Spasticity is a classic feature of cerebral palsy (CP), a persistent but dynamic disorder of movement and posture. CP is a symptom complex, not a specific disease. It results from brain lesions or anomalies arising in early development,8 including:
CP is classified on the basis of the extremities affected (monoplegic, diplegic, triplegic, hemiplegic, and quadriplegic) and the predominant movement abnormality, including:
Dystonia, athetosis, and chorea are hyperkinetic movement disorders, also known as dyskinetic movements. In contrast, spasticity is a hypertonic but isokinetic movement disorder.
Epilepsy is commonly associated with CP and can further impair the individual’s quality of life. The risk of epilepsy varies in different subtypes of CP, being most frequent in quadriplegics (50%) and least frequent in diplegic patients (27%).16,17 Therefore, epilepsy is likely related to the type of brain lesion. The relationship between epilepsy and a specific type of brain lesion is not fully understood.
The percentage of CP patients with epilepsy and the time course for development of epilepsy differ according to the type of brain lesion. Okumura and colleagues18 studied the relationship between epilepsy in the first 5 years of life in patients with CP and the type of brain lesions found on magnetic resonance imaging (MRI). Of 130 patients, 14 had congenital anomaly and 116 had perinatal injury. Overall, 37 (31%) of the 130 patients had epilepsy, similar to other studies, in which epilepsy incidence ranges from 25% to 45%.16–19
Partial seizures occurred in 12 patients, infantile spasms in 20, and generalized seizures in 5. Patients with congenital anomaly had a significantly higher incidence and an earlier age of onset of epilepsy than those with perinatal injury. Among perinatal injury patients, those with term injury (with or without preterm injury) showed a higher incidence and a later onset of epilepsy than those with only preterm injury.18
Spasticity is a classic feature of MS, the most common demyelinating disease. MS is characterized by the dissemination of demyelinating events in time and space. After demyelination occurs, destroyed myelin is phagocytosed by macrophages, and gliosis ensues. In most patients, the course is characterized by exacerbations and remissions, but a pattern of steady or stepwise progression can occur.
In MS, spasticity results from plaques of demyelination in the upper motor neuron fibers (i.e., pyramidal tract) in the brain or spinal cord.4
Paroxysmal neurologic disturbances of spinal cord origin, so-called spinal cord seizures, can also result from demyelinating lesions and can be difficult to distinguish from spasticity. They have also been associated with intravenous dye placement, transverse myelitis, and traumatic spinal cord injury.5
These seizures are characterized by tonic spasm in the extremities, often accompanied by painful dysesthesia. They are transient, usually lasting no more than 2 minutes. They may occur spontaneously, but commonly are precipitated by tactile stimulation or movement of the extremity.
Clinical differentiation from spasticity is critical, because these seizures may respond to antiepileptic drugs such as carbamazepine.6 These seizures may limit the rehabilitation of patients with idiopathic transverse myelopathy unless they are recognized and appropriate drug therapy is initiated.7
Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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