Calf Atrophy

I'm 33 years old and have experienced bilateral calf atrophy over the past few years and have essentially lost all muscle mass in both of my medial gastroc muscles.  I have had 2 EMG's with the one performed at mayo suggesting a neuropathy or amyotrophy.  My CPK has been in the high 300's and MRI did not reveal any problems in my back and the MRI in my legs showed diffuse bilateral fatty infiltration and atrophy of the medial and lateral gastocs.   My Nerve Cunduction Studies Came back completely normal.  THE EMG showed increased insertion potential for both the medial and lateral gastrocs with spontaneous fibrillations some CRD's and some MUP's that were long in duration and High in Amplitude.  The Timbialis Anterior and Posterior showed normal insertion Activity with some long duration and High amplitude changes.  The Thoracic Paraspinals showed increased insertion potential but no other changes.  I am confused and questioning what may be causing this.  The found neurogenic changes were non length dependent.  One neuro had felt it may be myoshi myopathy however my ATHENA test for dysferlin came back normal.  Since visiting mayo I have been experiencing a few fasciculations daily.   Primarily single ones that are visible in my lower legs.  Maybe 2 times per month I experience fasiculations elsewhere in my body, upper legs or arm. And 3-5 times per month fasiculations in that are more annoying like repetive twitching.  I have been concerned about ALS and the fasciculation have been worriesome.  Not sure if I just notice them now or if they have been going on for a long time.  How concerned with ALS should I be?  Mayo had noted the changes are related to the L5 S1 innervated nerves.  How slow is  the slowest moving type of ALS.  I know I have had this calf atrophy for at least 3 years but unsure if it progressing?    Please help with any suggestions.

[dr_simran]

Hello Dear,
You probably have Benign calf amyotrophy.
Benign calf amyotrophy is a variant of the benign focal amyotrophy disorders. The etiology for these disorders is unknown

The gastrocnemius weakness and wasting were bilateral.. Initial progression of symptoms is followed by disease stabilization. No history of poliomyelitis or family history of neuromuscular disease. Creatine kinase values are elevated. The electromyographic and muscle histopathologic findings are consistent with a chronic neuropathic disorder. Despite the restricted calf muscle involvement clinically, the electromyographic abnormalities suggested more diffuse lower limb involvement.

The benign focal amyotrophy disorders are a clinically heterogeneous group of disorders causing weakness and atrophy of the upper or lower extremities.These disorders are distinguished from other more common forms of motor neuron disease by the restricted limb involvement, absence of upper motor neuron signs, and slow progression for months to years followed by disease stabilization

The criteria for the diagnosis is insidiously progressive unilateral or bilateral calf muscle atrophy or weakness, no known antecedent injury, (3) no sensory symptoms,  no known medical or neurologic disorders that could cause muscle weakness or atrophy, no magnetic resonance imaging evidence of L5 or S1 nerve root disease.

ALS does not seem to be your diagnosis.You should consult your physican and aim at the treatment of Benign calf amyotrophy.
Refer http://archneur.ama-assn.org/cgi/content/full/60/10/1415

Best