The duration of anticonvulsant treatment varies according to seizure type and epilepsy syndrome. For most children, anticonvulsant medications can be weaned off after 2 years without seizures. There are some exceptions. Forexample, children with juvenile myoclonic epilepsy, progressive myoclonic epilepsy, atypical absence seizures, and Lennox-Gastaut syndrome usually require treatment for life. Children who have other neurological comorbidities, seizures that were initially difficult to control, orpersistently epileptiform EEGs are at highest risk for recurrence when therapy is discontinued.
Although cognitively normal children with epilepsy havethe same rates of injury as normal healthy children, thereare important safety considerations for people with epilepsy.The risk of drowning is high, so swimming and bathing mustonly occur under direct adult supervision. Children shoulduse appropriate helmets for sports such as bicycling or iceskating. There is no contraindication to participation in contact sports, but scuba diving, hang gliding, and free climbing are not safe for people with epilepsy. Each country andindividual states have specific laws regarding driving for people with epilepsy. Most require a period of seizure freedombefore issuing a driving permit.
Weakness is a decreased ability to voluntarily and actively movemuscles. This may be generalized or localized to one aspectof the body. Hypotonia is a state of low muscle resistance to movement. Hypotonia can be associated with weakness, but insome cases is present with normal motor strength. The differential diagnosis for weakness is extensive (Table 182-1).
Weakness and hypotonia may be due to disorders of upper motor neurons or lower motor neurons. Upper motor neurons originatein the cerebral motor cortex; their axons form the corticospinaltract ending in the spinal cord and control voluntary motor activity. The anterior horn cells, their motor roots, peripheral motornerves, neuromuscular junctions, and muscles represent the lower motor neurons and muscle units. Maintenance of normal strength, tone, and coordination requires integrated communication throughout this complex system, including the cerebral cortex,cerebellum, brainstem, thalamus, basal ganglia, and spinal cord.
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Weakness caused by upper motor neuron disease differs fromweakness produced by lower motor units (Table 182-2). Dysfunction of the upper motor neuron causes loss of voluntary
Neuromuscular junction Myasthenia gravis (juvenile, transient neonatal, congenital) Botulism
Muscle Muscular dystrophies (Duchenne, Becker, limb-girdle) Myotonic dystrophies Congenital myopathies Metabolic myopathies Dermatomyositis Polymyositis neuron, the final common pathway producing muscle activity, leads to total absence of movement with hypotonia. Function is best tested by measuring the strength of individual muscle groups or, in a young child, by observing the ability to perform tasks requiring particular muscle groups (e.g., walk up or down stairs, arise from the ground, walk on toes or heels, raise the hands above the head, squeeze a ball).
Tumors, trauma, infections, demyelinating syndromes, infarction, metabolic diseases, and degenerative diseases may injure the corticospinal tract, producing an upper motor neuron pattern of weakness coupled with increased deep tendon reflexes, spasticity, and extensor plantar responses (Babinski sign).
The distribution of weakness depends on the location of the lesion. A tumor in the left parietal region may produce a right hemiparesis. A brainstem glioma may produce a slowly progressive quadriparesis. A diffuse disorder of myelin synthesis, such as a leukodystrophy, would produce a progressive symmetrical quadriparesis.
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