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OBJECTIVES: This study confirms the effectiveness of pretreatment video-based psychoeducation on stress management and relaxation in reducing depression, anxiety, and uncertainty among patients with breast cancer. METHODS: We conducted a nonrandomized trial with 86 pretreatment patients with breast cancer who were divided equally into intervention and control groups, and stratified according to cancer stages and patient ages. Omitting the excluded participants, 35 intervention group and 36 control group participants were asked to complete the Hospital Anxiety and Depression Scale and Universal Uncertainty in Illness Scale (UUIS) before the psychoeducational intervention (baseline, hereafter "BL ") as well as 1 and 3 months later. Then, a 2 group (intervention and control groups) × 3 time points (BL and 1 and 3 months post-intervention) mixed models repeated measures (MMRM) analysis was implemented. RESULTS: Analysis confirmed interaction between 2 group × 3 time points for depression, anxiety, and UUIS. Multiple comparisons revealed that each score in the intervention group was significantly lower 1 and 3 months post-intervention compared to BL. Meanwhile, in the control group, the depression score was significantly higher at 3 months post-intervention compared to pre-intervention. The anxiety scores and UUIS of the same group were not significantly different between 1 and 3 months post-intervention. The effect size values 3 months post-intervention were -0.57 for depression, -0.25 for anxiety, and 0.05 for uncertainty. SIGNIFICANCE OF RESULTS: Pretreatment psychoeducation reduced depression, anxiety, and uncertainty in the intervention group of patients with breast cancer compared to the control group. The effect sizes at 3 months post-intervention were moderate for depression and small for anxiety. These results suggest the effectiveness of psychoeducation for patients with breast cancer, using videos on stress management and relaxation, early at the pretreatment stage.
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BACKGROUND AND PURPOSE: Our aim was to study the efficacy of robotic therapy as an adjuvant to standard therapy during poststroke rehabilitation. METHODS: Prospective, open, blinded end point, randomized, multicenter exploratory clinical trial in Japan of 60 individuals with mild to moderate hemiplegia 4 to 8 weeks post stroke randomized to receive standard therapy plus 40 minutes of either robotic or self-guided therapy for 6 weeks (7 days/week). Upper extremity impairment before and after intervention was measured using the Fugl-Meyer assessment, Wolf Motor Function Test, and Motor Activity Log. RESULTS: Robotic therapy significantly improved Fugl-Meyer assessment flexor synergy (2.1±2.7 versus -0.1±2.4; P<0.01) and proximal upper extremity (4.8±5.0 versus 1.9±5.5; P<0.05) compared with self-guided therapy. No significant changes in Wolf Motor Function Test or Motor Activity Log were observed. Robotic therapy also significantly improved Fugl-Meyer assessment proximal upper extremity among low-functioning patients (baseline Fugl-Meyer assessment score <30) and among patients with Wolf Motor Function Test ≥120 at baseline compared with self-guided therapy (P<0.05 for both). CONCLUSIONS: Robotic therapy as an adjuvant to standard rehabilitation may improve upper extremity recovery in moderately impaired poststroke patients. Results of this exploratory study should be interpreted with caution. CLINICAL TRIAL REGISTRATION: URL: http://www.umin.ac.jp/. Unique identifier: UMIN000001619.
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Hemiplejía/rehabilitación , Evaluación de Resultado en la Atención de Salud , Robótica/métodos , Rehabilitación de Accidente Cerebrovascular/métodos , Accidente Cerebrovascular/complicaciones , Extremidad Superior/fisiopatología , Adulto , Anciano , Anciano de 80 o más Años , Femenino , Hemiplejía/etiología , Humanos , Masculino , Persona de Mediana Edad , Rehabilitación de Accidente Cerebrovascular/instrumentación , Adulto JovenRESUMEN
Bunina bodies (BBs) are small eosinophilic neuronal cytoplasmic inclusions (NCIs) found in the remaining lower motor neurons (LMNs) of patients with sporadic amyotrophic lateral sclerosis (SALS), being a specific feature of the cellular pathology. We examined a case of SALS, unassociated with TDP-43 or C9ORF72 mutation, of 12 years duration in a 75-year-old man, who had received artificial respiratory support for 9 years, and showed widespread multisystem degeneration with TDP-43 pathology. Interestingly, in this patient, many NCIs reminiscent of BBs were observed in the oculomotor nucleus, medullary reticular formation and cerebellar dentate nucleus. As BBs in the cerebellar dentate nucleus have not been previously described, we performed ultrastructural and immunohistochemical studies of these NCIs to gain further insight into the nature of BBs. In each region, the ultrastructural features of these NCIs were shown to be identical to those of BBs previously described in LMNs. These three regions and the relatively well preserved sacral anterior horns (S1 and S2) and facial motor nucleus were immunostained with antibodies against cystatin C (CC) and TDP-43. Importantly, it was revealed that BBs exhibiting immunoreactivity for CC were a feature of LMNs, but not of non-motor neurons, and that in the cerebellar dentate nucleus, the ratio of neurons with BBs and TDP-43 inclusions/neurons with BBs was significantly lower than in other regions. These findings suggest that the occurrence of BBs with CC immunoreactivity is intrinsically associated with the particular cellular properties of LMNs, and that the mechanism responsible for the formation of BBs is distinct from that for TDP-43 inclusions.
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Esclerosis Amiotrófica Lateral/patología , Encéfalo/patología , Cuerpos de Inclusión/patología , Neuronas Motoras/ultraestructura , Neuronas/ultraestructura , Médula Espinal/patología , Esclerosis Amiotrófica Lateral/terapia , Humanos , Masculino , Persona de Mediana Edad , Respiración ArtificialRESUMEN
BACKGROUND: We evaluated whether the Walkaide® device could effectively improve walking ability and lower extremity function in post-stroke patients with foot drop. Patients aged 20-85 years with an initial stroke within ≤6 months and a functional ambulation classification score of 3 or 4 were eligible. MATERIALS AND METHODS: Patients were randomly allocated to the functional electrical stimulation (FES) or control group at a 1:1 ratio. A 40 min training program using Walkaide was additionally performed by the FES group five times per week for 8 weeks. The control group received the 40 min training program without FES. RESULTS: A total of 203 patients were allocated to the FES (n = 102) or control (n = 101) groups. Patients who did not receive the intervention or whose data were unavailable were excluded. Finally, the primary outcome data of 184 patients (n = 92 in each group) were analyzed. The mean change in the maximum distance during the 6-MWT (primary outcome) was 68.37 ± 62.42 m and 57.50 ± 68.17 m in the FES and control groups (difference: 10.86 m; 95% confidence interval: -8.26 to 29.98, p = 0.26), respectively. CONCLUSIONS: In Japanese post-stroke patients with foot drop, FES did not significantly improve the 6 min walk distance during the convalescent phase. The trial was registered at UMIN000020604.
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Spinocerebellar ataxia (SCA) type 17-digenic TBP/STUB1 disease (SCA17-DI) has been recently segregated from SCA17, caused by digenic inheritance of two gene mutations - intermediate polyglutamine-encoding CAG/CAA repeat expansions (polyQ) in TBP (TBP41 - 49) and STUB1 heterozygosity - the former being associated with SCA17, and the latter with SCA48 and SCAR16 (autosomal recessive). In SCA17, most patients carry intermediate TBP41 - 49 alleles but show incomplete penetrance, and the missing heritability can be explained by a new entity whereby TBP41 - 49 requires the STUB1 variant to be symptomatic. The STUB1 gene encodes the chaperone-associated E3 ubiquitin ligase (CHIP) involved in ubiquitin-mediated proteasomal control of protein homeostasis. However, reports of the neuropathology are limited and role of STUB1 mutations in SCA17-DI remain unknown. Here we report the clinicopathologic features of identical twin siblings, one of whom was autopsied and was found to carry an intermediate allele (41 and 38 CAG/CAA repeats) in TBP and a heterozygous missense mutation in STUB1 (p.P243L). These patients developed autosomal recessive Huntington's disease-like symptoms. Brain MRI showed diffuse atrophy of the cerebellum and T2WI revealed hyperintense lesions in the basal ganglia and periventricular deep white matter. The brain histopathology of the patient shared features characteristic of SCA17, such as degeneration of the cerebellar cortex and caudate nucleus, and presence of 1C2-positive neurons. Here we show that mutant CHIP fails to generate the polyubiquitin chain due to disrupted folding of the entire U box domain, thereby affecting the E3 activity of CHIP. When encountering patients with cerebellar ataxia, especially those with Huntington's disease-like symptoms, genetic testing for STUB1 as well as TBP should be conducted for diagnosis of SCA17-DI, even in cases of sporadic or autosomal recessive inheritance.
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Enfermedad de Huntington , Ataxias Espinocerebelosas , Humanos , Neuropatología , Autopsia , Ataxias Espinocerebelosas/genética , Ubiquitina-Proteína Ligasas/genéticaRESUMEN
A 66-year-old, right-handed male, was admitted to our hospital with difficulty in recognizing faces and colors. He had suffered a stroke in the right occipital region three years earlier that had induced left homonymous hemianopsia, but not prosopagnosia. A neurological examination revealed prosopagnosia, color agnosia, constructional apraxia, and topographical disorientation, but not either hemineglect or dressing apraxia. The patient was unable to distinguish faces of familiar persons such as his family and friends, as well as those of unfamiliar persons such as doctors and nurses. Brain MRI demonstrated an old infarction in the right medial occipital lobe and a new hemorrhagic infarction in the left medial occipital lobe, including the fusiform and lingual gyrus. It is unclear whether a purely right medial occipital lesion can be responsible for prosopagnosia, or whether bilateral medial occipital lesions are necessary for this occurrence. The current case indicated that bilateral medial occipital lesions play an important role in inducing porsopagnosia.
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Infarto Cerebral/complicaciones , Lóbulo Occipital/irrigación sanguínea , Prosopagnosia/etiología , Anciano , Lateralidad Funcional/fisiología , Hemianopsia/etiología , Humanos , MasculinoRESUMEN
A 47-year-old right-handed man was admitted to our hospital for rehabilitation after right basal ganglion hematoma. On day 57, he noticed a supernumerary motor phantom limb (SPL) involving his right arm, originating at the level of the elbow. The most notable finding of his SPL was the motor characteristic. When the subject had the intention to move the upper paralyzed limb simultaneously with the trainer's facilitating action, he said "there is another arm." The intention to move the paralyzed arm alone or passive movement of the paralyzed arm did not induce the SPL. He showed a severe left sensorimotor impairment and mild hemineglect, but no neglect syndromes of the body (e.g., asomatognosia, somatoparaphrenia, personification and misoplegia, or anosognosia) were observed. Brain MRI demonstrated a hematoma in the right temporal lobe subcortex, subfrontal cortex, putamen, internal capsule, and thalamus. Single-photon emission computed tomography images showed more widespread hypoperfusion in the right hemisphere in comparison to the lesions on MRI. However, the premotor cortex was preserved. Our case is different from Staub's case in that SPL was not induced by the intention to move the paralyzed limb alone; rather, it was induced when the patient intended to move the paralyzed limb with a trainer's simultaneous facilitating action. The SPL may reflect that an abnormal closed-loop function of the thalamocortical system underlies the phantom phenomenon. However, despite the severe motor and sensory impairment, the afferent pathway from the periphery to the premotor cortex may have been partially preserved, and this may have been related to the induction of SPL.
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A 76-year-old man who rapidly developed quadriparesis was admitted to our hospital. MRI showed an epidural mass extending from C4 to C6, displacing the spinal cord anteriorly. It showed isointensity on the T1-weighted imagines, hyperintensity on the T2-weighted images, and diffuse hyperintensity with gadolinium enhancement. Plain radiographs, CT and MRI showed no evidence of bone involvement. Serum immunoelectrophoresis disclosed M-components of IgA and lambda light chains. This is the first report that an epidural myeloma in the cervical spinal cord caused compression of the cord without evidence of bone involvement.
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Mieloma Múltiple/diagnóstico , Compresión de la Médula Espinal/etiología , Anciano , Espacio Epidural , Humanos , Imagen por Resonancia Magnética , Masculino , Mieloma Múltiple/complicaciones , CuadriplejíaRESUMEN
The origin of patchy white matter hyperintensities commonly seen in the elderly on magnetic resonance (MR) images with long repetition time (TR) is still controversial. We describe MR findings in older patients in whom white matter hyperintensities were attenuated by compression of the cerebral hemisphere from a chronic subdural hematoma. These sequential MR findings substantiate the hypothesis that leukoaraiosis may arise when drainage of the bulk flow of brain interstitial fluid is disturbed.