Distal Arm Weakness

Author(s):  
Aziz Shaibani

Distal arm weakness may be caused by involvement of the intrinsic hand muscles (interossi, thenar and hypothenar muscles, lumbricals) or extrinsic hand muscles (long finger flexors and extensors). ALS is typical for the former type, and IBM is typical for the latter type. Incoordination of skilled finger movement due to cerebellar disease is associated with normal strength. Poor mobility due to joints pain and swelling should not be confused with muscle weakness. Mononeuropathies such as ulnar, radial, median, and AIN,lesions usually cause differential loss of function. Myasthenia sometimes causes weakness of the wrist and finger extensors. A small but distinct group of distal hereditary myopathies should always be borne in mind. Progressive sensorimotor neuropathies are usually associated with sensory symptoms. Multifocal motor neuropathy can be a diagnostic challenge.

Author(s):  
Aziz Shaibani

Distal arm weakness may be caused by involvement of the intrinsic hand muscles (interossi, thenar and hypothenar muscles, lumbricals) or extrinsic hands muscles (long fingers flexors and extensors). Amyotrophic lateral sclerosis (ALS) is typical of the former type, and inclusion body myositis (IBM) is typical for the later type. Incoordination of skilled finger movement due to cerebellar disease is associated with normal strength. Poor mobility due to joint pain and swelling should not be confused with muscle weakness. Mononeuropathies such as ulnar, radial, median, and anterior interosseus nerve lesions usually cause differential loss of function. Myasthenia gravis sometimes causes weakness of the wrist and finger extensors. A small but distinct group of distal hereditary myopathies should always be kept in mind. Progressive sensorimotor neuropathies are usually associated with sensory symptoms. Multifocal motor neuropathy can be a challenging diagnosis.


2012 ◽  
Vol 7 (2) ◽  
pp. 124 ◽  
Author(s):  
Jean-Marc Léger ◽  
Eugen Gavriliuc ◽  
◽  

Multifocal motor neuropathy (MMN) is a rare, clinically well-defined condition within the spectrum of chronic, immune-mediated neuropathies. A typical patient history involves slowly or stepwise progressive, predominantly distal, asymmetrical limb weakness and muscle wasting, most frequently in the arm, that may have developed over a period of years. As a rare condition, MMN may present a diagnostic challenge for non-specialists and some patients may wait years for a correct diagnosis. Timely and accurate diagnosis is essential for patients with MMN. Unlike some motor neuropathies, MMN is treatable with intravenous immunoglobulin and untreated patients are likely to experience progressive muscle weakness that may result in serious functional impairment and impaired quality of life. The aim of this article is therefore to provide a guide for non-specialist neurologists to the clinical recognition and differential diagnosis of MMN.


US Neurology ◽  
2016 ◽  
Vol 12 (01) ◽  
pp. 17
Author(s):  
Richard A Rison ◽  
◽  
Said R Beydoun ◽  

Multifocal motor neuropathy (MMN) is a rare, treatable neuropathy, but good long-term outcomes are dependent on early treatment. Appropriate diagnostic criteria exist for MMN, but it has a heterogeneous clinical presentation, and, when confined to a small group of nerves, its clinical presentation can overlap with entrapment neuropathies. Electrodiagnosis is a useful diagnostic technique but occasionally MMN can be misdiagnosed as entrapment neuropathies. Misdiagnosis should rarely occur since the nerve involvement in MMN is usually not at sites of common nerve entrapment, and the impact of misdiagnosis can be substantial. The treatments of these conditions differ significantly: intravenous immunoglobulin is the standard therapy for MMN, while treatment options for entrapment neuropathies include conservative treatment, such as splinting, corticosteroids, or surgery. Such treatment in MMN may worsen symptoms, potentially leading to progressive motor symptoms, including muscle weakness, atrophy, and significant motor disability. Two exemplary cases are presented, which highlight the importance of differential diagnosis of these conditions. Emerging technologies, such as high-resolution sonography and magnetic resonance neurography, will aid in defining future diagnostic criteria of MMN.


2019 ◽  
Vol 130 (10) ◽  
pp. e210-e211
Author(s):  
Keisuke Kido ◽  
Manabu Inoue ◽  
Yuta Terada ◽  
Toshiaki Hamano

2006 ◽  
Vol 95 (6) ◽  
pp. 3371-3383 ◽  
Author(s):  
James P. Coxon ◽  
Cathy M. Stinear ◽  
Winston D. Byblow

Volitional inhibition is the voluntary prevention of a prepared movement. Here we ask whether primary motor cortex (M1) is a site of convergence of cortical activity associated with movement preparation and volitional inhibition. Volitional inhibition was studied by presenting a stop signal before execution of an anticipated response that requires a key lift to intercept a revolving dial. Motor evoked potentials (MEPs) were elicited in intrinsic hand muscles by transcranial magnetic stimulation (TMS) to assess corticomotor excitability and short interval intracortical inhibition (sICI) during task performance. The closer the stop cue was presented to the anticipated response, the harder it was for subjects to inhibit their response. Corticomotor pathway excitability was temporally modulated during volitional inhibition. Using subthreshold TMS, corticomotor excitability was reduced for Stop trials relative to Go trials from 140 ms after the cue. sICI was significantly greater for Stop trials compared with Go trials at a time that preceded the onset of muscle activity associated with the anticipated response. These results provide evidence that volitional inhibition is exerted at a cortical level and that inhibitory networks within M1 contribute to volitional inhibition of prepared action.


2004 ◽  
Vol 33 (3) ◽  
pp. 237-242 ◽  
Author(s):  
Vinay Chaudhry ◽  
Andrea M. Corse ◽  
David R. Cornblath ◽  
Ralph W. Kuncl ◽  
Daniel B. Drachman ◽  
...  

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