1428 SECTION 11 Problems Related to Movement and Coordination
main side effect of opioids is constipation, so the patient may
need to take a stool softener or laxative. Clonidine (Catapres)
and propranolol (Inderal) are also effective in some patients.
DEGENERATIVE NEUROLOGIC DISORDERS
Degenerative nerve diseases lead to nerve damage that worsens
as the disease progresses. These diseases affect many activities,
including balance, movement, speech, and respiratory and
heart function. There are more than 200 degenerative neuro-
logic disorders. These include the disorders discussed in the
remainder of this chapter, as well as disorders such as cerebellar
degeneration, Friedreich’s ataxia, Creutzfeldt-Jakob disease, and
neurofibromatosis. Some have no known cause. However, many
of these diseases have a genetic basis. Most degenerative nerve
diseases have no cure. Treatment aims to reduce symptoms and
help the patient maintain an optimal level of function.
Patients with these diseases have similar concerns and prob-
lems. They must deal with not only their disease, but also the
impact that the disease has on their quality of life. Many patients
have concerns regarding safety, mobility, self-care, and coping.
The patient and family often require psychosocial support, espe-
cially as the disease progresses and the patient’s disability gets
worse.
MULTIPLE SCLEROSIS
Multiple sclerosis (MS) is a chronic, progressive, degenerative
disorder of the CNS characterized by disseminated demyelin-
ation of nerve fibers of the brain and spinal cord. The onset of
MS is usually between 20 and 50 years of age, although it can
occur in young teens and much older adults. Women are
affected two to three times more often than men.
MS is five times more prevalent in temperate climates
(between 45 and 65 degrees of latitude), such as those found in
the northern United States, Canada, and Europe, as compared
with tropical regions. Migration from one geographic area to
another may alter a person’s risk of developing MS. Immigrants
and their descendants tend to take on the risk level (either
higher or lower) of the area to which they move. However, the
change in risk may not appear immediately. For example,
African Americans (in the United States) have a prevalence rate
that is 40% that of European Americans, whereas Africans (in
Africa) are thought to have a prevalence rate that is approxi-
mately 1% that of European Americans. The variations in inci-
dence of MS suggest that geography, ethnicity, and other factors
interact in a complex way to cause MS.16
Etiology and Pathophysiology
The cause of MS is unknown, although research suggests that it
is unlikely MS is related to a single cause. Researchers believe
the disease develops in a genetically susceptible person as a
result of environmental exposure, like an infection. Multiple
genes are believed to be involved in the inherited susceptibility
to MS, and first-, second-, and third-degree relatives of patients
with MS are at an increased risk.16
Possible precipitating factors include infection, smoking,
physical injury, emotional stress, excessive fatigue, pregnancy,
and a poor state of health. The role of precipitating factors such
as exposure to pathogenic agents is controversial. It is possible
that their association with MS is random and that there is no
cause-and-effect relationship.
Myelin sheath
Neuron
Axon of nerve fiber
A
Node of Ranvier
B
C
D
FIG. 59-3 Pathogenesis of multiple sclerosis. A, Normal nerve cell with
myelin sheath. B, Normal axon. C, Myelin breakdown. D, Myelin totally
disrupted; axon not functioning.
Three pathologic processes characterize MS: chronic inflam-
mation, demyelination, and gliosis (scarring) in the CNS. The
primary neuropathologic condition is an autoimmune process
orchestrated by activated T cells (lymphocytes). An environ-
mental factor or virus in genetically susceptible individuals may
initially trigger this process. The activated T cells in the systemic
circulation migrate to the CNS, disrupting the blood-brain
barrier. This is likely the initial event in the development of MS.
Subsequent antigen-antibody reaction within the CNS activates
the inflammatory response and leads to the demyelination of
axons.
Initially, attacks on the myelin sheaths of the neurons in the
brain and spinal cord result in damage to the myelin sheath (Fig.
59-3, A to C). However, the nerve fiber is not affected. Transmis-
sion of nerve impulses still occurs, though transmission is
slowed. The patient may complain of a noticeable impairment
of function (e.g., weakness). However, the myelin can regener-
ate, and when it does, symptoms disappear. At that point, the
patient experiences a remission.
As ongoing inflammation occurs, the nearby oligodendro-
cytes are affected, and the myelin loses the ability to regenerate.
Eventually damage occurs to the underlying axon. Nerve
impulse transmission is disrupted, resulting in the permanent
loss of nerve function (Fig. 59-3, D). As inflammation subsides,
glial scar tissue replaces the damaged tissue, leading to the
formation of hard, sclerotic plaques (Fig. 59-4). These plaques
are found throughout the white matter of the CNS.
Clinical Manifestations
The onset of MS is often insidious and gradual, with vague
symptoms occurring intermittently over months or years that
often dissuade the patient from seeking medical attention. Thus
the disease may not be diagnosed until long after the onset of
the first symptom. The disease is characterized by chronic, pro-
gressive deterioration in some patients, and remissions and ex-
acerbations in others. With repeated exacerbations, the overall
trend is progressive deterioration in neurologic function.