168 PART 2 Cardinal Manifestations and Presentation of Diseases
TABLE 24-2 Causes of Episodic Generalized Weakness
1. Electrolyte disturbances, e.g., hypokalemia, hyperkalemia, hypercalcemia,
hypernatremia, hyponatremia, hypophosphatemia, hypermagnesemia
2. Muscle disorders
a. Channelopathies (periodic paralyses)
b. Metabolic defects of muscle (impaired carbohydrate or fatty acid
utilization; abnormal mitochondrial function)
3. Neuromuscular junction disorders
a. Myasthenia gravis
b. Lambert-Eaton myasthenic syndrome
4. Central nervous system disorders
a. Transient ischemic attacks of the brainstem
b. Transient global cerebral ischemia
c. Multiple sclerosis
5. Lack of voluntary effort
a. Anxiety
b. Pain or discomfort
c. Somatization disorder
Normal somatic sensation reflects a continuous monitoring process,
little of which reaches consciousness under ordinary conditions. By
contrast, disordered sensation, particularly when experienced as
painful, is alarming and dominates the patient’s attention. Physicians
should be able to recognize abnormal sensations by how they are
described, know their type and likely site of origin, and understand
their implications. Pain is considered separately in Chap. 13.
■ POSITIVE AND NEGATIVE SYMPTOMS
Abnormal sensory symptoms can be divided into two categories:
positive and negative. The prototypical positive symptom is tingling
(pins and needles); other positive sensory phenomena include itch and
altered sensations that are described as pricking, bandlike, lightning-like
shooting feelings (lancinations), aching, knifelike, twisting, drawing,
25 Numbness, Tingling,
and Sensory Loss
Stephen L. Hauser
SUBACUTE OR CHRONIC QUADRIPARESIS Quadriparesis due to upper
motor neuron disease may develop over weeks to years from chronic
myelopathies, multiple sclerosis, brain or spinal tumors, chronic subdural hematomas, and various metabolic, toxic, and infectious disorders. It may also result from lower motor neuron disease, a chronic
neuropathy (in which weakness is often most profound distally), or
myopathic weakness (typically proximal).
When quadriparesis develops acutely in obtunded patients, evaluation begins with a CT scan of the brain. If upper motor neuron signs
have developed acutely but the patient is alert, the initial test is usually
an MRI of the cervical cord. When onset has been gradual, disorders of
the cerebral hemispheres, brainstem, and cervical spinal cord can usually be distinguished clinically, and imaging is directed first at the clinically suspected site of pathology. If weakness is lower motor neuron,
myopathic, or uncertain in origin, laboratory studies can determine
the levels of muscle enzymes and electrolytes, and EMG and nerve
conduction studies help to localize the pathologic process (Chap. 449).
Monoparesis Monoparesis usually is due to lower motor neuron
disease, with or without associated sensory involvement. Upper motor
neuron weakness occasionally presents as a monoparesis of distal and
nonantigravity muscles. Myopathic weakness rarely is limited to one
limb.
ACUTE MONOPARESIS If weakness is predominantly distal and of
upper motor neuron type and is not associated with sensory impairment or pain, focal cortical ischemia is likely (Chap. 427); diagnostic
possibilities are similar to those for acute hemiparesis. Sensory loss
and pain usually accompany acute lower motor neuron weakness;
the weakness commonly localizes to a single nerve root or peripheral
nerve, but occasionally reflects plexus involvement. If lower motor
neuron weakness is likely, evaluation begins with EMG and nerve
conduction studies.
SUBACUTE OR CHRONIC MONOPARESIS Weakness and atrophy that
develop over weeks or months are usually of lower motor neuron
origin. When associated with sensory symptoms, a peripheral cause
(nerve, root, or plexus) is likely; otherwise, anterior horn cell disease
should be considered. In either case, an electrodiagnostic study is indicated. If weakness is of the upper motor neuron type, a discrete cortical
(precentral gyrus) or cord lesion may be responsible, and appropriate
imaging is performed.
Distal Weakness Involvement of two or more limbs distally suggests lower motor neuron or peripheral nerve disease. Acute distal
lower-limb weakness results occasionally from an acute toxic polyneuropathy or cauda equina syndrome. Distal symmetric weakness usually
develops over weeks, months, or years and, when associated with
numbness, is due to peripheral neuropathy (Chap. 446). Anterior horn
cell disease may begin distally but is typically asymmetric and without
accompanying numbness (Chap. 437). Rarely, myopathies present with
distal weakness (Chap. 449). Electrodiagnostic studies help localize the
disorder (Fig. 24-3).
Proximal Weakness Myopathy often produces symmetric weakness of the pelvic or shoulder girdle muscles (Chap. 449). Diseases of
the neuromuscular junction, such as myasthenia gravis (Chap. 448),
may present with symmetric proximal weakness often associated with
ptosis, diplopia, or bulbar weakness and fluctuate in severity during
the day. In anterior horn cell disease, proximal weakness is usually
asymmetric, but it may be symmetric especially in genetic forms.
Numbness does not occur with any of these diseases. The evaluation
usually begins with determination of the serum creatine kinase level
and electrophysiologic studies.
Weakness in a Restricted Distribution Weakness may not fit
any of these patterns, being limited, for example, to the extraocular,
hemifacial, bulbar, or respiratory muscles. If it is unilateral, restricted
weakness usually is due to lower motor neuron or peripheral nerve disease, such as in a facial palsy. Weakness of part of a limb is commonly
due to a peripheral nerve lesion such as an entrapment neuropathy.
Relatively symmetric weakness of extraocular or bulbar muscles frequently is due to a myopathy (Chap. 449) or neuromuscular junction
disorder (Chap. 448). Bilateral facial palsy with areflexia suggests
Guillain-Barré syndrome (Chap. 447). Worsening of relatively symmetric weakness with fatigue is characteristic of neuromuscular junction disorders. Asymmetric bulbar weakness usually is due to motor
neuron disease. Weakness limited to respiratory muscles is uncommon
and usually is due to motor neuron disease, myasthenia gravis, or
polymyositis/dermatomyositis (Chap. 365).
Acknowledgment
The editors acknowledge the contributions of Michael J. Aminoff to earlier
editions of this chapter.
■ FURTHER READING
Brazis P et al: Localization in Clinical Neurology, 7th ed. Philadelphia,
Lippincott William & Wilkins, 2016.
Campbell WW, Barohn RJ: DeJong’s The Neurological Examination,
8th ed. Philadelphia, Lippincott William & Wilkins, 2019.
Guarantors of Brain: Aids to the Examination of the Peripheral Nervous System, 4th ed. Edinburgh, Saunders, 2000.
169 Numbness, Tingling, and Sensory Loss CHAPTER 25
deformation of the skin or stretch of muscles). Each type of receptor
has its own set of sensitivities to specific stimuli, size and distinctness
of receptive fields, and adaptational qualities.
Afferent peripheral nerve fibers conveying somatosensory information from the limbs and trunk traverse the dorsal roots and enter the
dorsal horn of the spinal cord (Fig. 25-1); the cell bodies of first-order
neurons are located in the dorsal root ganglia (DRG). In an analogous
fashion, sensations from the face and head are conveyed through the
trigeminal system (Fig. 441-2). Once fiber tracts enter the spinal cord,
the polysynaptic projections of the smaller fibers (unmyelinated and
small myelinated), which subserve mainly nociception, itch, temperature sensibility, and touch, cross and ascend in the opposite anterior
and lateral columns of the spinal cord, through the brainstem, to the
ventral posterolateral (VPL) nucleus of the thalamus and ultimately
project to the postcentral gyrus of the parietal cortex and other cortical
areas (Chap. 13). This is the spinothalamic pathway or anterolateral
system. The larger fibers, which subserve tactile and position sense
and kinesthesia, project rostrally in the posterior and posterolateral
columns on the same side of the spinal cord and make their first synapse in the gracile or cuneate nucleus of the lower medulla. Axons of
second-order neurons decussate and ascend in the medial lemniscus
located medially in the medulla and in the tegmentum of the pons and
midbrain and synapse in the VPL nucleus; third-order neurons project
to parietal cortex as well as to other cortical areas. This large-fiber
system is referred to as the posterior column–medial lemniscal pathway
(lemniscal, for short). Although the fiber types and functions that
make up the spinothalamic and lemniscal systems are relatively well
known, many other fibers, particularly those associated with touch,
pressure, and position sense, ascend in a diffusely distributed pattern
both ipsilaterally and contralaterally in the anterolateral quadrants of
the spinal cord. This explains why a complete lesion of the posterior
columns of the spinal cord may be associated with little sensory deficit
on examination.
APPROACH TO THE PATIENT
Clinical Examination of Sensation
The main components of the sensory examination are tests of primary sensation (pain, touch, vibration, joint position, and thermal
sensation) (Table 25-1). The examiner must depend on patient
responses, and this complicates interpretation. Further, examination may be limited in some patients. In a stuporous patient, for
example, sensory examination is reduced to observing the briskness
of withdrawal in response to a pinch or another noxious stimulus.
Comparison of responses on the two sides of the body is essential.
In an alert but uncooperative patient, it may not be possible to
examine cutaneous sensation, but some idea of proprioceptive
function may be gained by noting the patient’s best performance of
movements requiring balance and precision.
In patients with sensory complaints, testing should begin in the
center of the affected region and proceed radially until sensation is
perceived as normal. The distribution of any abnormality is defined
and compared to root and peripheral nerve territories (Figs. 25-2
and 25-3). Some patients present with sensory symptoms that do
not fit an anatomic localization and are accompanied by either no
abnormalities or gross inconsistencies on examination. The examiner should consider in such cases the possibility of a psychologic
cause (see “Psychogenic Symptoms,” below). Sensory examination
of a patient who has no neurologic complaints can be brief and
consist of pinprick, touch, and vibration testing in the hands and
feet plus evaluation of stance and gait, including the Romberg
maneuver (Chap. V6). Evaluation of stance and gait also tests the
integrity of motor and cerebellar systems.
PRIMARY SENSATION
The sense of pain usually is tested with a clean pin, which is then
discarded. The patient is asked to close the eyes and focus on the
pricking or unpleasant quality of the stimulus, not just the pressure
pulling, tightening, burning, searing, electrical, or raw feelings. Such
symptoms are often painful.
Positive phenomena usually result from trains of impulses generated
at sites of lowered threshold or heightened excitability along a peripheral or central sensory pathway. The nature and severity of the abnormal sensation depend on the number, rate, timing, and distribution of
ectopic impulses and the type and function of nervous tissue in which
they arise. Because positive phenomena represent excessive activity in
sensory pathways, they are not necessarily associated with a sensory
deficit (loss) on examination.
Negative phenomena represent loss of sensory function and are
characterized by diminished or absent feeling that often is experienced
as numbness and by abnormal findings on sensory examination. In
disorders affecting peripheral sensation, at least one-half of the afferent
axons innervating a particular site are probably lost or functionless
before a sensory deficit can be demonstrated by clinical examination. If
the rate of loss is slow, however, lack of cutaneous feeling may be unnoticed by the patient and difficult to demonstrate on examination, even
though few sensory fibers are functioning; if it is rapid, both positive
and negative phenomena are usually conspicuous. Subclinical degrees
of sensory dysfunction may be revealed by sensory nerve conduction
studies or somatosensory-evoked potentials.
Whereas sensory symptoms may be either positive or negative,
sensory signs on examination are always a measure of negative
phenomena.
■ TERMINOLOGY
Paresthesias and dysesthesias are general terms used to denote positive
sensory symptoms. The term paresthesias typically refers to tingling or
pins-and-needles sensations but may include a wide variety of other
abnormal sensations, except pain; it sometimes implies that the abnormal sensations are perceived spontaneously. The more general term
dysesthesias denotes all types of abnormal sensations, including painful
ones, regardless of whether a stimulus is evident.
Another set of terms refers to sensory abnormalities found on
examination. Hypesthesia or hypoesthesia refers to a reduction of
cutaneous sensation to a specific type of testing such as pressure, light
touch, and warm or cold stimuli; anesthesia, to a complete absence
of skin sensation to the same stimuli plus pinprick; and hypalgesia
or analgesia, to reduced or absent pain perception (nociception).
Hyperesthesia means pain or increased sensitivity in response to touch.
Similarly, allodynia describes the situation in which a nonpainful stimulus, once perceived, is experienced as painful, even excruciating. An
example is elicitation of a painful sensation by application of a vibrating
tuning fork. Hyperalgesia denotes severe pain in response to a mildly
noxious stimulus, and hyperpathia, a broad term, encompasses all the
phenomena described by hyperesthesia, allodynia, and hyperalgesia.
With hyperpathia, the threshold for a sensory stimulus is increased and
perception is delayed, but once felt, it is unduly painful.
Disorders of deep sensation arising from muscle spindles, tendons,
and joints affect proprioception (position sense). Manifestations
include imbalance (particularly with eyes closed or in the dark),
clumsiness of precision movements, and unsteadiness of gait, which
are referred to collectively as sensory ataxia. Other findings on examination usually, but not invariably, include reduced or absent joint
position and vibratory sensibility and absent deep tendon reflexes in
the affected limbs. The Romberg sign is positive, which means that the
patient sways markedly or topples when asked to stand with feet close
together and eyes closed. In severe states of deafferentation involving
deep sensation, the patient cannot walk or stand unaided or even sit
unsupported. Continuous involuntary movements (pseudoathetosis) of
the outstretched hands and fingers occur, particularly with eyes closed.
■ ANATOMY OF SENSATION
Cutaneous receptors are classified by the type of stimulus that optimally excites them. They consist of naked nerve endings (nociceptors,
which respond to tissue-damaging stimuli, and thermoreceptors,
which respond to noninjurious thermal stimuli) and encapsulated
terminals (several types of mechanoreceptor, activated by physical
170 PART 2 Cardinal Manifestations and Presentation of Diseases
Internal
capsule
Thalamus
Leg Trunk
Arm
Face
Ventral
posterolateral
nucleus of
thalamus
Medial lemniscus
Spinothalamic tract
Spinothalamic tract
Principal sensory
nucleus of V
Nucleus of
funiculus gracilis
Nucleus of
funiculus cuneatus
Nucleus of
spinal tract V
Posterior column
fibers
MIDBRAIN
PONS
MEDULLA
SPINAL CORD
Post-central
cortex
FIGURE 25-1 The main somatosensory pathways. The spinothalamic tract (pain, thermal sense) and the posterior column–lemniscal system (touch, pressure, joint position)
are shown. Offshoots from the ascending anterolateral fasciculus (spinothalamic tract) to nuclei in the medulla, pons, and mesencephalon and nuclear terminations of the
tract are indicated. (Reproduced with permission from AH Ropper, MA Samuels: Adams and Victor’s Principles of Neurology, 9th ed. New York, McGraw-Hill, 2009.)
TABLE 25-1 Testing Primary Sensation
SENSE TEST DEVICE ENDINGS ACTIVATED FIBER SIZE MEDIATING CENTRAL PATHWAY
Pain Pinprick Cutaneous nociceptors Small SpTh, also D
Temperature, heat Warm metal object Cutaneous thermoreceptors for hot Small SpTh
Temperature, cold Cold metal object Cutaneous thermoreceptors for cold Small SpTh
Touch Cotton wisp, fine brush Cutaneous mechanoreceptors, also
naked endings
Large and small Lem, also D and SpTh
Vibration Tuning fork, 128 Hz Mechanoreceptors, especially pacinian
corpuscles
Large Lem, also D
Joint position Passive movement of specific
joints
Joint capsule and tendon endings,
muscle spindles
Large Lem, also D
Abbreviations: D, diffuse ascending projections in ipsilateral and contralateral anterolateral columns; Lem, posterior column and lemniscal projection, ipsilateral; SpTh,
spinothalamic projection, contralateral.
or touch sensation elicited. Areas of hypalgesia should be mapped
by proceeding radially from the most hypalgesic site. Temperature
sensation to both hot and cold is best tested with small containers
filled with water of the desired temperature. An alternative way to
test cold sensation is to touch a metal object, such as a tuning fork
at room temperature, to the skin. For testing warm temperatures,
the tuning fork or another metal object may be held under warm
water of the desired temperature and then used. The appreciation
of both cold and warmth should be tested because different receptors respond to each. Touch usually is tested with a wisp of cotton,
171 Numbness, Tingling, and Sensory Loss CHAPTER 25
FIGURE 25-2 The cutaneous fields of peripheral nerves. (Reproduced with permission from W Haymaker, B Woodhall: Peripheral Nerve Injuries, 2nd ed. Philadelphia,
Saunders, 1953.)
Great auricular n.
Ant. cut. n. of neck
Ant.
cut.
rami
of
thor.
n’s.
T2
3
4
5
6
7
8
9
10
11
12
Lat.
cut.
rami
Supraclavicular n’s.
Med. cut. n. of arm
& intercostobrachial n.
Med. cut. n.
of forearm
Iliohypogastric n.
Genital
branch of
genitofem.
n.
Dorsal n. of penis
Scrotal branch of perineal n.
Obturator n.
Lat. cut. n. of calf
(from common peroneal n.)
Superficial peroneal n.
(from common peroneal n.)
Deep peroneal n.
(from common peroneal n.)
Intermed. & med. cut. n’s.
of thigh (from femoral n.)
Lat. cut. n. of thigh
Lat. cut. of forearm
(from musculocut. n.)
Lower lat. cut. n. of arm
(from radial n.)
Axillary n.
(circumflex)
I
II
III
Ilioinguinal n.
Femoral
branch
of genitofemoral n.
(lumbo-inguinal n.)
Saphenous n.
(from femoral n.)
Med. & lat. plantar n’s.
(from posttibial n.)
Sural n.
(from tibial n.)
Radial n.
Median n.
Ulnar n.
Great auricular n.
Greater
Lesser n.} occipital nerves
Ant. cut. n. of neck
T2
3
4
5
6
7
8
9
10
11
12
T1
L1
S1
Post. rami of
lumbar sacral
& coccygeal n’s.
Lat.
cut.
rami
Post.
cut.
rami
of
thor.
n’s.
C5
C6 Supraclavicular n’s.
Med. cut. n. of arm
& intercostobrachial n.
Post. cut. n. of forearm
(from radial n.)
Lat. cut. n. of forearm
(from musculocut n.) Med.
cut. n.
of
forearm
Obturator n.
Superficial peroneal n.
(from common peroneal n.)
Lat. cut. n.of calf
(from common femoral n.)
Inf. med.
cluneal n. Inf. lat.
cluneal n’s.
Lat. plantar n.
Saphenous n.
Sural n.
Calcanean branches
of tibial & sural n’s.
Med.
plantar n. Lat.
plantar n.
Superficial
peroneal n.
Inf. med. n. of thigh
Post cut. n. of thigh
Lower
Lat. cut. of arm
(from radial n.)
Post cut. n. of arm
(from radial n.)
Axillary n.
(circumflex)
Iliohypogastric n.
Saphenous n.
(from femoral n.)
Med. cut. n. of thigh
(from femoral n.)
Calcanean branches of
sural & tibial n’s.
Sural n. (from tibial n.)
Radial n.
Median n.
Ulnar n.
minimizing pressure on the skin. In general, it is better to avoid
testing touch on hairy skin because of the profusion of the sensory
endings that surround each hair follicle. The patient is tested with
the eyes closed and should respond as soon as the stimulus is perceived, indicating its location.
Joint position testing is a measure of proprioception. With the
patient’s eyes closed, joint position is tested in the distal interphalangeal joint of the great toe and fingers. The digit is held
by its sides, distal to the joint being tested, and moved passively
while more proximal joints are stabilized—the patient indicates the
change in position or direction of movement. If errors are made,
more proximal joints are tested. A test of proximal joint position
sense, primarily at the shoulder, is performed by asking the patient
to bring the two index fingers together with arms extended and
eyes closed. Normal individuals can do this accurately, with errors
of 1 cm or less.
The sense of vibration is tested with an oscillating tuning fork
that vibrates at 128 Hz. Vibration is tested over bony points, beginning distally; in the feet, it is tested over the dorsal surface of the
distal phalanx of the big toes and at the malleoli of the ankles, and in
the hands, it is tested dorsally at the distal phalanx of the fingers. If
abnormalities are found, more proximal sites should be examined.
Vibratory thresholds at the same site in the patient and the examiner may be compared for control purposes.
CORTICAL SENSATION
The most commonly used tests of cortical function are two-point
discrimination, touch localization, and bilateral simultaneous stimulation, and tests for graphesthesia and stereognosis. Abnormalities
T2
T2
T2
T1
C3
C3
C2
C4
C4
C5
C5
C6 C6
C8
C7
C7
C8
T4
T4
T6
T6
T8
T8
T10
T10
T12
T12
L1
L2
L3
L3
L4
L4 L5
L5
L5
L1
L3
S1
S2
S2
S1
S1
S3 S4S5
L
2
T1
FIGURE 25-3 Distribution of the sensory spinal roots on the surface of the body
(dermatomes). (Reproduced with permission from D Sinclair: Mechanisms of
Cutaneous Sensation. Oxford, UK, Oxford University Press, 1981 through PLS Clear.)
172 PART 2 Cardinal Manifestations and Presentation of Diseases
of these sensory tests, in the presence of normal primary sensation
in an alert cooperative patient, signify a lesion of the parietal cortex
or thalamocortical projections. If primary sensation is altered, these
cortical discriminative functions usually will be abnormal also.
Comparisons should always be made between analogous sites on
the two sides of the body because the deficit with a specific parietal
lesion is likely to be unilateral.
Two-point discrimination can be tested with calipers, the points
of which may be set from 2 mm to several centimeters apart and
then applied simultaneously to the test site. On the fingertips, a normal individual can distinguish about a 3-mm separation of points.
Touch localization is performed by light pressure for an instant
with the examiner’s fingertip or a wisp of cotton wool; the patient,
whose eyes are closed, is required to identify the site of touch. Bilateral simultaneous stimulation at analogous sites (e.g., the dorsum of
both hands) can be carried out to determine whether the perception of touch is extinguished consistently on one side (extinction or
neglect). Graphesthesia refers to the capacity to recognize, with eyes
closed, letters or numbers drawn by the examiner’s fingertip on the
palm of the hand. Once again, interside comparison is of prime
importance. Inability to recognize numbers or letters is termed
agraphesthesia.
Stereognosis refers to the ability to identify common objects by
palpation, recognizing their shape, texture, and size. Common
standard objects such as keys, paper clips, and coins are best used.
Patients with normal stereognosis should be able to distinguish a
dime from a penny and a nickel from a quarter without looking.
Patients should feel the object with only one hand at a time. If they
are unable to identify it in one hand, it should be placed in the other
for comparison. Individuals who are unable to identify common
objects and coins in one hand but can do so in the other are said to
have astereognosis of the abnormal hand.
QUANTITATIVE SENSORY TESTING
Effective sensory testing devices are commercially available. Quantitative sensory testing is particularly useful for serial evaluation
of cutaneous sensation in clinical trials. Threshold testing for
touch and vibratory and thermal sensation is the most widely used
application.
ELECTRODIAGNOSTIC STUDIES AND NERVE BIOPSY
Nerve conduction studies and nerve biopsy are important means of
investigating the peripheral nervous system, but they do not evaluate the function or structure of cutaneous receptors and free nerve
endings or of unmyelinated or thinly myelinated nerve fibers in the
nerve trunks. Skin biopsy can be used to evaluate these structures
in the dermis and epidermis.
■ LOCALIZATION OF SENSORY ABNORMALITIES
Sensory symptoms and signs can result from lesions at many different
levels of the nervous system from the parietal cortex to the peripheral
sensory receptor. Noting their distribution and nature is the most
important way to localize their source. Their extent, configuration,
symmetry, quality, and severity are the key observations.
Dysesthesias without sensory findings by examination may be
difficult to interpret. To illustrate, tingling dysesthesias in an acral
distribution (hands and feet) can be systemic in origin, for example,
secondary to hyperventilation, or induced by a medication such as acetazolamide. Distal dysesthesias can also be an early event in an evolving
polyneuropathy or may herald a myelopathy, such as from vitamin
B12 deficiency. Sometimes, distal dysesthesias have no definable basis.
In contrast, dysesthesias that correspond in distribution to that of a
particular peripheral nerve structure denote a lesion at that site. For
instance, dysesthesias restricted to the fifth digit and the adjacent onehalf of the fourth finger on one hand reliably point to disorder of the
ulnar nerve, most commonly at the elbow.
Nerve and Root In focal nerve trunk lesions, sensory abnormalities are readily mapped and generally have discrete boundaries
(Figs. 25-2 and 25-3). Root (“radicular”) lesions frequently are accompanied by deep, aching pain along the course of the related nerve trunk.
With compression of a fifth lumbar (L5) or first sacral (S1) root, as
from a ruptured intervertebral disk, sciatica (radicular pain relating to
the sciatic nerve trunk) is a common manifestation (Chap. 17). With a
lesion affecting a single root, sensory deficits may be minimal or absent
because adjacent root territories overlap extensively.
Isolated mononeuropathies may cause symptoms beyond the territory supplied by the affected nerve, but abnormalities on examination
typically are confined to expected anatomic boundaries. In multiple
mononeuropathies, symptoms and signs occur in discrete territories
supplied by different individual nerves and—as more nerves are
affected—may simulate a polyneuropathy if deficits become confluent.
With polyneuropathies, sensory deficits are generally graded, distal,
and symmetric in distribution (Chap. 446). Dysesthesias, followed
by numbness, begin in the toes and ascend symmetrically. When
dysesthesias reach the knees, they usually also have appeared in the
fingertips. The process is nerve length–dependent, and the deficit is
often described as “stocking glove” in type. Involvement of both hands
and feet also occurs with lesions of the upper cervical cord or the
brainstem, but an upper level of the sensory disturbance may then be
found on the trunk and other evidence of a central lesion may be present, such as sphincter involvement or signs of an upper motor neuron
lesion (Chap. 24). Although most polyneuropathies are pansensory
and affect all modalities of sensation, selective sensory dysfunction
according to nerve fiber size may occur. Small-fiber polyneuropathies
are characterized by burning, painful dysesthesias with reduced pinprick and thermal sensation but with sparing of proprioception, motor
function, and deep tendon reflexes. Touch is involved variably; when
it is spared, the sensory pattern is referred to as exhibiting sensory dissociation. Sensory dissociation may occur also with spinal cord lesions
(Chap. 442). Large-fiber polyneuropathies are characterized by vibration and position sense deficits, imbalance, absent tendon reflexes,
and variable motor dysfunction but preservation of most cutaneous
sensation. Dysesthesias, if present at all, tend to be tingling or bandlike
in quality.
Sensory neuronopathy (or ganglionopathy) is characterized by
widespread but asymmetric sensory loss occurring in a non-lengthdependent manner so that it may occur proximally or distally, and in
the arms, legs, or both. Pain and numbness progress to sensory ataxia
and impairment of all sensory modalities over time. This condition
is usually paraneoplastic or idiopathic in origin (Chaps. 94 and 445)
or related to an autoimmune disease, particularly Sjögren’s syndrome
(Chap. 361).
Spinal Cord (See also Chap. 442) If the spinal cord is transected,
all sensation is lost below the level of transection. Bladder and bowel
function also are lost, as is motor function. Lateral hemisection of the
spinal cord produces the Brown-Séquard syndrome, with absent pain
and temperature sensation contralaterally and loss of proprioceptive
sensation and power ipsilaterally below the lesion (see Figs. 25-1 and
442-1); ipsilateral pain or hyperesthesia may also occur.
Numbness or paresthesias in both feet may arise from a spinal cord
lesion; this is especially likely when the upper level of the sensory loss
extends to the trunk. When all extremities are affected, the lesion
is probably in the cervical region or brainstem unless a peripheral
neuropathy is responsible. The presence of upper motor neuron signs
(Chap. 24) supports a central lesion; a hyperesthetic band on the trunk
may suggest the level of involvement.
A dissociated sensory loss can reflect spinothalamic tract involvement in the spinal cord, especially if the deficit is unilateral and has
an upper level on the torso. Bilateral spinothalamic tract involvement
occurs with lesions affecting the center of the spinal cord, such as in
syringomyelia. There is a dissociated sensory loss with impairment of
pinprick and temperature appreciation but relative preservation of light
touch, position sense, and vibration appreciation.
Dysfunction of the posterior columns in the spinal cord or of the
posterior root entry zone may lead to a bandlike sensation around
the trunk or a feeling of tight pressure in one or more limbs. Flexion
173 Gait Disorders, Imbalance, and Falls CHAPTER 26
of the neck sometimes leads to an electric shock–like sensation that
radiates down the back and into the legs (Lhermitte’s sign) in patients
with a cervical lesion affecting the posterior columns, such as from
multiple sclerosis, cervical spondylosis, or following irradiation to the
cervical region.
Brainstem Crossed patterns of sensory disturbance, in which one
side of the face and the opposite side of the body are affected, localize to
the lateral medulla. Here a small lesion may damage both the ipsilateral
descending trigeminal tract and the ascending spinothalamic fibers
subserving the opposite arm, leg, and hemitorso (see “Lateral medullary syndrome” in Fig. 426-7). A lesion in the tegmentum of the pons
and midbrain, where the lemniscal and spinothalamic tracts merge,
causes pansensory loss contralaterally.
Thalamus Hemisensory disturbance with tingling numbness from
head to foot is often thalamic in origin but also can arise from the anterior parietal region. If abrupt in onset, the lesion is likely to be due to
a small stroke (lacunar infarction), particularly if localized to the thalamus. Occasionally, with lesions affecting the VPL nucleus or adjacent
white matter, a syndrome of thalamic pain, also called Déjerine-Roussy
syndrome, may ensue. The persistent, unrelenting unilateral pain often
is described in dramatic terms.
Cortex With lesions of the parietal lobe involving either the cortex
or subjacent white matter, the most prominent symptoms are contralateral hemineglect, hemi-inattention, and a tendency not to use the
affected hand and arm. On cortical sensory testing (e.g., two-point discrimination, graphesthesia), abnormalities are often found but primary
sensation is usually intact. Anterior parietal infarction may present as a
pseudothalamic syndrome with contralateral loss of primary sensation
from head to toe. Dysesthesias or a sense of numbness and, rarely, a
painful state may also occur.
Focal Sensory Seizures These seizures generally are due to lesions
in the area of the postcentral or precentral gyrus. The principal symptom of focal sensory seizures is tingling, but additional, more complex
sensations may occur, such as a rushing feeling, a sense of warmth, or a
sense of movement without detectable motion. Symptoms typically are
unilateral; commonly begin in the arm or hand, face, or foot; and often
spread in a manner that reflects the cortical representation of different
bodily parts, as in a Jacksonian march. Their duration is variable; seizures may be transient, lasting only for seconds, or persist for an hour
or more. Focal motor features may supervene, often becoming generalized with loss of consciousness and tonic-clonic jerking.
Psychogenic Symptoms Sensory symptoms may have a psychogenic basis. Such symptoms may be generalized or have an anatomic
boundary that is difficult to explain neurologically, for example, circumferentially at the groin or shoulder or around a specific joint. Pain
is common, but the nature and intensity of any sensory disturbances
are variable. The diagnosis should not be one of exclusion but based on
suggestive findings that are otherwise difficult to explain, such as midline splitting of impaired vibration, pinprick, or light touch appreciation; variability or poor reproducibility of sensory deficits; or normal
performance of tasks requiring sensory input that is seemingly abnormal on formal testing, such as good performance with eyes closed of
the finger-to-nose test despite an apparent loss of position sense in the
upper limb. The side with abnormal sensation may be confused when
the limbs are placed in an unusual position, such as crossed behind
the back. Sensory complaints should not be regarded as psychogenic
simply because they are unusual.
■ TREATMENT
Management is based on treatment of the underlying condition. Symptomatic treatment of acute and chronic pain is discussed in Chap. 13.
Dysesthesias, when severe and persistent, may respond to anticonvulsants (carbamazepine, 100–1000 mg/d; gabapentin, 300–3600 mg/d; or
pregabalin, 50–300 mg/d), antidepressants (amitriptyline, 25–150 mg/d;
nortriptyline, 25–150 mg/d; desipramine, 100–300 mg/d; or venlafaxine,
75–225 mg/d).
Acknowledgments
The editors acknowledge the contributions of Michael J. Aminoff to earlier
editions of this chapter.
■ FURTHER READING
Brazis P et al: Localization in Clinical Neurology, 7th ed. Philadelphia,
Lippincott William & Wilkins, 2016.
Campbell WW, Barohn RJ: DeJong’s the Neurologic Examination,
8th ed. Philadelphia, Wolters Kluwer, 2020.
Waxman S: Clinical Neuroanatomy, 29th ed. New York, McGraw Hill
Education, 2020.
PREVALENCE, MORBIDITY,
AND MORTALITY
Gait and balance problems are common in the elderly and contribute
to the risk of falls and injury. Gait disorders have been described in
15% of individuals aged >65. By age 80, one person in four will use
a mechanical aid to assist with ambulation. Among those aged ≥85,
the prevalence of gait abnormality approaches 40%. In epidemiologic
studies, gait disorders are consistently identified as a major risk factor
for falls and injury.
ANATOMY AND PHYSIOLOGY
An upright bipedal gait depends on the successful integration of postural control and locomotion. These functions are widely distributed in
the central nervous system. The biomechanics of bipedal walking are
complex, and the performance is easily compromised by a neurologic
deficit at any level. Command and control centers in the brainstem,
cerebellum, and forebrain modify the action of spinal pattern generators to promote stepping. While a form of “fictive locomotion” can
be elicited from quadrupedal animals after spinal transection, this
capacity is limited in primates. Step generation in primates is dependent on locomotor centers in the pontine tegmentum, midbrain, and
subthalamic region. Locomotor synergies are executed through the
reticular formation and descending pathways in the ventromedial
spinal cord. Cerebral control provides a goal and purpose for walking
and is involved in avoidance of obstacles and adaptation of locomotor
programs to context and terrain.
Postural control requires the maintenance of the center of mass
over the base of support through the gait cycle. Unconscious postural
adjustments maintain standing balance: long latency responses are
measurable in the leg muscles, beginning 110 milliseconds after a perturbation. Forward motion of the center of mass provides propulsive
force for stepping, but failure to maintain the center of mass within stability limits results in falls. The anatomic substrate for dynamic balance
has not been well defined, but the vestibular nucleus and midline cerebellum contribute to balance control in animals. Patients with damage
to these structures have impaired balance while standing and walking.
Standing balance depends on good-quality sensory information
about the position of the body center with respect to the environment, support surface, and gravitational forces. Sensory information
for postural control is primarily generated by the visual system, the
vestibular system, and proprioceptive receptors in the muscle spindles
and joints. A healthy redundancy of sensory afferent information is
generally available, but loss of two of the three pathways is sufficient to
compromise standing balance. Balance disorders in older individuals
26 Gait Disorders,
Imbalance, and Falls
Jessica M. Baker
174 PART 2 Cardinal Manifestations and Presentation of Diseases
sometimes result from multiple insults in the peripheral sensory systems (e.g., visual loss, vestibular deficit, peripheral neuropathy) that
critically degrade the quality of afferent information needed for balance stability.
Older patients with cognitive impairment appear to be particularly
prone to falls and injury. There is a growing body of literature on the
use of attentional resources to manage gait and balance. Walking is
generally considered to be unconscious and automatic, but the ability
to walk while attending to a cognitive task (dual-task walking) may be
compromised in the elderly. Older patients with deficits in executive
function may have particular difficulty in managing the attentional
resources needed for dynamic balance when distracted.
DISORDERS OF GAIT
Disorders of gait may be attributed to neurologic and nonneurologic
causes, although significant overlap often exists. The antalgic gait
results from avoidance of pain associated with weight bearing and is
commonly seen in osteoarthritis. Asymmetry is a common feature of
gait disorders due to contractures and other orthopedic deformities.
Impaired vision rounds out the list of common nonneurologic causes
of gait disorders.
Neurologic gait disorders are disabling and equally important to
address. The heterogeneity of gait disorders observed in clinical practice reflects the large network of neural systems involved in the task.
Walking is vulnerable to neurologic disease at every level. Gait disorders have been classified descriptively on the basis of abnormal physiology and biomechanics. One problem with this approach is that many
failing gaits look fundamentally similar. This overlap reflects common
patterns of adaptation to threatened balance stability and declining
performance. The gait disorder observed clinically must be viewed as
the product of a neurologic deficit and a functional adaptation. Unique
features of the failing gait are often overwhelmed by the adaptive
response. Some common patterns of abnormal gait are summarized
next. Gait disorders can also be classified by etiology (Table 26-1).
■ CAUTIOUS GAIT
The term cautious gait is used to describe the patient who walks with
an abbreviated stride, widened base, and lowered center of mass, as
if walking on a slippery surface. Arms are often held abducted. This
disorder is both common and nonspecific. It is, in essence, an adaptation to a perceived postural threat. There may be an associated fear of
falling. This disorder can be observed in more than one-third of older
TABLE 26-1 Prevalence of Neurologic Gait Disorders
NEUROLOGIC GAIT DISORDER NO. (%)a TOTAL NUMBERb CAUSES (NO.)
Single neurologic gait disorder 81 (69%)
Sensory ataxic 22 (18%) 46 Peripheral sensory neuropathy (46)
Parkinsonian 19 (16%) 34 Parkinson’s disease (18), drug-induced parkinsonism (8), dementia with
parkinsonism (4), parkinsonism (4)
Higher level 9 (8%) 31 Vascular encephalopathy (20), normal pressure hydrocephalus (1), severe
dementia (7), hypoxic ischemic encephalopathy (1), unknown (1)
Cerebellar ataxic 7 (6%) 10 Cerebellar stroke (3), cerebellar lesion due to multiple sclerosis (1), severe
essential tremor (3), postvaccinal cerebellitis (1), chronic alcohol abuse (1),
multiple system atrophy (1)
Cautious 7 (6%) 7 Idiopathic, associated fear of falling (7)
Paretic/hypotonic 6 (5%) 14 Neurogenic claudication (7), diabetic neuropathy (1), nerve lesion due to trauma or
surgery (4), distal paraparesis after Guillain-Barré syndrome (1), unknown (2)
Spastic 6 (5%) 7 Ischemic stroke (3), intracerebral hemorrhage (3), congenital (1)
Vestibular ataxic 4 (3%) 6 Bilateral vestibulopathy (3), recent vestribular neuronitis (1), recent Ménière’s
attack (1), acoustic neuroma with surgery (1)
Dyskinetic 1 (1%) 4 Levodopa-induced dyskinesia (3), chorea (1)
Multiple neurologic gait disorders 36 (30%)
Total 117
a
Percentage of individuals with a single gait disorder. b
Includes individuals with multiple gait disorders.
Note: Of 117 patients with a neurologic gait disorder, 81 had a single neurologic gait disorder; the remainder (36) had multiple neurologic gait disorders.
Source: Reproduced with modifications from P Mahlknecht et al: PLoS One 8:e69627, 2013.
patients with gait impairment. Physical therapy often improves walking
to the degree that follow-up observation may reveal a more specific
underlying disorder.
■ STIFF-LEGGED GAIT
Spastic gait is characterized by stiffness in the legs, an imbalance of
muscle tone, and a tendency to circumduct and scuff the feet. The
disorder reflects compromise of corticospinal command and overactivity of spinal reflexes. The patient may walk on the toes. In extreme
instances, the legs cross due to increased tone in the adductors
(“scissoring” gait). Upper motor neuron signs are present on physical
examination. The disorder may be cerebral or spinal in origin.
Myelopathy from cervical spondylosis is a common cause of spastic
or spastic-ataxic gait in the elderly. Demyelinating disease and trauma
are the leading causes of myelopathy in younger patients. In chronic
progressive myelopathy of unknown cause, a workup with laboratory
and imaging tests may establish a diagnosis. A structural lesion, such
as a tumor or a spinal vascular malformation, should be excluded with
appropriate testing. Spinal cord disorders are discussed in detail in
Chap. 442.
With cerebral spasticity, asymmetry is common, the upper extremities are usually involved, and dysarthria is often an associated feature.
Common causes include vascular disease (stroke), multiple sclerosis,
motor neuron disease, and perinatal nervous system injury (cerebral
palsy).
Other stiff-legged gaits include dystonia (Chap. 436) and stiff-person
syndrome (Chap. 94). Dystonia is a disorder characterized by sustained muscle contractions resulting in repetitive twisting movements
and abnormal posture. It often has a genetic basis. Dystonic spasms can
produce plantar flexion and inversion of the feet, sometimes with torsion of the trunk. In autoimmune stiff-person syndrome, exaggerated
lordosis of the lumbar spine and overactivation of antagonist muscles
restrict trunk and lower-limb movement and result in a wooden or
fixed posture.
■ PARKINSONISM, FREEZING GAIT, AND OTHER
MOVEMENT DISORDERSS
Parkinson’s disease (Chap. 435) is common, affecting 1% of the
population >65 years of age. The stooped posture, shuffling gait, and
decreased arm swing are characteristic and distinctive features. Patients
sometimes accelerate (festinate) with walking, display retropulsion,
or exhibit a tendency to turn en bloc. The step-to-step variability
175 Gait Disorders, Imbalance, and Falls CHAPTER 26
of the parkinsonian gait also contributes to falls, which are a major
source of morbidity, particularly later in the disease course. Dopamine
replacement improves step length, arm swing, turning speed, and gait
initiation. There is increasing evidence that deficits in cholinergic
circuits in the pedunculopontine nucleus and cortex contribute to the
gait disorder of Parkinson’s disease. Cholinesterase inhibitors such as
donepezil and rivastigmine have been shown in early studies to significantly decrease gait variability, instability, and fall frequency, even
in the absence of cognitive impairment, perhaps through improvement
in attention.
Freezing is defined as a brief, episodic absence of forward progression of the feet, despite the intention to walk. Freezing may be triggered
by approaching a narrow doorway or crowd, may be overcome by
visual cueing, and contributes to fall risk. Gait freezing is present in
approximately one-quarter of Parkinson’s patients within 5 years of
onset, and its frequency increases further over time. In treated patients,
end-of-dose gait freezing is a common problem that may improve with
more frequent administration of dopaminergic drugs or with use of
monoamine oxidase type B inhibitors such as rasagiline or selegiline
(Chap. 435).
Freezing of gait is also common in other neurodegenerative disorders associated with parkinsonism, including progressive supranuclear
palsy (PSP), multiple-system atrophy, and corticobasal degeneration.
Patients with these disorders frequently present with axial stiffness,
postural instability, and a shuffling, freezing gait while lacking the
characteristic pill-rolling tremor of Parkinson’s disease. The gait of PSP
is typically more erect compared with the stooped posture of typical
Parkinson’s disease, and falls within the first year also suggest the possibility of PSP. The gait of vascular parkinsonism tends to be broad-based
and shuffling with reduced arm swing bilaterally; disproportionate
involvement of gait early in the disease course differentiates this entity
from Parkinson’s disease.
Hyperkinetic movement disorders also produce characteristic and
recognizable disturbances in gait. In Huntington’s disease (Chap. 436),
the unpredictable occurrence of choreic movements gives the gait a
dancing quality. Tardive dyskinesia is the cause of many odd, stereotypic gait disorders seen in patients chronically exposed to antipsychotics and other drugs that block the D2
dopamine receptor. Orthostatic
tremor is a high-frequency, low-amplitude tremor predominantly
involving the lower extremities. Patients often report shakiness or
unsteadiness on standing and improvement with sitting or walking.
Falls are common. The tremor is often only appreciable by palpating
the legs while standing.
■ FRONTAL GAIT DISORDER
Frontal gait disorder, also known as higher-level gait disorder, is common in the elderly and has a variety of causes. The term is used to
describe a shuffling, freezing gait with imbalance, and other signs of
higher cerebral dysfunction. Typical features include a wide base of support, a short stride, shuffling along the floor, and difficulty with starts
and turns. Many patients exhibit a difficulty with gait initiation that is
descriptively characterized as the “slipping clutch” syndrome or gait ignition failure. The term lower-body parkinsonism is also used to describe
such patients. Strength is generally preserved, and patients are able to
make stepping movements when not standing and maintaining their
balance at the same time. This disorder is best considered a higher-level
motor control disorder, as opposed to an apraxia (Chap. 30), though
the term gait apraxia persists in the literature.
The most common cause of frontal gait disorder is vascular disease,
particularly subcortical small-vessel disease in the deep frontal white
matter and centrum ovale. Over three-quarters of patients with subcortical vascular dementia demonstrate gait abnormalities; decreased arm
swing and a stooped posture are particularly prevalent features. The clinical syndrome also includes dysarthria, pseudobulbar affect (emotional
disinhibition), increased tone, and hyperreflexia in the lower limbs.
Normal pressure (communicating) hydrocephalus (NPH) in adults
also presents with a similar gait disorder (Chap. 431). Other features
of the diagnostic triad (mental changes, incontinence) may be absent
in a substantial number of patients. MRI demonstrates ventricular
enlargement, an enlarged flow void about the aqueduct, periventricular
white matter change, and high-convexity tightness (disproportionate
widening of the sylvian fissures versus the cortical sulci). A lumbar
puncture or dynamic test is necessary to confirm a diagnosis of NPH.
Neurodegenerative dementias and mass lesions of the frontal lobes
cause a similar clinical picture and can be differentiated from vascular
disease and hydrocephalus by neuroimaging.
■ CEREBELLAR GAIT ATAXIA
Disorders of the cerebellum (Chap. 439) have a dramatic impact on
gait and balance. Cerebellar gait ataxia is characterized by a wide base
of support, lateral instability of the trunk, erratic foot placement, and
decompensation of balance when attempting to walk on a narrow base.
Difficulty maintaining balance when turning is often an early feature.
Patients are unable to walk tandem heel to toe and display truncal sway
in narrow-based or tandem stance. They show considerable variation
in their tendency to fall in daily life.
Causes of cerebellar ataxia in older patients include stroke, trauma,
tumor, and neurodegenerative disease such as multiple-system atrophy
(Chap. 440) and various forms of hereditary cerebellar degeneration
(Chap. 439). A short expansion at the site of the fragile X mutation
(fragile X premutation) has been associated with gait ataxia in older
men. Alcohol causes an acute and chronic cerebellar ataxia. In patients
with ataxia due to cerebellar degeneration, MRI demonstrates the
extent and topography of cerebellar atrophy.
■ SENSORY ATAXIA
As reviewed earlier in this chapter, balance depends on high-quality
afferent information from the visual and the vestibular systems and
proprioception. When this information is lost or degraded, balance
during locomotion is impaired and instability results. The sensory
ataxia of tabetic neurosyphilis is a classic example. The contemporary
equivalent is the patient with neuropathy affecting large fibers. Vitamin
B12 deficiency is a treatable cause of large-fiber sensory loss in the spinal
cord and peripheral nervous system. Joint position and vibration sense
are diminished in the lower limbs. The stance in such patients is destabilized by eye closure; they often look down at their feet when walking
and do poorly in the dark. Table 26-2 compares sensory ataxia with
cerebellar ataxia and frontal gait disorder.
TABLE 26-2 Features of Cerebellar Ataxia, Sensory Ataxia, and Frontal Gait Disorders
FEATURE CEREBELLAR ATAXIA SENSORY ATAXIA FRONTAL GAIT
Base of support Wide-based Narrow base, looks down Wide-based
Velocity Variable Slow Very slow
Stride Irregular, lurching Regular with path deviation Short, shuffling
Romberg test +/– Unsteady, falls +/–
Heel → shin Abnormal +/– Normal
Initiation Normal Normal Hesitant
Turns Unsteady +/– Hesitant, multistep
Postural instability + +++ ++++ Poor postural synergies rising from a chair
Falls Late event Frequent Frequent
176 PART 2 Cardinal Manifestations and Presentation of Diseases
■ NEUROMUSCULAR DISEASE
Patients with neuromuscular disease often have an abnormal gait,
occasionally as a presenting feature. With distal weakness (peripheral
neuropathy), the step height is increased to compensate for foot drop,
and the sole of the foot may slap on the floor during weight acceptance,
termed the steppage gait. Patients with myopathy or muscular dystrophy more typically exhibit proximal weakness. Weakness of the hip girdle may result in some degree of excess pelvic sway during locomotion.
The stooped posture of lumbar spinal stenosis ameliorates pain from
the compression of the cauda equina occurring with a more upright
posture while walking and may mimic early parkinsonism.
■ TOXIC AND METABOLIC DISORDERS
Chronic toxicity from medications and metabolic disturbances can
impair motor function and gait. Examination may reveal mental status
changes, asterixis, or myoclonus. Static equilibrium is disturbed, and
such patients are easily thrown off balance. Disequilibrium is particularly evident in patients with chronic renal disease and those with
hepatic failure, in whom asterixis may impair postural support. Sedative drugs, especially neuroleptics and long-acting benzodiazepines,
affect postural control and increase the risk for falls. These disorders
are especially important to recognize because they are often treatable.
■ FUNCTIONAL GAIT DISORDER
Functional neurologic disorders (formerly “psychogenic”) are common
in practice, and the presentation often involves gait. Sudden onset,
inconsistent deficits, waxing and waning course, incongruence of
symptoms with an organic lesion, and improvement with distraction
are key features. Phenomenology is variable; extreme slow motion,
an inappropriately overcautious gait, odd gyrations of posture with
wastage of muscular energy, astasia–abasia (inability to stand and
walk), bouncing, and foot stiffness (dystonia) have been described.
Falls are rare, and there are often discrepancies between examination
findings and the patient’s functional status. Preceding stress or trauma
is variably present, and its absence does not preclude the diagnosis of a
functional gait disorder. Functional gait disorders may be challenging
to diagnose and should be differentiated from the slowness and psychomotor retardation seen in certain patients with major depression.
APPROACH TO THE PATIENT
Slowly Progressive Disorder of Gait
When reviewing the history, it is helpful to inquire about the onset
and progression of disability. Initial awareness of an unsteady gait
often follows a fall. Stepwise evolution or sudden progression suggests vascular disease. Gait disorder may be associated with urinary
urgency and incontinence, particularly in patients with cervical
spine disease or hydrocephalus. It is always important to review the
use of alcohol and medications that affect gait and balance. Information on localization derived from the neurologic examination
can be helpful in narrowing the list of possible diagnoses.
Gait observation provides an immediate sense of the patient’s degree
of disability. Arthritic and antalgic gaits are recognized by observation,
although neurologic and orthopedic problems may coexist. Characteristic patterns of abnormality are sometimes seen, although, as stated
previously, failing gaits often look fundamentally similar. Cadence
(steps per minute), velocity, and stride length can be recorded by
timing a patient over a fixed distance. Watching the patient rise from a
chair provides a good functional assessment of balance.
Brain imaging studies may be informative in patients with an
undiagnosed disorder of gait. MRI is sensitive for cerebral lesions
of vascular or demyelinating disease and is a good screening test
for occult hydrocephalus. Patients with recurrent falls are at risk for
subdural hematoma. As mentioned earlier, many elderly patients
with gait and balance difficulty have white matter abnormalities
in the periventricular region and centrum semiovale. While these
lesions may be an incidental finding, a substantial burden of white
matter disease will ultimately impact cerebral control of locomotion.
DISORDERS OF BALANCE
■ DEFINITION, ETIOLOGY, AND MANIFESTATIONS
Balance is the ability to maintain equilibrium—a dynamic state in
which one’s center of mass is controlled with respect to the lower
extremities, gravity, and the support surface despite external perturbations. The reflexes required to maintain upright posture require input
from cerebellar, vestibular, and somatosensory systems; the premotor
cortex and corticospinal and reticulospinal tracts mediate output to
axial and proximal limb muscles. These responses are physiologically
complex, and the anatomic representation they entail is not well
understood. Failure can occur at any level and presents as difficulty
maintaining posture while standing and walking.
The history and physical examination may differentiate underlying
causes of imbalance. Patients with cerebellar ataxia do not generally
complain of dizziness, although balance is visibly impaired. Neurologic
examination reveals a variety of cerebellar signs. Postural compensation may prevent falls early on, but falls are inevitable with disease
progression. The progression of neurodegenerative ataxia is often measured by the number of years to loss of stable ambulation.
Vestibular disorders (Chap. 22) have symptoms and signs that
fall into three categories: (1) vertigo (the subjective inappropriate
perception or illusion of movement); (2) nystagmus (involuntary eye
movements); and (3) impaired standing balance. Not every patient has
all manifestations. Patients with vestibular deficits related to ototoxic
drugs may lack vertigo or obvious nystagmus, but their balance is
impaired on standing and walking, and they cannot navigate in the
dark. Laboratory testing is available to investigate vestibular deficits.
Somatosensory deficits also produce imbalance and falls. There is
often a subjective sense of insecure balance and fear of falling. Postural
control is compromised by eye closure (Romberg’s sign); these patients
also have difficulty navigating in the dark. A dramatic example is provided by the patient with autoimmune subacute sensory neuropathy,
which is sometimes a paraneoplastic disorder (Chap. 94). Compensatory strategies enable such patients to walk in the virtual absence of
proprioception, but the task requires active visual monitoring.
Patients with higher-level disorders of equilibrium have difficulty
maintaining balance in daily life and may present with falls. Their
awareness of balance impairment may be reduced. Patients taking
sedating medications are in this category.
■ FALLS
Falls are common in the elderly; over one-third of people aged >65 who
are living in the community fall each year. This number is even higher
in nursing homes and hospitals. Elderly people are not only at higher
risk for falls but are also more likely to suffer serious complications due
to medical comorbidities such as osteoporosis. Hip fractures result in
hospitalization, can lead to nursing home admission, and are associated with an increased mortality risk in the subsequent year. Falls may
result in brain or spinal injury, the history of which may be difficult
for the patient to provide. The proportion of spinal cord injuries due
to falls in individuals aged >65 years has doubled in the past decade,
perhaps due to increasing activity in this age group. Some falls result in
a prolonged time lying on the ground; fractures and CNS injury are a
particular concern in this context.
For each person who is physically disabled, there are others whose
functional independence is limited by anxiety and fear of falling.
Nearly one in five elderly individuals voluntarily restricts his or her
activity because of fear of falling. With loss of ambulation, the quality
of life diminishes, and rates of morbidity and mortality increase.
■ RISK FACTORS FOR FALLS
Risk factors for falls may be intrinsic (e.g., gait and balance disorders)
or extrinsic (e.g., polypharmacy, environmental factors); some risk factors are modifiable. The presence of multiple risk factors is associated
with a substantially increased risk of falls. Table 26-3 summarizes a
meta-analysis of studies establishing the principal risk factors for falls.
Polypharmacy (use of four or more prescription medications) has also
been identified as an important risk factor.
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