IgM antibodies to N-acetylgalactosaminyl GD1a in benign monomelic amyotrophy of the lower limb

Weiss, Michael D.

doi:10.1016/j.jns.2005.03.048

Cited by 3 publications

(3 citation statements)

References 18 publications

(18 reference statements)

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“…Only the arm weakness responded to IVIg. Motor neuropathies with conduction block presenting with lower limb weakness are extremely rare [57,58] and have been related to antibodies against GM 1 [57] or GD 1a [58], rather than GD 1b , as in our patient. This abnormality has not previously been associated with multifocal neuropathy with conduction block.…”

Section: Discussionmentioning

confidence: 50%

Monomelic neurogenic syndromes: A prospective study

Carvalho¹,

Swash²

2007

Journal of the Neurological Sciences

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Section: Discussionmentioning

confidence: 50%

Monomelic neurogenic syndromes: A prospective study

Carvalho¹,

Swash²

2007

Journal of the Neurological Sciences

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“…Third, the follow‐up time was not enough to differentiate BMALL from ALS in some patients. Commonly, a follow‐up > 3–4 years was considered a useful criterion to exclude the majority of patients with ALS (Berg‐Vos et al., 2003; Weiss, 2005). Although 28 of 37 patients had more than five‐year follow‐up plus disease duration, it was reasonable to follow‐up BMALL patients as long as possible.…”

Section: Discussionmentioning

confidence: 99%

“…The cause of BMALL and its relation to other anterior horn cell disorders, such as amyotrophic lateral sclerosis (ALS), are poorly understood (Guennoc et al., 2013). The possible pathogenesis seems to be associated with genetic factors (Fetoni et al., 2004), immunological antibodies (Khandelwal et al., 2006; Weiss, 2005), viral infection (McMillan et al., 2009; Vibha, 2015), and focal ischemia (Bella et al., 1992).…”

Section: Introductionmentioning

confidence: 99%

Benign monomelic amyotrophy of lower limb in a cohort of chinese patients

et al. 2021

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Background Benign monomelic amyotrophy of lower limb (BMALL) is a neurogenic syndrome representing an unclear field. Further studies might be helpful to elucidate uncertainties regarding causation, outcome, and the risk of progression to amyotrophic lateral sclerosis (ALS). Methods According to the inclusion and exclusion criteria, 37 patients with BMALL were retrospectively collected in three neuromuscular centers from January 2012 to October 2018. The detailed medical data were summarized. Multiple laboratory tests were examined. Routine electrophysiological examinations, muscle MRI of lower limbs, and muscle biopsy were conducted. Results The cohort included 24 male and 13 female cases with median age of onset 47 years. Muscle MRI revealed that the distribution of involved muscles matched with the extent of fat infiltration, so the pattern muscle atrophy can be divided into the following four types: six patients with thigh atrophy (type I), 14 patients with leg atrophy (type II); 10 patients with disproportionate atrophy in both thigh and leg (type III); and seven patients with well‐proportionate atrophy in both thigh and leg (type IV). Electrophysiological findings showed neurogenic pattern, spontaneous activity, and abnormal H reflex, which suggested a disorder of spinal anterior horn cell in the patients with types I‐III. However, no electrophysiological abnormalities were found in the patients with type IV. Muscle pathology varied from almost normal pattern to advanced neurogenic pattern in nine biopsied patients. Follow‐up showed that two patients with type II developed to ALS four years later, and all patients with type IV were in stable condition without any complaints. Conclusion Muscle MRI was useful to exactly localize the distribution of involved muscles in BMALL patients. The distribution of atrophic muscles can be roughly divided into four types based on the MRI features. The classification of distributing types might be as an indicator for the prognosis of BMALL.

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