Medical Doctors’ Knowledge of Libras in the Federal District and Deaf Patient Health Care

<p></p><p>ABSTRACT In medical schools, the teaching of Brazilian Sign Language (Libras) is limited and this scenario may result in difficulties when dealing with an important portion of the population: the deaf. According to the Brazilian Institute of Geography and Statistics (IBGE), nearly 24% of the Brazilian population has some kind of deficiency; belonging to what are known as vulnerable groups. Deafness is among the most prevalent deficiencies, and the medical practice being unable to attend a deaf patient is a public health problem that requires further discussion. The objective of the present study was to evaluate medical doctors’ knowledge of Libras and their perception of attending to a deaf patient. A crosssectional and descriptive study was designed and 101 medical doctors of the Brazilian Public Health System (Sistema Único de Saúde, SUS) were randomly chosen in the Federal District and answered a structured survey. We interviewed medical doctors with a mean age of 41 years from 24 different medical specialties. 92.1% of them had seen at least one deaf patient in their clinical practice. 76.2% of them considered the knowledge of Libras relevant to their practice, but only one declared basic knowledge of the language. Most of the medical doctors reported uncertainty and discomfort when attending a deaf patient. A significant number of doctors had already seen a deaf patient in their clinical practice, and most considered the knowledge of Libras important, especially those under the age of 55 years. The feeling of discomfort when dealing with a deaf patient possibly arises from not knowing Libras and being unable to communicate with the patient properly. We emphasize the importance of learning Libras before or during medical school and other health-related courses. Being aware that the deaf patient deserves full health assistance is fundamental, and it may improve specialized learning of Libras and consequently result in a better doctor-patient relationship.</p><p></p

Vesicular zinc staining in the <i>Fascia dentata</i> of Ctrl, MTLE and TLE-TD groups.

<p>MTLE (dark gray boxplots) had increased neo-Timm staining (showed as gray level intensity), when compared to Ctrl (white boxplots), in the inner molecular layer (IML, p<0.001). No difference was observed between TLE-TD (light gray boxplots) and Ctrl or MTLE. The * indicate difference from Ctrl. The dark circles indicate mean.</p

HLA-DR immunopositive area in hippocampal subfields of Ctrl, MTLE and TLE-TD groups.

<p>Compared to Ctrl (white boxplots), TLE groups had increased HLA-DR immunoreactivity (showed as percentage of immunopositive area) in outer molecular layer (OML), granule cell layer (GCL), CA4, and CA1 subfields (p<0.001). MTLE (dark gray boxplots) had increased HLA-DR immunoreactivity in inner molecular layer (IML), subgranule zone (SGZ), hilus, CA3, CA2, prosubiculum (PRO) and subiculum (SUB) (p<0.01). In IML, MTLE also presented increased HLA-DR immunoreactivity when compared to TLE-TD (p<0.001). The * indicate difference from Ctrl and ^# difference from TLE-TD.</p

Representative sections of MT-I/II immunohistochemistry in hippocampal subfields from Ctrl, TLE-TD and MTLE patients.

<p>MTLE patients had widespread increase in MT-I/II when compared to Ctrl, demonstrated by increased cellular and neuropil staining in C, F and I. In TLE-TD patients, increased MT-I/II expression was observed only in the <i>fascia dentata</i> (B) outer molecular layer (small black arrow) and subgranule zone (small white arrow), the entry point of the hippocampus. The representative images shown are from the <i>fascia dentata</i> (A–C), CA1 (D–F) and subiculum (G–I). Bar in I indicates 100 micrometers.</p

MT-I/II immunopositive area in hippocampal subfields of Ctrl, MTLE and TLE-TD groups.

<p>Compared to Ctrl (white boxplots), TLE groups had higher MT-I/II immunopositive area (showed as percentage of immunopositive area) in outer molecular layer (OML), inner molecular layer (IML) and subgranule zone (SGZ) (p<0.01). MTLE (dark gray boxplots) had increased MT-I/II immunoreactivity in granule cell layer (GCL), hilus, CA4, CA3, CA2, CA1, prosubiculum (PRO) and subiculum (SUB) (p<0.05), compared to Ctrl, and also in CA1 when compared to TLE-TD (p<0.001). The * indicate difference from Ctrl and ^#difference from TLE-TD.</p

MT-I/II immunopositive area in MTLE patients without and with secondary generalized seizures.

<p>Patients without secondary generalization (white boxplots) present increased MT-I/II immunopositivity (p<0.05) in the inner molecular layer (IML), granule cell layer (GCL), subgranule zone (SGZ), CA2 and CA1, when compared with patients that present secondary generalization (light gray boxplots). The ⁺ indicates difference between the groups.</p

GFAP immunopositive area in hippocampal subfields of Ctrl, MTLE and TLE-TD groups.

<p>Compared to Ctrl (white boxplots), MTLE (dark gray boxplots) and TLE-TD (light gray boxplots) groups had increased GFAP immunoreactivity (showed as percentage of immunopositive area) in outer molecular layer (OML), inner molecular layer (IML), granule cell layer (GCL), subgranule zone (SGZ), hilus, CA4 and CA3 (p<0.001), and MTLE groups had increased GFAP immunopositivity in CA2, CA1, prosubiculum (PRO) and subiculum (SUB), compared to Ctrl and TLE-TD (p<0.001). In the subiculum (SUB), TLE-TD had increased GFAP immunoreactivity, compared to Ctrl (p<0.001). The * indicate difference from Ctrl and ^# difference from TLE-TD.</p

Representative images of MT-I/II staining in several hippocampal subfields.

<p>Almost all stained cells have astrocyte morphology (indicated by small arrows in A–F), while neurons remained unstained (white cells pointed by large arrows in B). Only in few cases from Ctrl (E and F) and in one region of one case of TLE were observed cells with neuron morphology (large arrows in E and F). No stained neuron presented the strong staining of astrocytes. In Ctrl, neuropil presented a weak staining (indicated by black circle in F). In TLE the neuropil staining level was heterogeneous, as can be seen in CA1 sections depicted in C and D (indicated by white circles). The representative images shown are from the <i>fascia dentate</i> (A), <i>subiculum</i> (B and E), CA1 (C and D) and <i>hilus</i> (F) of Ctrl (E and F) and TLE cases (A–D). Bar in F indicates 100 micrometers.</p

Clinical history of patients with TLE (MTLE and TLE-TD) and Ctrl cases.

1<p>age of death for Ctrl and age at surgery for TLE.</p>#<p> = statistical difference to TLE-TD; Ctrl = control; MTLE = mesial temporal lobe epilepsy; TLE-TD = temporal lobe epilepsy associated with tumor or dysplasia.</p

Confocal images of astrocytes expressing MT-I/II in Ctrl and TLE cases.

<p>TLE (E–H) patients presented more astrocytes (GFAP immunoreactive cells, red in B, F, D, H and I) expressing MT-I/II (green in C, G, D, H and I, indicated by white arrows in D and H) than Ctrl (A–D). In a detailed view of H (I), MT-I/II expression can be observed in radial branches (large arrow), soma (small arrow) and nucleus (Hoeschst 33342 staining, white circle) of astrocytes. Astrocytes are GFAP immunoreactivity) Bars in H and I indicate 50 micrometers.</p