Posted by: Chris Maloney | September 11, 2011

Is Cerebral Palsy Curable As A Simple Deficiency?

Main pathway in growth regulation by the endoc...

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Cerebral Palsy is a terrible disease that robs infants of their ability to function over time.  Currently we treat it with aggressive physical therapy, but that is only moderately effective.

One of the most interesting things about Cerebral Palsy is that it occurs more often in small preterm infants.  When we look at the motor skills for preterm infants, most exhibit the signs of beginning Cerebral Palsy.  But by three months, almost all have gained normal function.

So is there some deficiency in preterm infants?  In studies of “resource poor” areas (I’m glad we’ve moved on from “third world”), Cerebral Palsy is hard to track.  But it appears to be no more common in those areas than in “resource rich” areas.  Any deficiency would be something common to both areas.

Some studies point to a positive effect of magnesium on the preterm brain.  It makes sense to think of magnesium helping with muscle tension, but it’s too simple to describe the breadth of the effects of Cerebral Palsy.

The obvious first choice would be a growth hormone deficiency.  Preterm infants would begin life without much growth hormone, but most would rapidly begin to secrete the hormone and catch up.  Only in those children without growth hormone on a continuing basis would Cerebral Palsy begin to appear, and likely only in those with severe deficiency.

We can check a hypothesis like growth hormone by checking if Cerebral Palsy patients are lower in growth hormone than control children.  They overwhelmingly are.

The next step is to test whether the introduction of growth hormone would improve the symptoms of Cerebral Palsy in children.  In a small pilot study just published, we find that the results are overwhelmingly positive.  The range of Cerebral Palsy symptoms improved with growth hormone supplementation.

I am certain the answer is more complicated than simply growth hormone replacement.  But for many children it is reasonable to assume we can improve symptoms by replacing the deficiency.

All studies are below for anyone who knows anyone with this illness.

Pak J Biol Sci. 2011 Apr 1;14(7):433-40.

Growth hormone deficiency in children and adolescents with
cerebral palsy: relation to gross motor function and degree of spasticity.

Hamza RT, Ismail MA, Hamed AI.


Department of Pediatrics, Faculty of Medicine, Ain Shams
University, Cairo, Egypt.


Children with Cerebral Palsy (CP) often have poor linear
growth during childhood with short final height. Thus, we aimed to assess serum
growth hormone (GH), insulin like growth factor-1 (IGF-1) and insulin like
growth factor binding protein-3 (IGFBP-3) levels among CP patients and their
relation to each of gross motor function and degree of spasticity. Fifty CP
children and adolescents were studied in comparison to 50 healthy age-, sex-
and pubertal stage-matched children and adolescents. All subjects were
subjected to clinical evaluation, Intelligence Quotient (IQ) assessment and
measurement of serum GH, IGF-1 and IGFBP-3. All auxological and hormonal
parameters were significantly lower among cases. Fifty two% of cases were
GH-deficient and 62% had reduced IGF-land IGFBP-3 levels. Gross Motor Function
Measure- 88 (GMFM-88) score correlated negatively with each of basal (r =
-0.71, p = 0.02) and peak stimulated GH (r =-0.88, p = <0.001); IGF-1 (r =
-0.64, p = 0.04) and IGFBP-3 (r = -0.69, p = 0.031). There were significant
negative correlations between the degree of spasticity assessed by Modified
Ashworth Scale and each of basal (r = -0.61, p = 0.032) and peak stimulated GH
(r = -0.78, p = 0.01); IGF-1 (r = -0.65, p = 0.041) and IGFBP-3 (r = -0.62, p =
0.035). Growth Hormone Deficiency (GHD) is prevalent in children with CP and
could be one of the causes of their short stature.

PMID: 21902055

Dev Med Child Neurol. 2011 Oct;53(10):933-7. doi: 10.1111/j.1469-8749.2011.04045.x.

The motor repertoire of extremely low-birthweight infants at
term in relation to their neurological outcome.

DE Vries N, Bos A.


Department of Paediatrics, Leeuwarden Medical Centre,
Leeuwarden  Division of Neonatology, Beatrix Children’s Hospital, University
Medical Center Groningen, University of Groningen, the Netherlands.


Aim  The aim of this study was to assess the motor
repertoire of extremely low-birthweight infants at term-equivalent age (TEA),
in relation to their neurological outcome. Method  Using Prechtl’s method, we
assessed both the quality of general movements and a detailed motor optimality
score in 13 extremely low-birthweight infants (four males; nine females; mean
gestational age 27.9wks, SD 2.9wks; mean birthweight 798g, SD 129g) at TEA, and
related them to general movements at the age of 3 months after term and
neurological outcome at the age of 2 years 6 months. Results  At TEA, 10 of the
13 infants had abnormal general movements. All infants showed abnormal leg
lifting with extended legs; nine showed stiff movements, three showed cramped
movements, and two showed cramped synchronized general movements. At 3 months, three infants still had abnormal general movements. Concurrent movements were abnormal in nine infants owing to monotony and jerkiness. Abnormal posture was seen in seven infants. None developed cerebral palsy; one infant showed cognitive and motor delay. Neurological outcome was not related to general movement quality and optimality score at TEA. Interpretation  Abnormal general movements at TEA are common in extremely low-birthweight infants. General movements often appear stiff and cramped with extended legs. At the age of 3 months after term, general movements are mostly normal, but concurrent movements are not. Nevertheless, these abnormalities do not imply an impaired neurological outcome such as cerebral palsy.

© The Authors. Developmental Medicine & Child Neurology
© 2011 Mac Keith Press.

PMID: 21896004

Ugeskr Laeger. 2011 Mar 28;173(13):962-5.

[Evidence exists for prophylactic magnesium sulphate as a
neuroprotector in premature births].

[Article in Danish]

Wolf HT, Hegaard HK, Huusom L, Greisen G, Hedegaard M.


Medicinsk Afdeling, Nykøbing Falster Sygehus, 4800 Nykøbing
Falster, Denmark.


Preterm birth increases the child’s risk of cerebral palsy.
Observational studies as well as randomized studies find that magnesium
sulphate given to women in preterm birth decreases such risk. A Cochrane
meta-analysis of the randomized studies shows no change in mortality, whereas
some observational studies find a mortality decrease. It is important to
identify the neuroprotective mechanism and to decide whether these results are
relevant in the current Danish obstetrical practice. Should we use magnesium
sulphate now or should questions about doses, time of administration and
maternal side effects be answered first?

PMID: 21453636

Ann Trop Paediatr. 2010;30(3):181-96.

A review of the incidence and prevalence, types and
aetiology of childhood cerebral palsy in resource-poor settings.

Gladstone M.


Department of Community Child Health, Alder Hey Children’s
NHS Foundation Trust, Liverpool, UK.



With 80% of children with disabilities living in
resource-poor settings, it is likely that there is a high prevalence of
cerebral palsy (CP) and neurological impairment in these settings. The
prevalence and incidence rates of disability, in particular of children with CP
in resource-poor settings, are difficult to access and clarify.


To review the recent literature relating to the prevalence,
incidence, type and aetiology of cerebral palsy in low-income settings.


A systematic search of studies published between 1990 and
2009 was performed using PubMed, Cinahl on Ovid, the Cochrane database, SCOPUS
and information from international disability organisations. All studies with
information about neurodisability, CP or disability in resource-poor settings
were included. Titles and/or abstracts of all studies were reviewed and full
texts of relevant studies were obtained.


Disparities in methodology, age range, classification
systems and populations made studies difficult to compare. Population-based
studies provided rates of childhood disability of 31-160/1000. When using
limited age ranges of 2-9 years with the Ten Question Questionnaire, rates were
82-160/1000 for children disability and 19-61/1000 for neurological impairment.
Rates of CP in population-based settings in China and India gave figures of
2-2.8/1000 births, similar to western settings. Hospital-based studies of CP
showed increased rates of spastic quadriplegia rather than diplegia or
hemiplegia and possibly increased rates of meningitis, jaundice and asphyxia
and lower rates of low birthweight and prematurity in CP populations. These
studies were small and not case-controlled or population-based.


Rates of CP and neurological impairment are difficult to
obtain in resource-poor settings. Methods of identifying children with CP and
causal factors and the effects of disability need to be better classified in
order to improve management and help shape preventive measures.

PMID: 20828451

Ther Clin Risk Manag. 2011;7:199-206. Epub 2011 May 30.

Effects of recombinant growth hormone (GH) replacement and
psychomotor and cognitive stimulation in the neurodevelopment of GH-deficient
(GHD) children with cerebral palsy: a pilot study.

Devesa J, Alonso B, Casteleiro N, Couto P, Castañón B, Zas
E, Reimunde P.


Medical Center “Proyecto Foltra”, Cacheiras (Teo),
A Coruña, Spain;


Cerebral palsy (CP) is the main cause of physical disability
in childhood and is an important health issue that has a strong socioeconomic
impact. There is no effective treatment for CP and therapeutic approaches
report only partial benefits for affected people. In this study we assessed the
effects of growth hormone (GH) treatment combined with psychomotor and
cognitive stimulation in the neurodevelopment of children with CP and GH
deficiency (GHD). The study was carried out in 11 patients (7 boys and 4 girls;
4.12 ± 1.31 years) with GHD and CP who were treated with recombinant GH (rGH)
and psychomotor and cognitive stimulation during 2 months. Battelle Developmental
Inventory Screening Test (BDIST) was performed 2 months before commencing GH
treatment, just before commencing GH administration, and after 2 months of
combined treatment involving GH and cognitive stimulation. Psychomotor and
cognitive status did not change during the period in which only cognitive
stimulation was performed; however, significant improvements in personal and social skills, adaptive behavior, gross motor skills and total psychomotor abilities, receptive and total communication, cognitive skills and in the total score of the test (P < 0.01), and in fine motor skills and expressive communication (P < 0.02) were observed after the combined treatment period.
Therefore, GH replacement together with psychomotor and cognitive stimulation
seem to be useful for the appropriate neurodevelopment of children with GHD and

PMID: 21691590



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