Spastic diplegia

Spastic diplegia

Description, Causes and Risk Factors:

A type of cerebral palsy in which there is bilateral spasticity, with the lower extremities more severely affected.

Spastic diplegia is caused when the brain damage occurs in the outer layer of the brain, the cerebral cortex. Periventricular leukomalacia (PVL) is thought to be a cause of spastic diplegia. PVL is a term that means damage of the white-matter that surrounds the ventricles. This periventricular white-matter is especially vulnerable to injury in the premature infant because the blood supply system, and some of the cells that make up the white-matter are not fully developed. There is also developing evidence that infections present in the mother increases the risk of PVL. PVL has been reported to occur in 4% -- 15% of premature infants.

Spastic diplegia's particular type of brain damage inhibits the proper development of upper motor neuron function, impacting the motor cortex, the basal ganglia and the corticospinal tract. Nerve receptors in the spine leading to affected muscles become unable to properly absorb gamma aminobutyric acid (GABA), the amino acid that regulates muscle tone in humans. Without GABA absorption to those particular nerve rootlets (usually centred, in this case, around the sectors L1-S1 and L2-S2), affected nerves (here, the ones controlling the legs) perpetually fire the message for their corresponding muscles to permanently, rigidly contract, and the muscles become permanently hypertonic (spastic).

The abnormally high muscle tone that results creates lifelong difficulty with all voluntary and passive movement in the legs, and in general creates stress over time — depending on the severity of the condition in the individual, the constant spasticity ultimately produces pain, muscle/joint breakdown including tendinitis and arthritis, premature physical exhaustion (i.e., becoming physically exhausted even when you internally know that you have more energy than you are able to use), contractures, spasms, and progressively worse deformities/mis-alignments of bone structure around areas of the tightened musculature as the person's years progress. Severe arthritis, tendinitis, and similar breakdown can start as early as the spastic diplegic person's mid-20s (as a comprison, typical people with normal muscle tone are not at risk of arthritis, tendinitis, and similar breakdown until well into their 50s or 60s, if even then).

The patients with spastic diplegia had a higher incidence of spondylolysis and a greater average angle of lumbar lordosis than did the control group. Increased lordosis causes proportionally greater compressive and shearing forces in the posterior elements of the spine. The pars interarticularis is subject to higher mechanical stresses than other parts of the posterior elements and is therefore liable to fatigue fracture from the compression forces applied in the standing position. The increased compression force in the lordotic spine, applied at the site of repeated flexion/extension movements during walking, renders patients with spastic diplegia susceptible to spondylolysis. It was found only in the fifth lumbar vertebra. This vertebra, placed between the movable lumbar spine and the immovable sacrum, is situated like a cantilever, the lowest part of which bears the brunt of the increased compression force

Spastic diplegia makes up about 25-30% of all cerebral palsy, not taking into account post-neonatally acquired cerebral palsy. It does appear, however, that the percentage of people with spastic diplegia has dropped marginally since the 1970's. It does seem there are fewer people with spastic diplegia who fall into the moderate classification and although it is much less clear it may be that there are fewer people with spastic diplegia who fall into the mild classification.

The rate of spastic diplegia in postneonatally acquired cerebral palsy is significantly lower than in non-postneonatally acquired cerebral palsy.


Spastic diplegia symptoms include increased tension in a muscle. Normally, muscles coordinate in pairs; when one group of muscles contract (tighten), the other group relaxes. This allows free movement. When complications in brain-to-nerve-to-muscle communication occur, the balanced degree of muscle tension is disrupted. Muscles affected by spastic diplegia become active together which effectively blocks coordinated movement. Thus, the muscles in spastic diplegic patients are constantly stiff, or spastic.

Spastic diplegia generally affects the legs of a patient more than the arms. Patients have more extensive involvement of the lower extremity than the upper extremity which allows most patients to eventually walk. The gait of a person with spastic diplegia is typically characterized by a crouched gait. As a person walks one leg typically provides support while the other leg advances in preparation for its role of support limb in advance of the next step. The gait cycle (GS) describes this pattern of alternate limb support and advance. A crouched gait is where the knee is excessively flexed (bent) during stance and at the onset of push-off, which can make walking impossible without the aid of a walker. Both toe walking and flexed knees are common attributes and can be corrected with proper surgical treatment and gait analysis.


Most cases of spastic diplegia are diagnosed before the child is three. Developmental delay can be an early sign of spastic diplegia in infants and it is the sign parents most often notice and bring to the attention of their pediatrician. Babies with spastic diplegia may have unusual muscle tone. They may be rigid or stiff or they may seem floppy and unable to hold their head at a normal angle. The stiffness is caused by increased muscle tone (hypertonia), while floppiness is caused by decreased muscle tone (hyptonia). Sometimes a baby may begin appearing overly relaxed and then become increasingly stiff; this generally occurs at age two to three months.

Because spastic diplegia primarily associated with movement of the legs, a diagnosis frequently comes when a child starts showing signs of not meeting developmental milestones for walking. This occurs usually between the ages of 18 months and three years.

Before this time, an infant's legs may seem stiff, or may start out unusually floppy and gradually stiffen. The cause of this stiffness or floppiness is muscle tone, which has to do with the ability of muscle groups to lengthen and contract to produce movement. Too much muscle tone is called hypertonia, and too little is called hypotonia.

Some spastic diplegia is so mild that people with the disorder report only minor problems with balance and gait.


Therapy: The functional difficulties associated with spasticity will vary at different times in a person's life so the goal of any treatment to intervention is to maximize the function and minimize any of the disadvantages or consequences. Most therapy programs are family focused and community-based and usually designed to facilitate participation in the activities usual for a person's life stage.

Orthotics: The use of orthoses is quite common in people with spastic diplegia. There are different types of orthoses ranging from small particles that slip inside a normal shoe to ankle foot orthoses (AFOs) that extend from just below a person's need to just passed their toes around the back of their ankle. There are numerous types of orthoses and it will require professional assistance to prescribe the best ones most suitable to a person with spasticity and a certain time.

Oral medication: Baclofen etc.

Injected medication: Botox. This is the trade name for botulinum toxin which is the same drug that causes botulism. The drug is purified in laboratories and carefully controlled amounts are injected directly into muscles to weaken them and reduce the effects of spasticity temporarily. It is believed that the drug wears off between 3 and six months after administration but the effects can last considerably longer.

Intrathecal baclofen. This is the same drug that is taken orally except very small amounts are inserted directly into the spinal cord via catheter that is surgically inserted. A pump is also surgically inserted into the abdomen just under the skin. This pump ensures small amounts of the drug is continuously administered to maintain a reducing effect on spasticity. The pump can be refilled every three months and it will last approximately seven years before it needs to be replaced.

Phenol and alcohol. These drugs are administered by injection in a similar way to Botox. It is felt they have a similar but potentially permanent effect.

Surgical interventions: Orthopaedic surgery is quite common in people who have spastic diplegia. It can be used to reduce the effects of contracture, relocate dislocated joints, assist with the production of power during walking and alleviating pain.

Selective Dorsal Rhizotomy (SDR) is a neurosurgical procedure that carefully removes some of the sensory nerves that are sometimes implicated in making spasticity very debilitating. It is a lengthy and relatively new procedure which requires very careful assessment and consideration before a decision is made to go ahead. While this is a big procedure there is good reason to believe that for certain people the intervention can be useful.




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