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Anatomy, Physiology, and Dysfunction of the Diaphragm
Published in Massimo Zambon, Ultrasound of the Diaphragm and the Respiratory Muscles, 2022
The intensive care theatre is another setting in which diaphragmatic weakness occurs because of systemic conditions. In this setting, diaphragmatic hypotrophy ensues and is favoured by sepsis, multiorgan failure, hyperglycemia, muscle relaxants, and mechanical ventilation itself (even for brief periods). This is usually considered a consequence of critical-illness polyneuropathy and myopathy and has a multifactorial origin. In fact, besides simple diaphragmatic disuse, several conditions contribute to muscle atrophy hypophosphatemia, hypomagnesemia, hypokalemia, hypocalcemia, and thyroid disturbances. This issue is clinically prominent, since diaphragmatic hypotrophy prolongs ventilator dependency and its extent conditions the probability of weaning (47–49).
Birthweight: Studies in Humans *
Published in Ernest L. Abel, Smoking and Reproduction: An Annotated Bibliography, 2017
12.a.8. Goujard, J., Kaminski, M., Grelier, M., and Rumeau-Rouquette, C., En-quete etiologique sur l’hypotrophie foetale. Resultats d’une etude prospective dans les hopitaux de Paris (Etiological inquiry regarding foetal hypotrophy. Results of a prospective study in Parisian hospitals), Soz. Praventivmed., 19, 93—99, 1974. Prospective study of 5500 births found fetal hypotrophy occurring in 14.9% of babies born to smokers, 10.3% of babies born to women who stopped smoking during the first trimester of pregnancy, and 8.2% of babies born to nonsmokers. For women with prior histories of stillbirth, percentages of hypotrophy were 16.3 and 18.8% for nonsmokers and smokers, respectively. For women with prior history of neonatal hypotrophy, percentage of hypotrophy in this study was 33.0 and 40.7% for nonsmokers and smokers, respectively. For women with prior history of abortion, percentages of hypotrophy were 8.2 and 10.7% for nonsmokers and smokers, respectively.
Congenital pouch colon
Published in Prem Puri, Newborn Surgery, 2017
Amulya K. Saxena, Praveen Mathur
Histological studies of resected pouch colon demonstrate extreme variations in CPC. In most patients, acute and chronic inflammation of the mucosal and submucosal layers is present with varying degrees of hemorrhage along with the presence of disorganized muscle layers in the colon wall (Figure 69.2). Hypotrophy of the muscle layers has been observed, which is more predominant in the outer muscle layer of the pouch.22 Extreme variations in the muscle layer (both circular and longitudinal) have also been found, which include fibrosis, atrophy, and hypertrophy along with muscle disruption.23 Investigations have also shown variations, from the presence of normal colon wall with normal ganglion cells in some patients to a poorly developed colon wall musculature with decreased or absent ganglion cells in others.6,10,13,24 Interestingly, heterotrophic tissue such as gastric mucosa, small intestinal mucosa with characteristic villi, and pancreatic tissue has also been found in pouch specimens of CPC patients. 10,22
Value of Placental Examination in the Diagnostic Evaluation of Stillbirth
Published in Fetal and Pediatric Pathology, 2022
In agreement with the literature data [21,23], we found that placental hypoplasia was significantly associated with stillbirth related to the placental abnormalities (87% of cases) which were dominated by vascular lesions. Isolated placental hypoplasia was observed in 5/8 cases of the unexplained stillbirths. Similar cases were reported in the literature, but causal relationship between placental hypoplasia and stillbirth remains unclear as the fetal IUGR may escape diagnosis because of severe fetal maceration (mummification) and lack of full-body X-ray [14]. This may explain the low frequency of fetal hypotrophy in our series (16%) despite the significant proportion of the hypoplastic placentas. Ogunyemi et al., [8] report that stillbirths have 6.8 times higher risk to be small for gestational age compared with fetuses born alive at the same age (≥ 25 WG).
Did the prevalence of suprascapular neuropathy in professional volleyball players decrease with the changes occurred in serving technique?
Published in The Physician and Sportsmedicine, 2021
Daniele Mazza, Raffaele Iorio, Piergiorgio Drogo, Edoardo Gaj, Edoardo Viglietta, Giuseppe Rossi, Edoardo Monaco, Andrea Ferretti
If the suprascapular nerve is compressed proximally at the suprascapular notch, atrophy of both the supraspinatus and infraspinatus muscles will be found. Furthermore, proximal entrapment is usually accompanied by pain in the posterior region of the shoulder. Differently, distal entrapment at the spinoglenoid notch will result in selective atrophy of the infraspinatus muscle known as infraspinatus syndrome (IS) [9]. In IS, no further symptoms other than isolated muscle atrophy were reported. Indeed, at the spinoglenoid notch, the sensory branches have yet to leave the nerve [32]. In our study, none of the volleyball players complained of shoulder pain; in recent literature, IS has been considered a totally asymptomatic condition [16,18,19,23,29,32]. External rotation weakness assessed with specific text or dynamometric exams may be the only suspicion finding. Each case of hypotrophy in our study was accompanied by external rotation weakness as compared to the contralateral side. This is in line with the study of Witvrouw et al. [19] who found a significant reduction in external rotation strength of the affected side.
Novel FUS mutation Y526F causing rapidly progressive familial amyotrophic lateral sclerosis
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2021
Zhang-Yu Zou, Chun-Hui Che, Shu-Yan Feng, Xiu-Ying Fang, Hua-Pin Huang, Chang-Yun Liu
One patient carrying FUS p.R521C mutation was a man who developed muscular weakness of the left lower limb at the age of 33 years. One month later, muscle weakness of the left hand presented and gradually progressed proximally. Three months later he developed weakness of the right upper limb and had some difficulties in lifting his arms. Nine months after onset he was referred to our ALS center because of weakness of neck and development of head drop. Neurological examination showed the cranial nerves were spared except for weakness of the bilateral sternocleidomastoid muscles and trapezius (Medical Research Council MRC 3/5). The extensor muscles of the neck were atrophic and weak (MRC 2/5). Diffuse and severe muscular hypotrophy and weakness was found at the upper limbs (MRC 4/5 in distal limbs and MRC 2/5 in proximal limbs) and the left lower limbs (MRC 3/5). Diffuse fasciculations were observed at upper limbs. Deep tendon reflexes were reduced in upper limbs and brisk in lower limbs. Babinski and Hoffman’s signs were not elicited. He was cognitively normal. He scored 34/48 on ALSFRS-R. EMG demonstrated chronic and active denervation of the upper and lower limbs, thoracic, and sternocleidomastoid muscles. The disease progressed rapidly and the patient died 17 months after onset due to respiratory deficit. He had a healthy 9-year-old son. Both his parents were in their 50’s and healthy.