1.
[Locomotive syndrome and frailty. Frailty in patients with fall & fall-related fracture].
Harada, A
Clinical calcium. 2012;(4):27-33
Abstract
Among geriatric syndromes, fall and fall-related fractures are one of the leading causes of the elderly's need for long-term care. Hip fractures are the typical cases. The underlying diseases of locomotive syndrome, such as sarcopenia, musculoskeletal ambulation disorder symptom complex, and osteoporosis, are closely associated with fall and fall-related fractures. From the stand point of frailty, sarcopenia, which is considered the major cause of aging-associated declines in function and reserve across multiple physiologic systems, plays a role in fall and fall-related fractures. The common adverse health outcomes both in locomotive syndrome and frailty, is a decrease in walking function and muscle strength. Understanding the role of the underlying diseases of locomotive syndrome including osteoarthritis, osteoporosis within the frailty cycle is important for the future.
2.
[A case of idiopathic portal hypertension (IPH) with hypermanganemia presenting as spastic gait].
Obama, R, Tachikawa, H, Yoshii, F, Takeoka, T, Shinohara, Y
Rinsho shinkeigaku = Clinical neurology. 2002;(9):885-8
Abstract
A 48-year-old women was admitted to our hospital because of gradually developed spastic gait. She showed spasticity of the lower extremities with mild weakness. Laboratory tests disclosed decreased WBC and platelet counts and mild increases of transaminase and total bilirubin. Blood manganese level was markedly increased (6.0 micrograms/dl). Abdominal ultrasound showed splenomegaly, and abdominal angiography showed a dilatation of the portal and paraumbilical veins. T1-weighted MR images showed high signal intensities at the bilateral globus pallidus and cerebral peducles, and T2-weighted images showed high signal intensities at the bilateral deep white matter, posterior limbs of the internal capsule and right upper cervical spinal cord. Following the diagnosis of IPH, splenectomy was performed. The blood level of manganese decreased thereafter and her neurological deficits gradually improved. Hepatic diseases often show high signal intensities at the basal ganglia on T1-weighted images, and this seemed to be due to accumulation of manganese in our case. Because demyelination or axonal injury of the spinal cord are found in hepatic disease, we speculate that the high signal intensities at the spinal cord on T2-weighted images of our case reflect hepatic myelopathy, which may also be caused by high blood levels of manganese.