Neuropathy Treatment with G Therapy (Neuropathie traitement, Neuropathie Behandlung, Neuropatia trattamento, Neuropatia tratamento, Neuropatía tratamiento, الاعتلال العصبي العلاج, Neuropathia kezelés, Neuropati behandling, 神経障害 治療, 신경 장해 치료) USA, India
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Tel: 0091-98220-38464
Present Research In Chronic Neuropathy:
This is evidence based presentation of thirteen cases of peripheral neuropathies of different etio-pathologies of chronic duration, treated with my new formulation. All the cases were treated with the same combination, which contains G Therapy and additional potentised medicines. Hence forth called as G Therapy.
Original Nerve Conduction Velocity study reports are scanned & presented along with the case studies. They are in chronological order, i.e. Before Treatment, During Treatment, & After Treatment. As far as possible, for the same patient these studies were done at the same Laboratory with the same Neurologist. This gives us correct comparison of reports.
At various levels and periods the Neurologist were consulted for discussions about their findings in these cases. I am very happy to present their scientific opinions of this study report.
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Background:
Peripheral neuropathy is a major cause of morbidity the world over. Neuropathy can be caused by various causes viz. infections, nutritional deficiency, metabolic disorders, idiopathic, toxins, inherited disorders, ischemia & physical trauma. It can be a mononeuritis, polyneuritis with involvement of the autonomic nerves and associated with myelopathy, psychosis or affection of cranial nerves.
Damage to the nerve cell body or axon leads to axonal degeneration while lesions of the Schwann cell or disorder in the myelin synthesis leads to segmental demyelination. Clinical recovery is better in patients with demyelination alone, than with the combination of both axonal degeneration and demyelination or axonal degeneration alone. Earlier the neuropathy is diagnosed, there is likely to be less damage to the nerves & better is the prognosis. Management of neuropathy lies in treating the underlying cause, if known. Otherwise, it is treated empirically with vitamin supplements particularly thiamine, but also B6 & B12. Rehabilitative measures like physiotherapy, splints and protective shoes are advised. Diabetic Neuropathy may be slowed down by close control of the diabetes.
Immunomodulating or immuno – suppressive medicines have a role in autoimmune & inflammatory diseases.
Disussion:
Significant improvements in motor function were seen in the above thirteen cases after 5 to 8 weeks of Neuro G–Therapy whereas their clinical status was quite the same for more than two years, before starting this therapy.
Vitamin B12 deficiency is linked to peripheral neuropathy in 40% of cases. Folate deficiency is associated with depression in 50% of cases. Organic mental change, dementia and cognitive impairment occurs in approx. 25% of patients with either deficiency. Vitamin B12 deficiency is a prime factor in subacute combined degeneration of the spinal cord. It has been suggested that methylation processes are the biochemical basis of the neuropsychiatric manifestations of folate and vitamin B12 deficiencies. Methylation in the brain may play a role in certain types of dementia. In our experience with Neuro G-Therapy cognitive improvements were seen in patients of multi-infarct dementia.
In this study of starting Neuro G Therapy most cases have shown clinical improvements first and thereafter perceptible improvements were seen in NCV studies. What it signifies I really don't understand. Possibly the Neuro G Therapy is acting directly at the neurocellular level first, followed by axonal regeneration. Further electrophysiological study will throw more light on this breakthrough research and observation.
The Improvements:
Improvements in all the above cases could possibly be due to
- Axonal regeneration.
- Branching of normal axons.
- Increase in number of functioning axons reflecting increase in amplitude in NCV.
- Increase in nerve conduction velocity implying improved myelination of the conduction pathway.
- Neuro G–Therapy may be playing a role like Vit.B12 viz. methylation in the brain.
Summary:
Definite clinical & objective improvements were seen in all the thirteen cases of different etio – pathological, chronic cases of peripheral neuropathies. The neurophysiological studies in all cases after Neuro G-Therapy show that possibly it is acting as a nerve growth factor or stimulating the release of such factors. I feel, although this is a small pilot data, it is objective & so is most encouraging. Further research with ultra modern electro-physiological studies in more patients is necessary to define the utility of this safe therapy and to determine its maximum effectiveness.
Table 1:
| Case |
Diagnosis |
Duration of disability before starting Neuro G therapy |
Electrophysiological Studies before Neuro G Therapy |
Electrophysiological Studies after Neuro G Therapy |
Case 1: S. Agarwal 35 Years
Male |
Right sciatic nerve palsy due to fracture of right hip with central dislocation
L4 L5 complete palsy
S1 S2 partial palsy |
1 year, April 95 to April 96 |
Apr 96
The study reveals evidence of Right sciatic nerve palsy, above the branch to the right biceps, the common peroneal division is more affected and shows minimal regeneration while the posterior tibial division shows a fairly good regeneration pattern.
|
July 96
Study reveals improved velocities of all nerves; amplitudes of posterior tibial and sural too, show increase. Good regeneration pattern seen in gastrocnemius and biceps as compared to previous study.
|
Case 2: F. Zafir
29 Years
Male |
Accidental spinal chord injury
C4 C5 level Tetraplegia |
6 Years
March 88 to Jan 94 |
Dec 93
There is evidence of mild Right ulnar neuropathy (motor and sensory) EMG was done using concentric needle electrodes in the Rt. 1st D 10, Rt. ADM Rt. Triceps.
All muscles were silent at rest with hardly any units in the Rt. 1st 10 & ADM. There were a few units in the Rt. Triceps. On max. voluntary effort the interference pattern was reduced in all the muscles sampled.
Conclusion: EMG shows total absence of motor units from the muscles sampled. This could be due to an ant. Horn cell lesion or a severe UMN lesion.
|
May 94
Rt. D 10: Few units Rt. ADM: Few units
There is evidence of Rt. Ulnar neuropathy (motor + sensory) EMG was done using concentric needle electrodes in the Rt. D 10 Rt. ADM & Rt. Triceps. Compared in previous study there are units present in the above muscles, suggestive of some recovery in these muscles, especially the Triceps.
Apr 95
There is evidence of right ulnar neuropathy. EMG was done using concentric needle electrodes in the Rt. 1st D to ADM & Rt. Triceps. there isno spontaneous activity at rest. Few units could be recorded from all the muscles sampled with reduced interference pattern suggestive of a neurogenic lesion.
Aug 96
There is evidence of right ulnar neuropathy (sensory) Amplitude of Rt. ulnar SAP has improved. There is evidence of severe motor nerve degeneration in muscles supplied by C6-8 T1 roots bilaterally, which is most severe in C8-T1 root muscles. Site of lesion? Root? Anterior horn cell.
|
Case 3:
Mr. Kulkarni |
Known diabetic with Guillaine Barre Syndrome, invalidated (bedridden) |
2 Years
June 94 to May 96 |
June 94
There is evidence of severe sensory-motor neuropathy. The neuropathy appears mixed demyelinating & axonal degenerating type.
|
Aug 96
They study reveals evidence of a severe generalised axonal & demyelinating sensory motor neuropathy. As compared to previous study, responses of Rt. & Lt. Lateral popliteal, in posterior tibial & Rt. ulnar show worsening. Rt. median amplitudes have increased. Sensory velocities are lower.
|
Case 4: Mr. Ponkshe
37 years
Male |
Motor Nerve degeneration at ant. horn cell level |
5 & 1/2 years
Oct 92 to May 98
|
Feb 94
There isno sensory neuropathy. Study reveals evidence of motor nerve degeneration in muscles supplied by L4-L5-S1 roots at Root or Anterior horn cell level. Delayed 'H' of reflexes also suggest a proximal lesion.
Apr 98
Study reveals evidence of motor nerve degeneration in muscles supplied by L4-5-S1 roots with the Lt. L5 S1 root being maximally affected at root anterior horn cell level. No significant change as compared to previous record.
|
June 98
As compared to previous study. EMG in right lower limb is now normal. The left lower limb also shows improvement in the number of motor units. (Interference pattern)
Sept 98
Normal electrophysiologic study for lower limbs.
Jan 99
Normal electrophysiologic study for lower limbs.
|
|
Case 5: Omkar Shetye
8 years
Male
|
Hereditary sensory motor neuropathy |
8 Years
Since birth |
Nov 98
Gen. Sensory motor neuropathy axonal and demyelinating
|
Jan 99
NCV - The right common peroneal show improivemnt in amplitude but some slowing of conduction. The median sensory show improved latency and low amplitude as compared with Nov 98 study.
|
Table 2:
| Case |
Clinical status before Neuro G therapy |
Clinical Improvements after Neuro G therapy |
Time required for clinical improvements |
Time after which Electrophysiological improvements were seen |
Case 1: S. Agarwal 35 Years
Male |
Apr 95
Accident - Rt. Hip fracture with central dislocation. Right sciatic nerve palsy with foot drop.
Aug 95
Patient walking with walker & foot drop splint in non-weight bearing.
Jan 96
Range of motion of right hip is almost normal. Muscle power - normal & walking with elbow crutches SD curve of Anterior group muscles of leg shows denervated muscle.
|
Improvement in Rt. foot drop. Only mild TA tightness yields to stretch. |
3 months Apr 96 to Jul 96
|
3 months
|
Case 2: F. Zafir
29 Years
Male |
Accident Mar 98
Tetraplegia, C4-C5 level confined to wheelchair
Recurrent urinary tract infections
Constipation
Severe spasticity
Almost immobile
|
Complete voiding of the bladder & no further UTI
Regular bowel movements.
Voluntary locking of knees.
Reduction in spasticity
Ability to do sit ups with support.
|
4 months
|
5 months
|
Case 3: Mr. Kulkarni
58 years
Male |
Diabetic with GBS variant in Jun 94
Bedridden for more than one year.
Unable to get up from ling down position.
|
Improvements noted after 2 months & after one year of Neuro G therapy. He could rise to sitting postion from the supine position, stand & walk with support.
|
2 months to 1 year
|
6 months
|
Case 4: Mr. Ponkshe
37 years
Male |
Weakness in lower limb
Imbalance while walking climbing, driving.
Tingling & numbness in fingers & toes.
Cannot sit in one posture for long.
|
No weakness or strain in lower limb muscles.
Can walk, climb, jog, swim, drive confidently.
Mild, occasional tingling an numbness.
No imbalance & can sit in one posture for long.
|
1 month |
1 month |
|
Case 5: Omkar Shetye
8 years
Male
|
Crawling
Can stand without support only for a few seconds.
Walks with support only with foot drop and valgus deformity of foot.
Many scratches on hands and legs.
|
Motor conditions same.
No new injuries on arms & legs
|
2 months
|
3 months
|
New 1: Evidence Based Study Report on Neuronal Regeneration with G Therapy
New 2: Evidence Based Study Report on Neuronal Regeneration with G Therapy
New 3: Evidence Based Study Report on Neuronal Regeneration with G Therapy
New 4: Evidence Based Study Report on Neuronal Regeneration with G Therapy
Neuropathy: Epilepsy with Sensory Motor Neuropathy Treatment
Neuropathy: Progressive Cerebellar Ataxia with Motor Neuropathy Treatment with G Therapy
Neuropathy: Monoplegia of right arm (Erb's Palsy) Treatment with G Therapy
Neuropathy: Acute Axonal Sensory Motor Neuropathy Treatment with G Therapy
Neuropathy: Hereditary Spastic Cerebellar Ataxia Treatment and Neuropathy Treatment with G Therapy
Neuropathy: Motor Neuropathy Treatment with Seizure Disorder and Scholastic Backwardness Treatment with G Therapy
Neuropathy: Post Traumatic Cerebellar Ataxia with Sensory Neuropathy Treatment with G Therapy
Neuropathy: Hereditary Sensory Motor Neuropathy Treatment - Axonal and Demyelinating Neuropathy Treatment with G Therapy
Neuropathy: Motor Nerve Degeneration at Anterior Horn Cell Level Neuropathy Treatment with G Therapy
Neuropathy: Anterior Horn Cell Lesion Disease Treatment or U.M.N. Lesion Treatment with G Therapy
Neuropathy: Guillain Barre Syndrome Treatment with G Therapy
