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A guide to treating gait impairment with prolonged-release fampridine (Fampyra®) in patients with multiple sclerosis.
Ramió-Torrentà, L, Álvarez-Cermeño, JC, Arroyo, R, Casanova-Estruch, B, Fernández, O, García-Merino, JA, Hernández, MA, Izquierdo, G, Martínez-Yélamos, S, Meca, J, et al
Neurologia. 2018;(5):327-337
Abstract
INTRODUCTION Gait impairment, a frequent sign in multiple sclerosis (MS), places a major burden on patients since it results in progressive loss of personal and social autonomy, along with work productivity. This guide aims to provide recommendations on how to evaluate gait impairment and use prolonged-release fampridine (PR-fampridine) as treatment for MS patients with gait impairment in Spain. DEVELOPMENT PR-fampridine dosed at 10mg every 12hours is currently the only drug approved to treat gait impairment in adults with MS. Additionally, PR-fampridine has been shown in clinical practice to significantly improve quality of life (QoL) in patients who respond to treatment. Treatment response can be assessed with the Timed 25-Foot Walk (T25FW) or the 12-item MS Walking Scale (MSWS-12); tests should be completed before and after starting treatment. The minimum time recommended for evaluating treatment response is 2 weeks after treatment onset. Patients are considered responders and permitted to continue the treatment when they demonstrate a decrease in their T25FW time or an increase in MSWS-12 scores. A re-evaluation is recommended at least every 6 months. The SF-36 (Short Form-36) and the MSIS-29 (MS Impact Scale-29) tests are recommended for clinicians interested in performing a detailed QoL assessment. This drug is generally well-tolerated and has a good safety profile. It should be taken on an empty stomach and renal function must be monitored regularly. CONCLUSIONS These recommendations will help ensure safer and more efficient prescription practices and easier management of PR-fampridine as treatment for gait impairment in Spanish adults with MS.
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2.
Locomotion, cognition and influences of nutrition in ageing.
Ayers, E, Verghese, J
The Proceedings of the Nutrition Society. 2014;(2):302-8
Abstract
Gait and cognitive impairments in older adults can reflect the simultaneous existence of two syndromes that affect certain brain substrates and pathologies. Nutritional deficiencies, which are extremely common among elderly population worldwide, have potential to impact the existence and rehabilitation of both syndromes. Gait and cognition are controlled by brain circuits which are vulnerable to multiple age-related pathologies such as vascular diseases, inflammation and dementias that may be caused or accentuated by poor nutrition or deficiencies that lead to cognitive, gait or combined cognitive and gait impairments. The following review aims to link gait and cognitive classifications and provide an overview of the potential impact of nutritional deficiencies on both neurological and gait dysfunctions. The identification of common modifiable risk factors, such as poor nutrition, may serve as an important preventative strategy to reduce cognitive and mobility impairments and moderate the growing burden of dementia and disability worldwide.
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3.
[Fall risk and fracture. Falls and fractures in patients with neurological disorders].
Tamaoka, A
Clinical calcium. 2013;(5):679-85
Abstract
Neurological disorders are frequently associated with risk factors for falls, such as gait and balance disorders, deficits of lower extremity strength, sensation and coordination, in addition to cognitive impairments. Patients with various kinds of neurological disorders, including Parkinson's disease, Parkinson's syndrome, amyotrophic lateral sclerosis, peripheral neuropathy, stroke, etc, easily suffer from falls. To prevent falls among such patients, treatments of the underlying neurological diseases and assessments risk factors for falls are most important to cope effectively with these patients. In general, maintenance of the appropriate environment, consideration of the injury prevention, rehabilitation for increasing muscular strength, etc, are useful for the prevention of falls in patients with neurological disorders.
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4.
[Locomotive syndrome and frailty. Osteoporosis as an underlying disorder in the locomotive syndrome].
Hagino, H
Clinical calcium. 2012;(4):41-8
Abstract
Osteoporosis, a disorder related to locomotive syndrome, has been nicknamed "the silent disease" since it has no symptoms until fragility fracture occurs. However, a new fragility fracture cannot only reduce daily activity but can also increase fracture risk resulting in possible repetition of the fracture or other new fractures. As a result, daily living activities requiring mobility are often rapidly reduced and the quality of life can be considerably impaired. There are three strategies for preventing fragility fractures : prevention of falls, anti-osteoporosis treatment and hip protectors. A multidisciplinary approach including these strategies should be emphasized to impede the damaging process involved in fragility fracture.
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5.
[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.
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6.
[Sarcopenia in relation to locomotive syndrome and frailty].
Satake, S
Clinical calcium. 2012;(4):67-73
Abstract
One of the features of a change in our body composition with aging is a loss of muscle mass, which is called "sarcopenia" . This change may lead seniors to be dependent anothers for some activities in their daily lives. Although sarcopenia was primarily defined as a loss of muscle mass with aging, the definition has been changing and evolving to include either muscle weakness or decreased muscle performance with low muscle mass to attach greater importance to practical functions. Sarcopenia is thought to be one of the core features of frail status and also one of the causal diseases of locomotive syndrome which was proposed by the Japanese Orthopaedic Association in 2007. In our preliminary study, sarcopenia was related to a decreased sense of balance and the incidence of sarcopenia was higher in frailer seniors.
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7.
[Locomotive syndrome and frailty. Lumbar canal stenosis as an underlying disorder in the locomotive syndrome].
Sakai, Y
Clinical calcium. 2012;(4):59-66
Abstract
Lumbar canal stenosis most commonly affects the elderly population by entrapment of the cauda equine roots surrounding the spinal canal often associated with pain in the back and lower extremities, difficulty ambulating. The locomotive syndrome refers to high-risk conditions under requiring care services, and lumbar canal stenosis is an important underlying disease. As one of the key capacities of frailty identified muscluloskeletal function, the locomotive syndrome is considered to musculoskeletal frail syndrome. Surgical treatment should be recommended to take the pressure off the nerves in the lumbar spine when the conservative treatments failed, and several studies revealed that the surgery generally resulted in a preferable outcome in the lumbar canal stenosis patients. Among lumbar canal stenosis patients treated with surgery, locomotive syndrome was contained 44% and many of which were seen in thin females. The patients with locomotive syndrome had lower muscle volume both in the extremities and the trunk than those without locomotive syndrome, and surgical results were poorer in the activity of daily life whereas the pain relief was adequately obtained. Treatment of the lumbar canal stenosis should be attended to locomotive frailty, and muscle strengthening training should be incorporated into pre and postoperative therapy.
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8.
Gait termination: a review of experimental methods and the effects of ageing and gait pathologies.
Sparrow, WA, Tirosh, O
Gait & posture. 2005;(4):362-71
Abstract
The study of human gait has expanded and diversified to the extent that it is now possible to identify a substantive literature concerning a variety of gait tasks, such as gait initiation [Halliday SE, Winter DA, Frank JS, Patla AE, Prince F. The initiation of gait in young, elderly, and Parkinson's disease subjects. Gait Posture 1998;8:8-14; Mickelborough J, van der Linden ML, Tallis RC, Ennos AR. Muscle activity during gait initiation in normal elderly people. Gait Posture 2004;19:50-57], stepping over and across obstacles [Patla AE, Prentice SD, Robinson C, Newfold J. Visual control of locomotion: strategies for changing direction and for going over obstacles. J Exp Psych 1991;17:603-34; Chen, HC, Ashton-Miller JA, Alexander NB, Schultz AB. Effect of age and available response time on ability to step over an obstacle. J Gerontol 1994;49:227-33; Sparrow WA, Shinkfield AJ, Chow S, Begg RK. Gait characteristics in stepping over obstacles. Hum Mov Sci 1996;15:605-22; Begg RK, Sparrow WA, Lythgo ND. Time-domain analysis of foot-ground reaction forces in negotiating obstacles. Gait Posture 1998;7:99-109; Patla AE, Rietdyk S. Visual control of limb trajectory over obstacles during locomotion: effect of obstacle height and width. Gait Posture 1993;1:45-60] negotiating raised surfaces such as curbs and stairs [Begg RK, Sparrow WA. Gait characteristics of young and older individuals negotiating a raised surface: implications for the prevention of falls. J Gerontol Med Sci 2000;55A:147-54; Mcfayden BJ, Winter DA. An integrated biomechanical analysis of normal stair ascent and descent. J Biomech 1988;21:733-44]. In addition, increasing research interest in age-related declines in gait that might predispose individuals to falls has engendered a very extensive literature concerning ageing effects on gait. While rapid locomotor adjustments are common in the course of daily activities there has been no previous review of the findings concerning gait adaptations when walking is terminated both rapidly and unexpectedly. The aims of this review were first, to summarise the key research findings and methodological considerations from studies of termination. The second aim was to demonstrate the effects of ageing and gait pathologies on termination with respect to the regulation of step characteristics, lower-limb muscle activation patterns and foot-ground reaction forces.
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9.
Copper deficiency myelopathy produces a clinical picture like subacute combined degeneration.
Kumar, N, Gross, JB, Ahlskog, JE
Neurology. 2004;(1):33-9
Abstract
BACKGROUND Copper deficiency in ruminants is known to cause an ataxic myelopathy. Copper deficiency as a cause of progressive myelopathy in adults is underrecognized. OBJECTIVE To describe the clinical, biochemical, electrophysiologic, and imaging characteristics in 13 patients with myelopathy associated with copper deficiency. METHODS The records of patients with a copper deficiency-associated myelopathy were reviewed. Clinical characteristics, laboratory investigations, and responses to therapeutic intervention were summarized. RESULTS Thirteen such patients were found, 11 of them in a 15-month period. All patients presented with prominent gait difficulty, reflecting a sensory ataxia due to dorsal column dysfunction and lower limb spasticity. All patients had polyneuropathy. A high or high-normal serum zinc level was seen in 7 of the 11 patients for whom this information was available. Somatosensory evoked potential studies done in eight patients showed impaired conduction in central proprioceptive pathways. Dorsal column signal change on spine MRI was present in three patients. An initial clue to the diagnosis was a very low ceruloplasmin level; further tests of copper metabolism excluded Wilson disease. The cause remained unexplained in most patients. Oral copper supplementation restored normal or near-normal copper levels in 7 of the 12 patients in whom adequate follow-up data were available; parenteral supplementation restored normal level in 3 further patients. Copper supplementation prevented further neurologic deterioration, but the degree of actual improvement was variable. CONCLUSIONS Unrecognized copper deficiency appears to be a common cause of idiopathic myelopathy in adults. The clinical picture bears striking similarities to the syndrome of subacute combined degeneration associated with vitamin B12 deficiency. Early recognition and copper supplementation may prevent neurologic deterioration.
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10.
[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.