Page 1 of 1

Getting to the root of my BFS

PostPosted: September 16th, 2015, 7:40 am
by misterjuanperalta
Process of elimination:

Hypoglycaemia & Focal Seizures:

Hypoglycaemia, common in diabetic patients treated with insulin, can induce various neurological disturbances. Of these, seizures are the most common acute symptom, mainly of the generalized tonic-clonic type (myoclonus), with focal events only exceptionally being reported and documented. Hypoglycaemia can modify cortical excitability by determining an imbalance between excitation and inhibition; some brain structures, such as the temporal lobe and hippocampus, appear to be particularly susceptible to this insult. We describe a case of a 61-year-old diabetic patient in whom insulin-induced transient hypoglycaemia triggered a focal seizure of temporal origin that was well documented by EEG during 24-hour ambulatory monitoring. This is, to our knowledge, one of the few and well-documented cases of this type of seizure.


Tongue biting, particularly if it is lateral, is highly specific to generalized tonic-clonic seizures.


Hyperinsulinemia & Muscles:

The test subjects were made to have hyperinsulinemia and moderate hypoglycemia, the latter probably counteracted by overeating and increased glucagon secretion, as indicated by increased body weight and lower liver glycogen contents, respectively. Systemic insulin sensitivity was increased and measured with a hyperinsulinemic-euglycemic clamp technique. This was paralleled by an elevated glucose utilization estimated as uptake of 2-deoxyglucose in parametrial, retroperitoneal, and inguinal adipose tissues and the soleus and extensor digitorum longus muscles. Glycogen synthesis was also elevated in the soleus muscle. Muscle fiber composition changed with hyperinsulinemia and elevated 2-deoxyglucose uptake toward more fast-twitch, type II, particularly type IIb fibers, whereas the proportion of slow-twitch, type I fibers, diminished. Capillary density was elevated per unit muscle surface area as well as per muscle fiber. This was paralleled by increased insulin sensitivity systemically and in muscles. These results suggest that muscle fiber composition alterations may be a consequence rather than a cause of hyperinsulinemia and that capillarization rather than fiber composition is of importance for insulin sensitivity in muscle.


It has been shown (here) that muscle-specific over-expression of LPL causes muscle-specific insulin resistance by causing defects in muscle insulin signaling and action. Similarly, liver-specific over-expression of LPL causes liver-specific insulin resistance by causing defects in liver insulin signaling and action. These defects in insulin signaling and action are associated with increased intracellular fatty acid-derived metabolites in muscle and liver. Our findings clearly demonstrate that increased fatty acid delivery to muscle and liver impair insulin's ability to metabolize glucose in these tissues, and that these defects are likely to be secondary to blunted insulin signaling caused by increased intracellular fatty acid-derived metabolites. Furthermore, the tissue-specific nature of these defects demonstrates that locally derived fatty acid metabolites are capable of inducing profound insulin resistance in liver and muscle, independent of any circulating adipocyte-derived hormone, and thus suggests a very different target for reversing this condition.


Small Fiber Neuropathy & Benign Fasciculation Syndrome (BFS):

In 4 of the 14 patients (36%), the ENFD was significantly decreased in the calf, and normal at the thigh, and in 10 the ENFD was normal at both biopsy sites. Six of 11 patients tested (54%), had significantly decreased SGNFD; 2 at both the calf and thigh, 2 at the calf only, 1 at the thigh only, and 1 at the foot. It’s concluded that many patients with Benign Fasciculation Syndrome exhibit a significant decrease in SGNFD or ENFD, with the SGNFD preferentially affected. Small fiber neuropathy should be investigated as a potential cause or contributing factor to Benign Fasciculation Syndrome.

Source: ... ts/P01.139

We performed skin biopsies on consecutive patients with cramps but without neuropathic complaints. Twelve patients were biopsied, 8 with normal small-fiber sensation. Seven patients had decreased intra-epidermal nerve fiber density (IENFD), 2 with non-length-dependent loss. A cause for neuropathy was found in 1 patient with cramp-fasciculation syndrome. Creatine kinase was elevated in 8 patients, 4 with decreased IENFD. Muscle biopsy performed in 8 patients, but was diagnostic in only 1, with McArdle disease. Our data show that 60% of patients with muscle cramps (or fasciculations) who lack neuropathic complaints have SFN, as documented by decreased IENFD. Cramps (or fasciculations) may originate as local mediators of inflammation released by damaged small nerve that excite intramuscular nerves.

Source: ... neuropathy

Sleep Apnoea & Benign Fasciculation Syndrome (BFS):

A recent study proposed a new approach to treat the Cramps Syndrome and Benign Fasciculations through the identification and correction of sleep apnoea, which in most cases can be one of the triggers.


Endocrine Dysfunction:

In this study, out of the 37 patients who were diagnosed with endocrine myopathies, thyroid dysfunction was the most common cause (17 cases), followed by vitamin D deficiency in (9) nine, adrenal dysfunction in (6) six, parathyroid dysfunction in (3) three, and pituitary dysfunction in (2) two. Some patients had atypical presentation (E.G, tongue fasciculations in (1) one). Following the treatment regimen which was specific for a given myopathy, 26 patients recovered fully. In conclusion, we found varied clinical presentations of endocrine myopathies. All the patients with neuromuscular complaints should be investigated for endocrine causes because a significant number of them recovers fully with specific treatment.

Source: ... ast=Sharma

Celiac Disease, Gluten Sensitivity, Gluten Neuropathy, Gluten Ataxia & Associated Amyotrophy

This new study describes a case study involving 7 patients (5 male, 2 female) who were identified from a cohort of 540 patients with neurological manifestations of "Gluten related disorders (GRD)." These patients showed signs of "myoclonic tremor," which is an involuntary muscle twitching, which initially occurred in their face, tongue, one arm or one leg, "but then spread to affect other parts of the body."

Source: ... uman-brain

There’s more to the effect of wheat on the human brain. Other phenomena include:

– Migraine
– Carpal tunnel syndrome
– Seizures–especially temporal-lobe seizures
– Myelitis–inflammation of the lining of the spinal cord
– Psychiatric disease–depression, changes in personality, even psychosis or paranoid delusions and auditory hallucinations
– Gait disorders–i.e., difficulty walking
– Impaired reflexes or hyperreflexia (e.g, in the ankles or knees)
- Dysphagia (Celiac Disease)
- Hyperreflexia (Celiac Disease)

Source: ... m-feeling/
Source: ... e&q&f=true

In this case, a 28-year-old man had muscle fasciculations of 2 years. The fasciculations began in his eye and progressed to the lips and lower extremities. In addition, he had gastrointestinal distress and fatigue. The patient was previously diagnosed as having wheat allergy at the age of 24 but was not compliant with a gluten-free diet at that time. Food sensitivity testing revealed immunoglobulin G-based sensitivity to multiple foods, including many different grains and dairy products. The working diagnosis was gluten neuropathy. This report describes improvement in chronic, widespread muscle fasciculations and various other systemic symptoms with dietary changes. There is strong suspicion that this case represents one of gluten neuropathy, although testing for celiac disease specifically was not performed.


A 40-year-old Caucasian woman, with past medical history significant for depression, presented with a chief complaint of diffuse bone pain and proximal muscular weakness, mainly in the lower extremities and to a less extent in both shoulders for six months. The pain and weakness progressed to the point that she had difficulties in rising from a chair, holding her arms up and walking, and inability to ascend stairs. Clinical examination showed evidence of bilateral, proximal muscle atrophy and weakness in the upper and lower extremities, and hypoactive reflexes in four extremities. Her hip range of motion was limited and painful. She had a waddling gait pattern.... Investigations for malabsorption were carried out and IgA antiendomysial antibody and antigliadin IgA and IgG antibodies were found to be elevated. Esophagogastroduodenoscopy (EGD) with distal duodenal biopsy confirmed a diagnosis of celiac disease. With adherence to a gluten-free diet and calcium-vitamin D supplementation, the patient's condition improved remarkably within three months and she was able to walk pain free. Laboratory workup should include Phosphorus and Alkaline phosphatase, which were abnormal in this patient.


Celiac Disease, characterized by small bowel dysfunction and gluten intolerance, can be associated with neurological complications that include ophthalmoplegia, cerebellar ataxia, hyperreflexia, tremor and cognitive impairment. In cases where gluten ataxia is suspected, testing for anti-Purkinje cell antibodies should be considered.

Source: ... e&q&f=true

Twitching (Radiculopathy) & Dysarthria (CAD):

Excerpt: "An 87-year-old gentleman was admitted after sudden dysarthria and left facial palsy due to a right internal carotid artery occlusion. On examination, incidental spontaneous movements (including fasciculations) were seen at rest. Because there are other causes of radiculopathy besides nerve root compression, MRI is not always appropriate in the absence of pain or foot drop. Moreover, lumbar disk protrusions can be found in asymptomatic patients independent of age. Finally, an isolated chronic left L5 radiculopathy was diagnosed related to lumbar spondyloarthrosis (or osteoarthritis at the zygoapophyseal joint)."


Re: Getting to the root of my BFS

PostPosted: September 16th, 2015, 4:47 pm
by Xina535
THANK YOU For sharing this! I am HOPING to be seen at a neurological clinical on Oct 1st and will be working on my case history, symptoms and suggestions. This will help! And please post your updates/test results.

Re: Getting to the root of my BFS

PostPosted: September 17th, 2015, 5:23 am
by leroyb
Did either of you ever get your ceruloplasmin checked and what was it?

Re: Getting to the root of my BFS

PostPosted: September 17th, 2015, 11:31 am
by Xina535
I have no idea what that is or if I had it checked. Is it through blood?

Re: Getting to the root of my BFS

PostPosted: September 17th, 2015, 11:57 am
by misterjuanperalta
Yes, through blood. Tests not done on me yet.

Re: Getting to the root of my BFS

PostPosted: September 17th, 2015, 2:13 pm
by Xina535
oh - I googled and found this:


Lower-than-normal ceruloplasmin levels may indicate the following:
Wilson disease (a rare (UK incidence 1/100,000) copper storage disease)[10]
Menkes disease (Menkes kinky hair syndrome) (rare - UK incidence 1/100,000)
Overdose of Vitamin C
Copper deficiency


Greater-than-normal ceruloplasmin levels may indicate or be noticed in:
copper toxicity / zinc deficiency
oral contraceptive pill use[12]
acute and chronic inflammation (it is an acute-phase reactant)
rheumatoid arthritis
Alzheimer's disease[14]
Obsessive-compulsive disorder[16]

So I guess neither too low or too high is good, but the too high is what we REALLY don't want, right?