Chapter 60 Assessment of Neurologic Function
the muscle and the spinal
cord. The result of lower
motor neuron damage is
muscle paralysis. Reexes are
lost, and the muscle
becomes accid (limp) and
atrophied from disuse. If the
patient has injured the
spinal trunk and it can heal,
use of the muscles
connected to that section of
the spinal cord may be
regained. If the anterior
horn motor cells are
destroyed, however, the
nerves cannot regenerate
and the muscles are never
useful again. Flaccid
paralysis and atrophy of the
affected muscles are the
principal signs of lower
motor neuron disease.
Lower motor neuron lesions
can be the result of trauma,
infection (poliomyelitis),
toxins, vascular disorders,
congenital malformations,
degenerative processes, and
neoplasms. Compression of
nerve roots by herni- ated
intervertebral disks is a
common cause of lower
motor neu- ron dysfunction.
Coordination of
Movement. The
smoothness, accuracy, and
strength that characterize the
muscular movements of a
normal person are
attributable to the inuence
of the cerebellum and the
basal ganglia.
The cerebellum (refer to
Fig. 60-2), described earlier, is
located beneath the occipital
lobe of the cerebrum; it is
responsible for the
coordination, balance, and
timing of all muscular
movements that originate in
the motor centers of the
cerebral cortex. Through
the action of the
cerebellum, the
contractions of op- posing
muscle groups are adjusted
in relation to each other to
maximal mechanical
advantage; muscle
contractions can be sus-
tained evenly at the desired
tension and without
signicant uctuation, and
reciprocal movements can
be reproduced at high and
constant speed, in
stereotyped fashion and
with relatively little effort.
The basal ganglia, masses
of gray matter in the
1833
midbrain be- neath the effects of all neuromuscular Tumors, infection, or
cerebral hemispheres, border paralyzing agents must have abscess and increased
the lateral ventricles and lie worn off, and any other intracranial pressure can all
in proximity to the internal possible treatable causes of affect the cerebellum.
capsule. The basal ganglia neurologic impairment must Cerebellar signs, such as
be investigated. ataxia, incoordination, and
play an important role in seizures, as well as CSF
planning and coordinating obstruction and compression
motor movements and of the brain stem may be
posture. Complex neural seen. Signs of increased
connections link the basal intracranial pressure,
ganglia with the cerebral including vomiting,
cortex. The major effect of headache, and changes in
these structures is to inhibit vital signs and level of
unwanted muscular activity; consciousness, are especially
disorders of the basal ganglia common when CSF ow is
obstructed.
result in exaggerated, Destruction or
uncontrolled movements. dysfunction of the basal
Impaired cerebellar ganglia leads not to paralysis
function, which may occur but to muscle rigidity, with
as a result of an intracranial disturbances of posture and
injury or some type of an movement. Such patients
expanding mass (eg, a tend to have involuntary
hemorrhage, abscess, or movements. These may
tumor), results in loss of take the form of coarse
muscle tone, weakness, and tremors, most often in the
upper extremities,
fatigue. Depending on the particularly in the distal
area of the brain affected, portions; athetosis,
the patient has different movement of a slow,
motor symptoms or squirming, writhing,
responses. The patient may twisting type; or chorea,
demonstrate decorticate, marked by spasmodic,
decerebrate, or accid purposeless, irregular,
posturing, usually as a result uncoordinated motions of
of cerebral trauma (Bateman, the trunk and the
2001). For further extremities, and facial
grimacing. Disorders due
explanation of this, see to lesions of the basal
Figure 61-1 in Chapter 61. ganglia include Parkinsons
Decortication (decorticate disease, Huntingtons
posturing) is the result of disease (see Chap. 65), and
lesions of the internal capsule spasmodic torticollis.
or cerebral hemispheres; the
patient has exion and S
internal rotation of the arms E
and wrists and extension, N
inter- nal rotation, and S
plantar exion of the feet. O
Decerebration (de- cerebrate R
posturing), the result of Y
lesions at the midbrain, is
more ominous than S
decortication. The patient Y
has extension and external
S
rotation of the arms and
T
wrists and extension, plantar
exion, and internal E
rotation of the feet. Flaccid M
posturing is usually the
result of lower brain stem F
dysfunction; the patient has U
no motor function, is limp, N
and lacks motor tone. C
Flaccidity preceded by T
decerebration in a patient I
with cerebral injury indicates O
severe neurologic N
impairment, which may
Integrating Sensory
herald brain death. Impulses. The thalamus, a
However, before the major receiving and
declaration of brain death, transmitting center for the
the patient must have spinal afferent sensory nerves, is a
cord injury ruled out, the
large structure connected to whose axons cross to the
the midbrain. It lies next to opposite side and then
the third ventricle and proceed to the thalamus.
forms the oor of the lateral
ventricle (see Fig. 60-3). Sensory Losses.
The thalamus integrates all Destruction of a sensory
sensory impulses except nerve results in total loss of
olfaction. It plays a role in sensation in its area of
the conscious awareness of distribution. Transection of
pain and the recogni- tion the spinal cord yields
of variation in temperature complete anesthesia below
and touch. The thalamus is the level of injury. Selective
responsible for the sense of destruction or degeneration
movement and position and of the posterior columns of
the ability to recognize the the spinal cord is responsible
size, shape, and quality of for a loss of position and
objects. vibratory sense in segments
distal to the lesion, without
Receiving Sensory Impulses. loss of touch, pain, or
Afferent impulses travel from temperature perception. A
their points of origin to their lesion, such as a cyst, in the
destinations in the cerebral center of the spinal cord
cortex via the ascending causes dissociation of
pathways directly, or they sensation loss of pain
may cross at the level of the
spinal cord or in the
medulla, depending on the
type of sensation that is
registered. Sensory
information may be
integrated at the level of the
spinal cord or may be relayed
to the brain. Knowledge of
these pathways is important
for neurologic assessment
and for understanding
symptoms and their
relationship to various
lesions.
Sensory impulses enter the
spinal cord by way of the
posterior
root. These axons convey
sensations of heat, cold, and
pain and
enter the posterior gray
column of the cord, where
they make
connections with the cells of
secondary neurons. Pain
and temperature bers cross
immediately to the opposite
side of the cord and course
upward to the thalamus.
Fibers carrying sensations of
touch, light pressure, and
localization do not connect
immediately with the
second neuron but ascend
the cord for a variable
distance before entering the
gray matter and completing
this connection. The axon
of the secondary neuron
crosses the cord and
proceeds upward to the
thalamus.
Position and vibratory
sensation are produced by
stimuli arising from muscles,
joints, and bones. These
stimuli are
conveyed,uncrossed, all the
way to the brain stem by the
axon of the primary neuron.
In the medulla, synaptic
connections are made with
cells of the secondary neurons,
1834 Unit 14 NEUROLOGIC FUNCTION
at the level of the lesion. This occurs because the bers
carrying pain and temperature cross within the cord
immediately on entering; thus, any lesion that divides the cord
longitudinally divides these bers. Other sensory bers ascend
the cord for variable distances, some even to the medulla, before
crossing, thereby by passing the lesion and avoiding
destruction.
Lesions affecting the posterior spinal nerve roots may cause
impairment of tactile sensation, including intermittent severe
pain that is referred to their areas of distribution. Tingling of the
ngers and the toes can be a prominent symptom of spinal cord
disease, presumably due to degenerative changes in the sensory
bers that extend to the thalamus (ie, belonging to the
spinothalamic tract).
Assessment: The Neurologic Examination
HEALTH HISTORY
An important aspect of the neurologic assessment is the history
of the present illness. The initial interview provides an
excellent opportunity to systematically explore the patients
current condition and related events while simultaneously
observing overall appearance, mental status, posture,
movement and affect. Depending on the patients condition,
the nurse may need to rely on yes-or-no answers to questions, on
a review of the medical record, or input from the family or a
combination of these.
GENETICS IN NURSING PRACTICENeurologic Disorders
DISEASES AND CONDITIONS INFLUENCED
BY GENETIC FACTORS
Alzheimers disease
Amyotrophic lateral sclerosis (ALS)
Duchenne muscular dystrophy
Epilepsy
Friedrich ataxia
Huntington disease
Myotonic dystrophy
Neurobromatosis type I
Parkinsons disease
Spina bida
Tourette syndrome
NURSING ASSESSMENTS
FAMILY HISTORY ASSESSMENT
Assess for other similarly affected relatives with
neurologic impairment.
Inquire about age of onset (eg, present at birthspina PATIENTS ON THE WEB
bida;
developed in childhoodDuchenne muscular dystrophy;
developed in adulthoodHuntington disease, Alzheimers
disease, amyotrophic lateral sclerosis)
Inquire about the presence of related conditions such as men-
tal retardation and/or learning disabilities
(neurobromatosis
type I).
PHYSICAL ASSESSMENT
Assess for the presence of other physical features suggestive of
an underlying genetic condition, such as skin lesions seen in
neurobromatosis type 1 (caf-au-lait spots).
Assess for other congenital abnormalities (eg, cardiac, ocular).
Neurologic disease may be stable or progressive, with both
intermittent symptom-free periods as well as times with
uctuations in symptoms. The health history therefore includes
details about the onset, character, severity, location, duration,
and frequency of symptoms and signs; associated complaints;
precipitating, aggravating, and relieving factors; progression,
remission, and exacerbation; and the presence or absence of
similar symptoms among family members. The nurse may also
use the interview to inquire about any family history of genetic
diseases. See the Genetics chart for assessment guidelines and
Chapter 9 for additional information about genetics.
Included in the health history is a review of the medical
history, including a system-by-system evaluation. The nurse
should be aware of any history of trauma or falls that may have
involved the head or spinal cord. Questions regarding the use of
alcohol, medications, and recreational drugs are also included.
The history taking portion of the neurologic examination is
critical and, in many cases of neurologic disease, leads to an
accurate diagnosis.
CLINICAL MANIFESTATIONS
The clinical manifestations of neurologic disease are as varied
as the disease processes themselves. Symptoms can be subtle or
in- tense, uctuating or permanent, an inconvenience or
devastating. An introduction to some of the most common
symptoms associ-
MANAGEMENT SPECIFIC TO GENETICS
Inquire whether DNA mutation or other genetic testing has
been performed on affected family members.
If indicated, refer for further genetic counseling and
evalua- tion so that family members can discuss
inheritance, risk to
other family members, availability of genetic testing and
gene-based interventions.
Offer appropriate genetics information and resources.
Assess patients understanding of genetics information.
Provide support to families with newly diagnosed
genetic- related neurologic disorders.
Participate in management and coordination of care of pa-
tients with genetic conditions and individuals predisposed to
develop or pass on a genetic condition.
GENETICS RESOURCES FOR NURSES AND THEIR
Genetic Alliance: http://www.geneticalliance.org a
directory of support groups for patients and families
with genetic conditions
Gene Clinics: http://www.geneclinics.org a listing of
common genetic disorders with up-to-date clinical
summaries, genetic counseling and testing information
National Organization of Rare Disorders: http://www.
rarediseases.orga directory of support groups and
informa- tion for patients and families with rare genetic
disorders
OMIM: Online Mendelian Inheritance in Man: http://www.
nchi.nlm.nih.gov/omim/stats/html a complete listing of
inherited genetic conditions