic activity of grouped potentials. Following coagulation, no spontaneous EMG activity was any longer recorded in the neck muscles, in the majority of the cases.

Diagnosis, Differential↗