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Biomedical subjects

E Moraru

Publications and source records attributed to E Moraru.

At least 19 recordsLinked to original sources
PubMed2002

Relation between depression and anxiety in dystonic patients: implications for clinical management.

Past clinical research has identified depression as the most common psychiatric disorder associated with cervical dystonia (CD). The purpose of our study is to document different patterns of psychopathology, the frequency of psychiatric disorders, and possible correlation with the neurological disorder in patients with CD. Forty patients with CD were investigated to assess levels of psychopathology on two self-rated scales: the Beck Depression Inventory (BDI) and Symptom Check List (SCL-90). To determine the presence of psychiatric disorders, the patients were evaluated using the standard instrument in the DSM-III-R (Structured Clinical Interview Schedule, SCID). A small group of dystonic patients (12%) had higher levels of psychopathology, with significant amounts of concomitant anxiety and depression on the BDI and SCL-90. SCID criteria for at least one psychiatric disorder were fulfilled in 22 patients (55%), including both the lifetime and current diagnoses. The most frequent diagnostic categories were anxiety (40%) and major depressive disorders (37.5%). In 17 patients (42.5%), criteria for at least one lifetime diagnosis were fulfilled prior to the onset of CD. Psychiatric evaluation does not indicate one specific disorder associated with CD. The presence of anxiety and depression symptoms before and during the course of dystonia, without a possible causal relationship, could mean that the alteration of a chain of physiological events in the central nervous system may not lead to a single clinical picture. The relatively high overall lifetime prevalence of anxiety and depressive disorders may indicate the need for a broader diagnostic and therapeutic approach to patients with focal dystonia.

Adult↗
PubMed2001

Treatment of focal hyperhidrosis with botulinum toxin type A: long-term follow-up in 61 patients.

BACKGROUND: The blocking action of botulinum toxin type A (BTX-A) on cholinergically innervated sweat glands has been used successfully to treat patients with focal hyperhidrosis. OBJECTIVES: To investigate the long-term efficacy and safety of intradermal injections of BTX-A. METHODS: We performed an open-label study in 61 patients treated over a period of 3 years for axillary or palmar hyperhidrosis. A total dose of 400 mU BTX-A (Dysport) was injected into both axillae or 460 mU BTX-A (Dysport) into both palms. The injections were repeated after relapse. Objective quantification of sweat production was performed using digitized ninhydrin-stained sheets. RESULTS: Four weeks after BTX-A treatment the median reduction in sweat production was 71% compared with baseline (P < 0.001) in the axillary group and 42% (P = 0.005) in the palmar group. Subjective assessment of sweat production by the patients using a visual analogue scale (0, no sweating; 100, the most severe sweating) showed a significant reduction in both the axillary (P < 0.001) and palmar groups (P < 0.001). Secondary disturbances due to focal hyperhidrosis interfering with daily activities were markedly improved in both groups. The median time interval between the sets of injections was 34 weeks for axillary hyperhidrosis and 25 weeks for palmar hyperhidrosis. The treatment of palmar hyperhidrosis was complicated by transient but not disabling weakness of the small hand muscles in nine of 21 patients. CONCLUSIONS: Repeated intradermal injections of BTX-A in patients with axillary and palmar hyperhidrosis are as effective as first treatments.

Adult↗
PubMed2001

[Botulinum toxin in the treatment of focal hyperhidrosis].

INTRODUCTION: Botulinum A toxin (BTX-A) acts primarily at peripheral cholinergic synapses, inhibiting the release of acetylcholine. Initially it has been used to block the neuromuscular junction in focal dystonic and spastic syndromes. Recently there has been suggestions for potential clinical indications in non-muscular diseases where cholinergic terminals play a role. GUSTATORY SWEATING: In 1995 physicians reported a long-lasting anhidrotic effect of intracutaneous BTX-A injections in patients suffering from gustatory sweating (Frey's syndrome). Consequently, a number of clinical studies demonstrated good efficacy of intradermal injections of botulinumtoxin in patients with focal hyperhidrosis. FOCAL HYPERHIDROSIS OF THE PALMS AND AXILLAE: Focal hyperhidrosis is usually confined to the palms and axillae. Excessive sweating may be a social handicap and an occupational hazard. The management of focal hyperhidrosis remains controversial. Topical antiperspirants are only effective in very mild cases. Iontophoresis with tap water or anticholinergic drugs is messy and time consuming with only short-lived effect. Sympathectomy, the cornerstone of surgical management, is usually effective in palmar hyperhidrosis. Complications of this technique include surgical risks, postoperative and cosmetic problems and compensatory hyperhidrosis. AXILLARY HYPERHIDROSIS: Several studies confirmed that intracutaneous injections of botulinum toxin are useful in the majority of patients with axillary hyperhidrosis resistant to conventional treatment. In axillary hyperhidrosis total doses are ranging from 200-400 mU Dysport or from 80 to 130 mU Botox to reach a good clinical response. Injections are usually well tolerated and no serious side-effects have been observed. The mean duration of anhidrotic effect ranges between 3 and 9 weeks. PALMAR HYPERHIDROSIS: The use of botulinumtoxin in patients with palmar hyperhidrosis is rather difficult. The therapeutic window is smaller because injections are complicated by transient weakness of the small hand-muscles. Furthermore the injections at the palms are painful which can be overcomed by application of local anaesthetics or the blockade of the ulnar and median nerves. The duration of anhidrotic effect ranges from 20 to 50 weeks. CONCLUSION: Intracutaneous injections of botulinum-toxin should be offered to patients with focal hyperhidrosis of the palms and axillae causing serious social, psychologic and occupational problems, resistant to other conventional treatment options.

Axilla↗
PubMed1999

[Long-term treatment with botulinum toxin: dosage, treatment schedules and costs].

Local injection of botulinum toxin A (BTX) is considered as the treatment of choice for spasmodic torticollis (ST), blepharospasm (BS) and, with certain limitations, for hemifacial spasm (HFS). Long-term data from 89 patients with ST, 39 patients with BS and 15 patients with HFS were evaluated and subgroups of patients who received at least three (60 ST, 17 BS, 9 HFS), six (35 ST, 10 BS, 8 HFS) and nine (26 ST) re-injections were formed. These groups were investigated in regard of increases in the dosage of BTX and in regard of shorter treatment intervals in cases of repeated treatment. Annual drug costs were calculated from these data. Patients treated at least three times were asked to fill out a questionnaire concerning satisfaction and the quality of life after BTX treatment. Furthermore, the patients' "willingness to pay" for BTX treatment was investigated. Our calculations showed neither a significant increase in the dosage of BTX nor a significant reduction in the length of treatment intervals after 3 or 6 treatment sessions. Annual drug costs for BTX for the treatment of ST were 10,542 ATS, of BS 2847 ATS and of HFS 1029 ATS. 86.1% of patients with ST, 88.9% with BS and 100% with HFS were very satisfied or satisfied with the BTX treatment. In all 3 diagnostic groups, a significant mean improvement of quality of life was measured on a visual analogue scale (p < 0.001). We conclude that the injection of botulinum toxin A is a highly effective and cost effective treatment for ST, BS and HFS, and significantly increases the quality of life of all these patients.

Adult↗
PubMed1998

Psychiatric comorbidity in patients with spasmodic torticollis.

Several studies have reported raised levels of psychopathology based on self-rating scales in patients with spasmodic torticollis. Recent publications have also proposed that psychopathology, especially symptoms of depression, might be a reaction to dystonia or constitute a nonspecific reaction pattern. To determine the actual frequency of psychiatric disorders, we evaluated 44 patients with spasmodic torticollis (20 female, 24 male; mean age 43.6 years, SD 10.4) using the standard instrument for psychiatric diagnosis in the DSM-III-R (Structured Clinical Interview Schedule, SCID). The SCID permits retrospective diagnosis for most of the major psychiatric disorders, including the time before onset of dystonia. SCID criteria for at least one psychiatric disorder were fulfilled in 65.9% of patients, including both lifetime and current diagnosis. The most frequent diagnostic categories were panic disorder with or without agoraphobia (29.5%), major depressive disorder (25%), substance abuse (13.6%), and obsessive compulsive disorders (6.8%) were diagnosed less frequently. The patient-recalled onset of psychiatric symptoms preceded onset of torticollis symptoms in 43.2% of those investigated.

Adolescent↗
PubMed1986

Selective staining of large projection neurons by monoclonal antibody to a glycoprotein of PC12 cells.

A monoclonal antibody has been produced against glycoproteins prepared from PC12 cells. This antibody stains PC12 cells in a rimlike fashion, whether they are fixed or living. When neuronally differentiated PC12 cells are used, neurites as well as somata stain. In the presence of complement, the antibody is cytotoxic to PC12 cells. These lines of evidence suggest that at least some of the binding is to an exposed component of the plasma membrane in these cells. Biochemical experiments directed at identifying the antigen(s) indicate specific recognition of glycoproteins of apparent molecular weights of approximately 160 and 95 kDa by SDS-PAGE. The antibody appears to be directed against a determinant on the protein moiety. The larger species is likely to be the same as a glycoprotein previously described (Lee et al., 1981), which has been found in PC12 cells, but not in brain. The monoclonal antibody we have produced, however, selectively stains a subset of neurons in brain. Specifically, it binds to Purkinje cells in cerebellar cortex, pyramidal cells in cerebral cortex and hippocampus, ganglion cells in retina, and some neurons, generally large, in most brain structures examined. No glia or nonneural tissues stain. We suggest that the neurons recognized by this antibody may be the projection cells of each structure. However, in contrast to PC12 cells, the antigen(s) bound in this case appears to be predominantly internal. This interpretation is supported by the appearance of stained cells in tissue; by the failure of the antibody to stain live dissociated neurons from brain; and by its failure to lyse sympathetic neurons in the presence of complement. Western immunoblots show that there is glycoprotein present in brain that is recognized by the antibody, and that it is enriched in a crude microsomal fraction prepared from that tissue. This material migrates on SDS gels as two bands of 130 and 95 kDa.

Adrenal Gland Neoplasms↗
PubMed1985

Monoclonal antibodies to epitopes on different regions of the 200 000 dalton neurofilament protein. Probes for the geometry of the filament.

Neurofilaments in mammalian nervous tissues have three subunit proteins. These subunit proteins have apparent molecular masses of 200 (NF200), 150 (NF150) and 68 (NF68) kD. Biochemical assembly studies have indicated that the NF68 protein forms the core of the filament and that the other two proteins are associated proteins. Electron microscopy immunolocalization studies have been performed previously on isolated filaments and on filaments from neurons in culture, and have confirmed the localization of NF68 as a core filament protein and NF200 as a peripheral protein. We have raised two monoclonal antibodies to the NF200 components. Using immunogold labelled protein A, we have been able to localize these antibodies to tissue sections of adult cerebellum at the EM level. With this method, we have found that one of the monoclonal antibodies (NF2) shows a linear arrangement of gold particles directly on the filament, whereas the second monoclonal antibody (NF111) reacts with the filaments to give a periodic arrangement of gold particles. By immunoblotting against chymotryptic fragments of the NF200 protein, we have found that the mAB-NF111 reacts solely with a 160 kD piece, whereas the other monoclonal antibody reacts with both the 160 kD piece and the 40 kD piece. The latter piece was shown to be associated to the filament by binding studies with iodinated NF68. Thus the EM localization studies and the biochemical studies indicate that the two monoclonal antibodies react with different parts of the NF200 molecule, one binding to a part of the molecule which is located closer to the filament, and one to a more peripheral part of the molecule.

Animals↗
PubMed1978

On the mechanism of hyperglycemia and stimulation of growth hormone secretion by L-dopa.

The mechanism of hyperglycemia produced by L-dopa was studied in normal trained dogs with 3-3H-glucose infusion to measure rates of hepatic glucose output (production) and overall glucose uptake (utilization). Infusion of L-dopa (20 mg/kg/h) increased glucose production causing hyperglycemia. Despite the hyperglycemia plasma insulin did not increase nor did glucose uptake, indicating a relative inhibition of glucose utilization. These effects resemble those produced by epinephrine infusion. Pretreatment with a decarboxylase inhibitor, carbidopa, prevented the L-dopa effect to increase glucose production and no hyperglycemia occurred. Hyperglycemia was not prevented by pimozide, a dopamine receptor blocker, nor by propranolol but was prevented by phentolamine. L-Dopa also increased plasma growth hormone levels without affecting plasma cortisol. The effect on growth hormone was prevented by carbidopa and by phentolamine but not by pimozide; propranolol potentiated the rise in growth hormone. The data suggest that the L-dopa-induced hyperglycemia is due to a peripheral action, whereas stimulation of growth hormone secretion may be due to a central action of a L-dopa metabolite.

Animals↗
PubMed1977

On the mechanism of diazoxide-induced hyperglycemia.

Infusion of diazoxide (16.5 mg./kg. in 10 minutes) into normal unanesthetized dogs resulted in a prompt hyperglycemia due to increased hepatic glucose production as measured with a 3-3H-glucose primer-infusion technique. Plasma insulin and glucagon were decreased. Glucose uptake failed to increase. Diazoxide administration during period of alpha adrenergic receptor blockade with phentolamine still caused hyperglycemia and increased glucose production. Glucose uptake was inhibited despite adequate plasma insulin. Infusion of somatostatin along with insulin prevented the effects of diazoxide on plasma glucose and glucose production. It is concluded that diazoxide hyperglycemia is not due solely to decreased insulin secretion or increased epinephrine secretion and that glucagon is not a contributory factor. Diazoxide may act directly to increase glucose production and inhibit glucose uptake. Somatostatin appears capable of blocking the effect of diazoxide on glucose production by an unknown mechanism.

Animals↗
PubMedDate not supplied

[Recurrent respiratory manifestations in atopic dermatitis in small children].

The aim of the present study was the retrospective analysis (in the last 5 years) of 89 children, aged between 3 and 24 months of life, diagnosed with atopic dermatitis (D.A.) and wheezing, in comparison with a second group of 31 children admitted in the Paediatric Clinic for recurrent wheezing (R.W.) without atopic cutaneous signs. Evaluating the therapeutical response on the basis of the clinical and biological features for each child, we have noticed for the first group (with D.A.), the followings: 30% of patients didn't experience a favourable outcome and were complicated with "severe" asthma; 54% of subjects have manifested airway hyperreactivity (nocturnal and early morning cough); 81% of children have associated allergic rhinitis. The observations in the second group have suggested that, only in 12% of patients with R.W. has been manifested asthma as a major complication. The main risk factors for asthma in the first group were as follows: precocious atopic eczema, personal or family history of atopy, nourishment with non-maternal milk and passive smoke. We consider that asthma at infants and children is underestimated because of the difficulties of diagnosis at this age.

Asthma↗