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Biomedical subjects

A Constantinovici

Publications and source records attributed to A Constantinovici.

At least 37 records · Page 2Linked to original sources
PubMedDate not supplied

Dissociation of parietal and frontal somatosensory evoked potentials in central nervous system diseases.

The mean latency and waveform of early and late SEPs recorded on 50 and 200 ms were studied in 20 normal subjects, for the parietal (P), prerolandic (F) and prefrontal (pF) regions, ipsiand contralateral to the stimulated median nerve, using either the midfrontal or ear lobe electrode as reference. N17 (thalamic) potential occurred in the ipsilateral P and both F and pF regions (when using an ear lobe reference). The study was also performed in 145 patients with central nervous system diseases. Abnormal, especially early components were observed in 32 of 50 patients with multiple sclerosis. Abnormally delayed SEPs were found in 5 of 13 patients with brainstem lesions presenting sensory disorders. The patients with severe cortical parietal lesions (19 cases) or severe thalamic lesions (4 cases) had also severe abnormalities of all components of the SEPs in both P and F regions. A "dissociated" aspect of the SEPs, with absence of early components on the F side and normal components on the P side, occurred in patients with slight thalamic lesions, ataxic hemiparesis or pure motor deficits (prerosublandic lesions). Another dissociated aspect was noted between the normal early SEPs and the abnormal late components in patients with partial parietal lesions, aphasia or in children with acute sclerosing panencephalitis. These "dissociated" aspects of the SEP suggest different, independent afferent pathways, which may be selectively altered. The late components of the SEP may originate from the primary somatosensory cortex and depend on its integrity. Patients with only a pain sensory loss had abnormal late SEP components.

Brain Diseases↗
PubMedDate not supplied

[Transient global amnesia (a study of 30 cases)].

The authors have studied 30 patients with transient global amnesia aged between 49 and 76 years (median age of 63 years), without focal neurologic signs that have been followed for periods varying between 6 months and 10 years. Three of the patients had recurrent attacks of transient global amnesia, and another three had a stroke, although at some distance from the amnesia attack. Association was noted with certain risk factors including high blood pressure, and angiopathic changes of the eye fundus (in 50% of the patients), dyslipidemia (in 30%), diabetes (in 10%), and essential polyglobulia (in 7%). Coagulation studies including thrombelastograms were carried out in 22 patients, and demonstrated hypercoagulability in 50% of them. Changes in the arterial wall were noted in 85% of the 14 patients in whom carotid sphygmograms were recorded. The presence of these risk factors could explain the occurrence of cerebrovascular accidents in patients with transient global amnesia. Electroencephalograms performed immediately or a short time after the amnesia attack have evidenced in 18 patients rapid-type dysrhythmia, or diffuse theta waves, predominantly located in the deep layers of the left and right temporal areas. The EEG tracings were either flat or normal in the remaining 12 patients. Of the 30 patients presenting with global transient amnesia only two had migraine in antecedents, and another six had headache during the evolution of amnesia. The neurologic examination did not reveal any abnormality in 27 of the patients. Sequelar signs of neurological deficits were noted in the remaining three patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

The diagnostic value of somatosensory evoked potentials in the diseases of peripheral nervous system.

The mean latency value of somatosensory evoked potentials (SEP) recorded at the Erb's point, spinal and cortical level, was assessed in 20 normal subjects by percutaneous stimulation of the peripheral nerves (median, ulnar, superficial radial, tibial and peroneal). At the Erb's point and spinal cervical level, we distinguished the classically described potentials (N9, N13, N14) and the cortical "far-field" potentials such as: P17, N20, P24, N35 and sometimes P45. The central conduction time was calculated by determination of the interpeak latency N9-N13 and N13-N20 (for the upper limb) and LP-P37 for the lower one. A study of 100 patients with peripheral nerve diseases: 30 polyneuropathies, 50 radiculopathies, 9 cases with carpal tunnel syndrome, 5 with brachial plexus injury, 6 with compressive or traumatic diseases of the peripheral nerves, demonstrates the value of the SEPs in the assessment of the nervous lesion site (central or peripheral). In polyneuropathies, a decrease in amplitude and delayed latency of the N9 potential as well as delayed latency of the early cortical potentials on stimulation of the median and tibial nerves occurred. Delayed N9 and low amplitude with delayed latency spinal potential (N13 and LP) were found in radiculopathies. In myelopathies, the central spinal conduction time (N9-N13) was delayed and there were also delayed latencies of the cortical SEPs on lower limb stimulation. The patients with brachial plexus injury had a change in the N9 to N13 amplitude ratio, with prognostic value. Cortical recordings of the SEPs are also of special prognostic value and may suggest the surgical exploration when the axonal functional continuity is lost in brachial plexus injury and compressive or traumatic lesions of the peripheral nerves.

Adult↗
PubMedDate not supplied

Somatosensory evoked potentials in spinal cord diseases.

Somatosensory evoked potentials (SEPs) were studied in 115 patients with spinal cord diseases (multiple sclerosis, amyotrophic lateral sclerosis, cervical myelopathy, subacute combined degeneration, myelitis, spinal cord injury, tumours). The SEPs were recorded at three levels: parietal, spinal (cervical or lumbar), and at the Erb point. The central conduction time was also estimated (N9-N13 and lumbar potential (LP): LP-P37). The most sensitive test (95% abnormalities) was represented by the cortical recording of the SEPs when the tibial nerve was stimulated. The interval LP-P37 was increased, the SEPs being delayed or unrecordable and desynchronized (in cases of polyneuropathies only the latency was increased whereas the waveform was normal). In 50 patients with definite form of multiple sclerosis (MS) abnormalities of the cervical potential N13 were obtained in 96% of cases. The cortical SEPs to the median nerve stimulation were abnormal in 64% of cases only (32 patients). Of 10 patients with amyotrophic lateral sclerosis (ALS), cortical SEPs to the lower limb stimulation were abnormal in 6 patients (20%) and only 2 patients had also abnormal N13 and N20. Of 15 patients with cervical myelopathy, SEPs to the tibial nerve stimulation were abnormal and N9-N13 delayed in all but 2 patients. All the 5 patients with subacute combined degeneration had abnormal SEPs to the tibial nerve stimulation. In all the 15 patients with inflammatory spinal cord diseases, the SEPs were abnormal and the central conduction time was delayed. In 5 cases with spinal cord injury the SEPs were absent above the lesion. In 15 patients with tumoral compression SEPs to the stimulation of the nerve dependent on the sensitive root compressed as well as the lower limb SEPs were abnormal.

Adult↗
PubMedDate not supplied

The prognostic value of ventricular rupture in cerebral hemorrhage.

Analysis of 41 cerebral hemorrhage cases associated or not with intraparenchymatous hematoma and ventricular rupture shows the role played by these associated phenomena in the evaluation and prognosis of these patients. The death rate was 56.25% in simple cerebral hemorrhage, 100% in hemorrhage associated with hematoma, 30.76% in hemorrhage associated with ventricular rupture and 80% in hemorrhage associated with hematoma and ventricular rupture. The authors point out that the mere presence of ventricular rupture is not a really aggravating factor. A particular severity resulting from association of hemorrhage with hematoma seems to be due to the extension of the cerebral lesion produced by the two conditions associated.

Adult↗