Cerebral Palsy

By Philip McAllister, DC, BKin, ACRB, CSCS, RTP
Canadian Chiropractor Magazine: May 2003 Vol 8 (3); pp18-23

Dr. Philip McAllister is the clinical director of Back To Basics Chiropractic & Rehabilitation Centre in Guelph, Ont., which is a multi-disciplinary centre. Dr. McAllister specializes in treating patients with physical impairments as well as high-calibre athletes since graduating from the Southern California University of Health Sciences in 1995.

The Trigenics® technique is applied to an 11-year-old girl with cerebral palsy to improve her strength and range of motion.

Cerebral palsy is caused by damage to the brain that controls and coordinates muscular action. (3) Most often the damage occurs during pregnancy or labour, or shortly after birth. The brain injury is permanent, but it does not progress. (9) While it is not “curable” in the accepted definition of the term, training and therapy can help significantly improve the quality of life for a patient with cerebral palsy. (7)  Dr. William John Little described cerebral palsy in the nineteenth century, and thus it has also been known as Little’s disease. It’s also been referred to as static encephalopathy. (4)

The effects of cerebral palsy constitute an inability to control motor function, particularly muscle coordination. (1) Depending on which areas of the brain have been damaged, one or more of the following may occur: muscle tightness or spasm, involuntary movement, disturbance in gait and mobility; abnormal sensation and perception; impairment of sight, hearing or speech; seizures; mental retardation and learning disabilities. It can manifest itself in a range of severity. (4)

There are several injuries to a developing brain that may produce cerebral palsy. (5) The main cause is an insufficient amount of oxygen reaching the fetal or newborn brain, (3) which can take place if there is a premature separation of the placenta from the wall of the uterus, awkward birth position of the baby, labour that is too long or too abrupt, or interference with circulation in the umbilical cord can interrupt oxygen supply. (8) Premature birth, low birth weight, Rh or A-B-O blood type incompatibility between mother and infant, infection of the mother with German measles or other virus diseases in early pregnancy, and micro-organisms that attack the infant’s central nervous system are also risk factors. (10) In most cases the cause is related to the development and childbearing processes and since the condition is not inherited, it is often called congenital cerebral palsy.

A less common type is called acquired cerebral palsy, which usually occurs before two years of age. (1) Head injury is the most frequent cause, usually the result of motor vehicle accidents, falls, or child abuse. Another possible cause is brain infection. (6)


Natasha is a wonderful 11-year-old young lady. She was diagnosed with cerebral palsy at the age of six months due to a very traumatic delivery at birth. She weighs approximately 72 pounds and her height is approximately 52 inches. Natasha is non-verbal and she communicates with an augmentive assistance device on her power wheelchair, otherwise known as her talking computer.

She is very active and rides a modified bicycle at school on a daily basis. She uses a stander for schoolwork and eating and also has a Hart walker for motor retraining her gait on a daily basis. Natasha is very active in sports such as swimming, bowling, track 3 skiing, and horseback riding.

Natasha has a mixed type of cerebral palsy. She has the tight muscle tone of spastic cerebral palsy and the involuntary movements of athetoid cerebral palsy. (7) This happened because both the pyramidal and extrapyramidal areas of her brain were damaged from inadequate blood or oxygen supply when she was a fetus and during the trauma of her birth. (4)

Natasha is predominantly spastic in her motor dysfunction, but is otherwise excellent in her cognitive and mental capabilities. She is integrated into a normal grade 6 classroom environment, and she uses a computer for her schoolwork with the help of a head mouse.

Natasha has undergone extensive therapy and training over the past 11 years, ranging from augmentive therapy, communicative therapy, hyperbaric oxygen therapy for two years, Botox injections to her hamstrings and adductor muscles bilaterally over the course of several years, extensive physical therapy, and chiropractic manipulation.  Over the course of her lifetime these treatments have made some short-term strides, but no major changes have been documented in her coordination, strength, and range of motion.

The Trigenics® protocols (2) have been used on Natasha for the past few months, particularly with her bilateral hamstrings, adductors, gluteus, and psoas muscles. The results thus far have been phenomenal compared to any other therapies or treatments that Natasha has received.


The physical examination was focused on the lower extremities. Her predominant deficits were bilateral adduction and flexion of the lower extremities, causing a severe scissoring of her gait when assisted with walking.

Hip and knee range of motion are listed in Table 1 comparing pre- and post- treatment measures. Muscle strength was weak for the bilateral hamstrings and bilateral abductor musculature, with dominance of the bilateral quadriceps and adductors. Palpation revealed trigger points in the bilateral hamstrings and adductors of a fibrotic quality. Hypertonicity was noted in the bilateral psoas, adductors, and hamstring musculature. This is common to see in this type of cerebral palsy. (4)


 HIP (knee extended) Prior to treatment After 12 weeks of Trigenics treatment
Extension 0/15 bilaterally 10/15 (R), 9/15 (L)
Abduction 10/30 bilaterally 16/30 (R), 15/30 (L)
Adduction 30/45(R), 25/45(L) 38/45(R), 35/45(L)
Internal rotation 10/45(R), 15/45(L) 25/45(R), 31/45(L)
External rotation 35/45(R), 30/45(L) 40/45(R), 38/45(L)
HIP (knee flexed)
Flexion 110/120(R), 100/120(L) 120/120(R), 120/120(L)
Extension 0/15 bilaterally 7/15(R), 5/15(L)
Extension 0/15 bilaterally 7/15(R), 5/15(L)
Internal rotation 5/45(R), 10/45(L) 30/45(R), 27/45(L)
External rotation 25/45(R), 30/45(L) 36/45(R) 33/45(L)


Natasha’s presentation is typical for her neurological deficit. There are evident limitations to the performance of the examination due to her physical impairments. (3)



To the best of her abilities, Natasha was able to contract within her range of motion without pain. The following protocols were performed three times per week over 12 weeks. The explanation of abbreviations are as follows (2):

* (TS) Trigenics® Strengthening protocols

* (TL) Trigenics® Lengthening protocols

Natasha’s treatment plan included: psoas (TS, TL); gluteus maximus (general TS) myopoint locations, just lateral to its insertion midsacrum; sartorius (TS); rectus femoris (proximal attachment) (TS); rectus femoris (general TS); adductors  (TS, TL); hamstrings (prone TS); hamstrings (supine TS); hamstrings(TL). (2)

Natasha noticed overall increases in her range of motion, and said there was less discomfort in her movements compared to other stretches she had performed over the years. She also noticed an increase in the resistive strength of her

hamstrings and adductors in general. We are hopeful that this may be a viable strategy to avoid any surgical intervention for the scissoring gait. At this time Natasha has an easier time with her gait pattern movements while being assisted with her motions.

Measurements of strength were taken with a hand-held force dynamometer.  Table 2 indicates the changes observed.

Table 2: Post 12 weeks of Trigenics® protocols strength change

Muscle tested Right (Per cent increase) Left (Per cent increase) 
Hamstring 12.00 14.00
Psoas 22.00 27.00
Gluteus max. 8.00 6.00
Adductors 37.00 32.00
Sartorius 2.00 2.50
Rectus femoris 19.00 24.00

Cerebral palsy in Natasha’s case involves both pyramidal and extrapyramidal involvement. (4) Of particular interest is the establishment of the upper motor neuron lesions, such as weakness involving the extensors of the upper limbs and the flexors of the lower limbs, and the development of spasticity (most of which is related to the release of subcortical pathways from higher inhibition and consequent activation of the “gamma loop”). She also presents increased tendon reflexes, again due to the release of the spinal reflex from higher inhibitory control by both cortical and subcortical centres, and the development of extensor plantar responses (essentially a withdrawal reflex). (2)

Natasha has had great success with the Trigenics® protocols, as the results have indicated. It has been very helpful to improve the collateral muscles, as well as those directly tested in the case study. (2) Resetting the muscle tone of these areas is extremely important in helping to maintain mobility and function. (2)

As these results have been very favourable, and the patient has experienced an increase in her range of motion and functional strength, it is prudent that further testing with other patients be established.  The neuromuscular facilitation with the Trigenics® protocols has illustrated a very positive trend towards increasing range of motion and increasing functional strength deficits for neurological impairments such as cerebral palsy.  We look forward to further research and potentially positive outcomes as we have seen with Natasha’s data.



1.) Miller, Bachrach et al.  Cerebral Palsy: a guide for care.  2002. Hopkins Press
2.) Austin AO.  Trigenics theory.  2002 The Trigenics® Institute of Neuromuscular Medicine.
3.) Miller G, Clark G.  The cerebral palsies: Causes, consequences and management.  1998
4.) Bobath K. Neurophysiological basis for the treatment of cerebral palsy.1991
5.) Levitt S. Treatment of cerebral palsy and motor delay.  1995,
6.) McDonald ET. Treating cerebral palsy.  1987,
7.) Dormans JP, Pellegrino L. Caring for children with cerebral palsy: a team approach.  1998
8.) Thompson GH. Comprehensive management of cerebral palsy.  2000
9.) Galjaard H. et al.  Early detection and management of cerebral palsy (Topics in Neurosciences) 1988