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Neuronal Ceroid Lipofuscinosis In 7 Year Old Child What Can Homeopathy Do?

A case presentation of progressive myoclonic epilepsy, recently diagnosed by a pediatric neurophysician probably as neurological ceroid lipofuscosis in a child aged around seven years old.

To begin, this child developed seizures at the age of 3-4 years  old, then followed the mental detoriation with paralysis and muscle wasting of all limbs and loss of speech.

Presently, the child has repeated respiratory tract infections, and more recently for a few days, a loud wheeze with difficulty in swallowing even liquids.

The pediatrician failed to give any relief to these symptoms. I had prescribed antimonium tart LM based upon present respiratory complaints, which gave him relief. The child is better with respect to his respiratory complaints, but now we have to deal with his myoclonic epilepsy/neurological ceroid lipofuscosis. The details of this case are as follows:

  • During his mother's pregnancy, she had suppressed her emotional annoyance and torture when her husband took money from her parents.
  • The mother's disposition was very mild, timid and she suppressed her emotions making her very weak, pale and emaciated.

  • It was during this period in time that she had conceived. After giving birth, the child was very good with no complaints.  

  • Later on the child would get frequent scrotal inflammation that used to be treated with allopathic medicines and sometimes I treated with belladona.

  • The child began to shriek during sleep.  He used to go to a room during his sleep and sit in the corner of room in a state of fright. He would not allow anybody to come near to him and he had to be waken from his sleep state, after which he would be quiet.

  • Gradually he started falling down and then siezures in his head started. His upper limbs, lower limbs were affected, then loss of speech as the slow paralysis progressed with emaciation of parts.

To summarize, the following points are important

  1. Ailments after suppressed grief (in mother)
  2. Scrotal inflammation recurrent
  3. Night terrors
  4. Seizures started in head and spread to other parts (to begin with he used blink his eyes and jerks in head started.)
  5. Myoclonic siezures followed by loss of speech, difficulty in swallowing and paralysis of extremities.
  6. Emaciation and atrophy
  7. Atrophic changes have been reported in optic nerve.
  8. Child had ravenous appetite and even now child responds to smell of food He cries if he smells odors of food (demands to feed him)
  9. Child earlier was introverted and reserved with aversion for company
  10. Child sensitive to noises and crowds.
  11. He was warm blooded preferring cold water and weather.

Pediatric neurophysician has diagnosed this condition as Neurological ceroid lipofuscinosis.

Medscape | The neuronal ceroid lipofuscinoses (NCLs), also known as Batten disease, are a group of neurodegenerative disorders. They are considered the most common of the neurogenetic storage diseases with a prevalence of 1 in 12,500 in some populations. They are associated with variable yet progressive symptoms including seizures, dementia, visual loss, and/or cerebral atrophy. In 1826, Stengel described the first patients—4 siblings in Norway. Batten made the first clinicopathologic correlation in 1903 and referred to NCL as familial cerebromacular degeneration. Batten was also the first person to differentiate NCL from Tay-Sachs disease in 1914. Vogt, Spielmeyer, Bielschowsky, and Kufs also described older patients with similar symptoms.

In 1939, Klenk discovered increased gangliosides in Tay-Sachs disease but in not juvenile amaurotic idiocy (an early name for NCL). NCL was later so named because of the accumulation of autofluorescent lipopigments resembling ceroid and lipofuscin. In 1959, Koppang described English setters with the same phenotype as patients with NCL. Although NCLs are generally autosomal recessive disorders, in 1971 Boehme also described autosomal dominant inheritance of the same disease in the Parry family of New Jersey. The enzymatic abnormalities were better defined in the 1980s and the molecular genetics have now being described in some variants of NCL. A database of NCL mutations is maintained and can be found here.[1]

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Psora is in background 



1. Generalities, heat, sensation of.

2. Generalities, emaciation.

3. Generalities, night agg.

4. Stomach, appetite, ravenous. 

5. Skin, eruption, suppressed.

6. Generalities, convulsion.

Sensitive to noise and smell of food is also Psoric symptoms and under in effect of SULPHUR.

Gud evening and wish u Peace.

I just wanted a small clarification regarding the use of sulphur, where concurrent water intake after the dose result on to any adverse effects, if so then what may be the probable cause.


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