Has anyone benefited from TMS therapy

[jlbiggs]

I have had FND for four years now. As we all know basically Our recovery is up to us. I tried so many modalitiesAnd been making progress very slowly. I've spent a lot of by money and it's almost gone now so the level I have left I don't want to waste. Jim messed therapy is six weeks along five times every week. My copayment alone is going to be $1300. I just wanted to know if anyone else's tried it into what success before I spend the money. Any input would be greatly appreciated...

[Junebeatle]

I did TMS, it helped me with the depression, memory loss, & fatigue. As far as muscle movements & attacks it didn’t. Everyone is different though, Saffron seems to help my muscle mis-firing all over body + Valium for sleep. Good luck 🍀. You may be different, I’m 100% glad with TMS results. I’m actually going to try again to get off Valium entirely.

[jlbiggs in reply to Junebeatle]

Thank you for your reply

I'm not really that depressed but my movements are worsened with anxiety and I was hoping it would alleviate some of that. I know it's fairly effective for depression I just was wondering how muchIt help with anxiety. If you don't mind me askingHow many times a week to do it and for how long Each session and for how many weeks?

[Junebeatle in reply to jlbiggs]

I had severe anxiety this past year when my FND returned in April 2018 (had been in remission for years).Unfortunately I for the first time ever had to take a Benzodiazepines because my movements were waking me up. I know TMS works for a lot of folks anxiety, I was able to cut back Valium from 15mg to 7.5mg at least with TMS. I did 46 sessions 5 days per week each one varying between 45min-60min.

I had never had depression until this past year when FND took away my exercise and my whole body. I think it’s definitely worth a try. I was an impossible case and this saved my life!

[jlbiggs in reply to Junebeatle]

I want to try but my co-pay is going to be $35 a session so five times I costA significant amount of money but if it works well worth it. Thank you again for your reply

[Junebeatle in reply to jlbiggs]

In my opinion it was well worth it! Anything to help with this dreadful illness. Did you see the latest FND research I had posted showing we have excessive levels of glutamate in the limbic regions of our brains...glutamate is highly excitatory leading to anxiety & also unfortunately neuronal loss (it’s implicated in Alzheimer’s progression for instance) You may want to print it & take with you to TMS consult.

[Junebeatle in reply to Junebeatle]

Hysterical' Motor Symptoms Explained?

Batya Swift Yasgur, MA, LSW

June 17, 2019

1

Abnormally high levels of limbic glutamate may be at the root of unexplained functional motor symptoms (FMS) that previously have been attributed to "hysteria."

Researches used magnetic resonance spectroscopy (MRS) to evaluate N-acetylaspartate (NAA) levels; myo-inositol (MI) levels; choline (Cho) levels; the sum of glutamate and glutamine (Glx); and creatine (Cr) content in two brain regions of patients with FMS and compared those results to results obtained from healthy control persons.

They found increased levels of Glx/Cr content in the anterior cingulate cortex/medial prefrontal cortex (ACC/mPFC) in patients with FMS but normal levels in the occipital cortex (OCC) compared to control persons.

These increased levels correlated with FMS-related alexithymia and anxiety as well as symptom severity.

"We assessed by MRS patients by glutamate and glutamine in a group of patients with FMS and in a group of healthy age- and sex-matched controls, testing the limbic areas of the cerebral cortex and, as a control region, the visual cortex and also clinically through a number of clinical scales," senior author Alberto Priori, MD, PhD, of the Aldo Revelli Research Center at the University of Milan, Italy, told Medscape Medical News.

"We found that glutamate is abnormally increased in the limbic but not in the visual cortex of patients and that the increase correlated with the severity of motor and psychological disturbances," he added.

The study was published online June 5 in Neurology.

Frequent, Still Mysterious

"Functional neurological disorders are very difficult to be treated and very expensive for the national health systems worldwide," said Priori, whose research group "deals with the biology of this frequent but still mysterious condition."

Functional neurologic symptoms are "what historically was called 'hysteria,' a condition known for a long time in the medical literature and thought to be linked to unresolved conflicts and purely psychological problems," he continued.

He noted that Sigmund Freud developed psychoanalysis "mostly to resolve functional problems."

For several years, Priori's group has focused on clarifying the biological mechanisms underlying these disturbances. They "decided as a first step to study the brain neurochemistry of our patients with a noninvasive technique," he said.

They chose to study the limbic system because it is thought to be involved in FMS. They used MRS to quantify several brain metabolites: NAA, which is a neural and axonal integrity marker; MI, an inflammatory marker; and Cho, which is involved in cell membrane synthesis and degradation.

They also studied glutamate — the major excitatory neurotransmitter — and Glx and Cr in the ACC/mPFC and in the OCC.

The researchers also examined correlations between limbic metabolite content and FMS-related clinical features: motor symptom severity, alexithymia, anxiety, depression, and quality of life in 10 patients with FMS and 10 age- and sex-matched control persons (mean [SD] age, 47.10 years [17.00 years] and 44.3 years [12.85 years], respectively).

Participants were required to complete the Mini–Mental State Examination, the Hamilton Depression Rating Scale (HAM-D), the Hamilton Anxiety Rating Scale (HAM-A), the 20-Item Toronto Alexithymia Scale (TAS-20), and the EuroQol 5D (EQ-5D).

Patients with nonremittent symptoms (gait disorder [30%], tremor [20%], dystonia [20%], myoclonus [10%], and functional mixed disorder [20%]) were included in the trial.

Participants had to be free of any other neurologic disorders, including dementia, and medical diseases and to have no overlap between functional disorders and other movement disorders.

Prime Mover

Control participants had normal rating scores for psychopathology. Two case patients had major depressive disorders, and one had panic disorder.

Three case patients were taking selective serotonin reuptake inhibitors, and four were taking benzodiazepines, which they stopped taking 5 days before undergoing MRS.

The case patients were found to have high scores in depression and anxiety, as assessed by the HAM-D and HAM-A; high scores on the TAS- 20; and low quality of life, as measured by the EQ-5D.

Glx/Cr was found on MRS to be higher in case patients with FMS than in healthy control persons in the ACC/mPFC but not in the OCC, as determined on the basis of a two-way ANOVA calculation that showed a significant interaction between the factors "brain site" and "group" (P = .001).

Moreover, post hoc analysis showed an increase in Glx/Cr in the ACC/mPFC in case patients vs healthy control persons (mean ± SD: 1.52 ± 0.56, vs 0.677 ± 0.050, respectively; P = .0005).

These findings remained, even when HAM-D, HAM-A, and TAS-20 scores were entered as a covariate in the same model.

There were no differences between case patients and control persons with regard to NAA/Cr, Cho/Cr, or MI/Cr either in the ACC/mPFC or in the OCC.

When the researchers conducted a correlation analysis between Glx/Cr and psychological scales, they found that in the overall population, the Glx/Cr in the ACC/mPFC correlated with anxiety (HAM-A, ρ = 0.732; P = .003) and alexithymia (TAS-20, ρ = 0.432; P = .02).

In case patients, Glx/Cr content in the ACC/mPFC was also correlated with the severity of functional motor symptoms.

"Glutamate is the major excitatory neurotransmitter in the brain. There are two hypotheses that could explain our findings. Firstly, the increased glutamate could be the prime mover creating an abnormal excitatory output from the limbic to the motor areas of the cerebral cortex.

"Alternatively, increase glutamate could be secondary to downregluation of its receptors or to impaired activity of its degrading enzymes," Priori said.

He noted that his group is currently conducting further research that "will better clarify this issue."

Intriguing Implications

Commenting on the study for Medscape Medical News, Carine Maurer, MD, PhD, assistant professor of neurology and associated director, Medical Scientist Training Program, Stony Brook University School of Medicine, New York, who was not involved with the study, noted that the sample size is "quite small and findings will need to be replicated in larger studies."

Nevertheless, the study "provides intriguing evidence for abnormally increased paralimbic glutamate/glutamine in patients with FMD, as measured by MRS," she said.

The study augments previous research that suggests there are neurobiological differences in patients with FMD, including the presence of group-level differences in functional and structural imaging findings.

Although the authors report that metabolic changes correlated with severity of motor symptoms, "this finding needs to be interpreted cautiously, given limitations in scales used to assess FMD symptom severity," she said.

Nevertheless, "for the practicing clinician, from a practical point of view, this helps with conceptualization of the disorder and patient education," she said.

Moreover, she said, the findings have "intriguing implications for future research and suggests that drugs targeting the NMDA [N-methyl-D-aspartate] receptor may be promising as future pharmacological targets."

"Unexplained functional neurological symptoms, historically known as hysteria, are recognized a neurochemical abnormality that could be targeted by the specific treatments for this condition," Priori said.

Such treatments include psychotherapy, rehabilitation, and drugs, he said.

He noted that several classes of drugs currently available for other indications can influence the glutamatergic system "and could therefore be useful for these patients."

The study was partly supported by the Aldo Ravelli Research Center on Neurotechnology and Experimental Brain Therapeutics at the Department of Health Sciences, University of Milan, Italy. Priori and Maurer have disclosed no relevant financial relationships. The other authors' disclosures are listed in the original article.

Neurology. Published online June 5, 2019. Abstract

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Medscape Medical News © 2019

Cite this: 'Hysterical' Motor Symptoms Explained? - Medscape - Jun 17, 2019.

[jlbiggs in reply to Junebeatle]

Yes I had read it and found it very interesting but did not see any kind of remedy or course of action. How do you treat

[Junebeatle in reply to jlbiggs]

I’m not a psychiatrist, but it sounds like something to regulate the excessive glutamate levels in the brain. I know the ALS drug Rilutek can do this & they are having some success in treatment resistant cases of OCD (some of them have excessive glutamates, not Serotonin) Also some NMDA receptor drugs target glutamates, those may be useful. Saffron I think helps NMDA receptors & it’s helped my FND during the daytime. I would print & take with you to TMS doctor, see what his input is. Can TMS directly influence this neuro chemical glitch?