Muscle bulk generally is not affected by upper motor neuron lesions,
24 Neurologic Causes of
Weakness and Paralysis
Stephen L. Hauser
Normal motor function involves integrated muscle activity that is mod-
ulated by the activity of the cerebral cortex, basal ganglia, cerebellum,
red nucleus, brainstem reticular formation, lateral vestibular nucleus,
and spinal cord. Motor system dysfunction leads to weakness or paral-
ysis, discussed in this chapter, or to ataxia (Chap. 439) or abnormal
movements (Chap. 436). Weakness is a reduction in the power that
can be exerted by one or more muscles. It must be distinguished from
increased fatigability (i.e., the inability to sustain the performance of
an activity that should be normal for a person of the same age, sex,
and size), limitation in function due to pain or articular stiffness, or
impaired motor activity because severe proprioceptive sensory loss pre-
vents adequate feedback information about the direction and power of
movements. It is also distinct from bradykinesia (in which increased
time is required for full power to be exerted) and apraxia, a disorder
of planning and initiating a skilled or learned movement unrelated to a
significant motor or sensory deficit (Chap. 30).
Paralysis or the suffix “-plegia” indicates weakness so severe that a
muscle cannot be contracted at all, whereas paresis refers to less severe
weakness. The prefix “hemi-” refers to one-half of the body, “para-” to
both legs, and “quadri-” to all four limbs.
The distribution of weakness helps to localize the underlying lesion.
Weakness from involvement of upper motor neurons occurs particu-
larly in the extensors and abductors of the upper limb and the flexors
of the lower limb. Lower motor neuron weakness depends on whether
involvement is at the level of the anterior horn cells, nerve root, limb
plexus, or peripheral nerve—only muscles supplied by the affected
structure are weak. Myopathic weakness is generally most marked in
proximal muscles. Weakness from impaired neuromuscular transmis-
sion has no specific pattern of involvement.
Weakness often is accompanied by other neurologic abnormalities
that help indicate the site of the responsible lesion (Table 24-1).
Tone is the resistance of a muscle to passive stretch. Increased tone
may be of several types. Spasticity is the increase in tone associated with
disease of upper motor neurons. It is velocity dependent, has a sudden
release after reaching a maximum (the “clasp-knife” phenomenon),
and predominantly affects the antigravity muscles (i.e., upper-limb
flexors and lower-limb extensors). Rigidity is hypertonia that is present
throughout the range of motion (a “lead pipe” or “plastic” stiffness) and
affects flexors and extensors equally; it sometimes has a cogwheel qual-
ity that is enhanced by voluntary movement of the contralateral limb
(reinforcement). Rigidity occurs with certain extrapyramidal disorders,
such as Parkinson’s disease. Paratonia (or gegenhalten) is increased tone
that varies irregularly in a manner seemingly related to the degree of
relaxation, is present throughout the range of motion, and affects flex-
ors and extensors equally; it usually results from disease of the frontal
lobes. Weakness with decreased tone (flaccidity) or normal tone occurs
with disorders of motor units. A motor unit consists of a single lower
motor neuron and all the muscle fibers that it innervates.
TABLE 24-1 Signs That Distinguish the Origin of Weakness
SIGN UPPER MOTOR NEURON LOWER MOTOR NEURON
Atrophy None Severe
Fasciculations None Common
Tone Spastic Decreased
Distribution of weakness Pyramidal/regional Distal/segmental
Muscle stretch reflexes Hyperactive Hypoactive/absent
Babinski sign Present Absent
165
although mild disuse atrophy eventually may occur. By contrast, atro-
phy is often conspicuous when a lower motor neuron lesion is respon-
sible for weakness and also may occur with advanced muscle disease.
Muscle stretch (tendon) reflexes are usually increased with upper
motor neuron lesions but may be decreased or absent for a variable
period immediately after onset of an acute lesion. Hyperreflexia is
usually—but not invariably—accompanied by loss of cutaneous reflexes
(such as superficial abdominals; Chap. 422) and, in particular, by an
extensor plantar (Babinski) response. The muscle stretch reflexes are
depressed with lower motor neuron lesions directly involving specific
CHAPTER 24 Neurologic Causes of Weakness and Paralysis
reflex arcs. They generally are preserved in patients with myopathic
weakness except in advanced stages, when they sometimes are atten-
uated. In disorders of the neuromuscular junction, reflex responses
may be affected by preceding voluntary activity of affected muscles;
such activity may lead to enhancement of initially depressed reflexes in
Lambert-Eaton myasthenic syndrome and, conversely, to depression of
initially normal reflexes in myasthenia gravis (Chap. 448).
The distinction of neuropathic (lower motor neuron) from myo-
pathic weakness is sometimes difficult clinically, although distal weak-
ness is likely to be neuropathic, and symmetric proximal weakness
myopathic. Fasciculations (visible or palpable twitches within a muscle
due to the spontaneous discharge of a motor unit) and early atrophy
indicate that weakness is neuropathic.
■ PATHOGENESIS
Upper Motor Neuron Weakness Lesions of the upper motor
neurons or their descending axons to the spinal cord (Fig. 24-1) pro-
duce weakness through decreased activation of lower motor neurons.
In general, distal muscle groups are affected more severely than prox-
imal ones, and axial movements are spared unless the lesion is severe
and bilateral. Spasticity is typical but may not be present acutely. Rapid
repetitive movements are slowed and coarse, but normal rhythmicity is
maintained. With corticobulbar involvement, weakness occurs in the
lower face and tongue; extraocular, upper facial, pharyngeal, and jaw
muscles are typically spared. Bilateral corticobulbar lesions produce a
pseudobulbar palsy: dysarthria, dysphagia, dysphonia, and emotional
lability accompany bilateral facial weakness and a brisk jaw jerk.
Electromyogram (EMG) (Chap. 446) shows that with weakness of the
upper motor neuron type, motor units have a diminished maximal
discharge frequency.
Lower Motor Neuron Weakness This pattern results from dis-
orders of lower motor neurons in the brainstem motor nuclei and the
anterior horn of the spinal cord or from dysfunction of the axons of
these neurons as they pass to skeletal muscle (Fig. 24-2). Weakness is
due to a decrease in the number of muscle fibers that can be activated
through a loss of α motor neurons or disruption of their connections to
muscle. Loss of γ motor neurons does not cause weakness but decreases
tension on the muscle spindles, which decreases muscle tone and atten-
uates the stretch reflexes. An absent stretch reflex suggests involvement
of spindle afferent fibers.
When a motor unit becomes diseased, especially in anterior horn
cell diseases, it may discharge spontaneously, producing fasciculations.
When α motor neurons or their axons degenerate, the denervated
muscle fibers also may discharge spontaneously. These single muscle
MYOPATHIC PSYCHOGENIC
Mild None
None None
Normal/decreased Variable/paratonia
Proximal Variable/inconsistent with daily
activities
Normal/hypoactive Normal
Absent Absent
 166
Corticospinal

Sh Trunk
der
Hip
Afferent

Wr ow
tract

oul

Fin st
Elb
neuron

um s
Knee

i
Th ger
b
ck
Ankle Ne
Brow
Toes
Eyelid
Nares
Lips
Tongue
Larynx
γ
α

Alpha and gamma

PART 2

motor neurons

Red nucleus
Reticular nuclei
Cardinal Manifestations and Presentation of Diseases

Motor end plates on

Vestibular nuclei voluntary muscle
Vestibulospinal tract Rubrospinal tract (extrafusal fibers)

Lateral corticospinal
Reticulospinal tract tract
Lateral
corticospinal tract
Rubrospinal
(ventrolateral)
tract
Ventromedial
bulbospinal
tracts
FIGURE 24-1 The corticospinal and bulbospinal upper motor neuron pathways.
Upper motor neurons have their cell bodies in layer V of the primary motor cortex
(the precentral gyrus, or Brodmann area 4) and in the premotor and supplemental
motor cortex (area 6). The upper motor neurons in the primary motor cortex
are somatotopically organized (right side of figure). Axons of the upper motor
neurons descend through the subcortical white matter and the posterior limb of
the internal capsule. Axons of the pyramidal or corticospinal system descend
through the brainstem in the cerebral peduncle of the midbrain, the basis pontis,
and the medullary pyramids. At the cervicomedullary junction, most corticospinal
axons decussate into the contralateral corticospinal tract of the lateral spinal
cord, but 10–30% remain ipsilateral in the anterior spinal cord. Corticospinal
neurons synapse on premotor interneurons, but some—especially in the cervical
enlargement and those connecting with motor neurons to distal limb muscles—
make direct monosynaptic connections with lower motor neurons. They innervate
most densely the lower motor neurons of hand muscles and are involved in
the execution of learned, fine movements. Corticobulbar neurons are similar to
corticospinal neurons but innervate brainstem motor nuclei. Bulbospinal upper
motor neurons influence strength and tone but are not part of the pyramidal system.
The descending ventromedial bulbospinal pathways originate in the tectum of the
midbrain (tectospinal pathway), the vestibular nuclei (vestibulospinal pathway), and
the reticular formation (reticulospinal pathway). These pathways influence axial and
proximal muscles and are involved in the maintenance of posture and integrated
movements of the limbs and trunk. The descending ventrolateral bulbospinal
pathways, which originate predominantly in the red nucleus (rubrospinal pathway),
facilitate distal limb muscles. The bulbospinal system sometimes is referred to as
the extrapyramidal upper motor neuron system. In all figures, nerve cell bodies and
axon terminals are shown, respectively, as closed circles and forks.
fiber discharges, or fibrillation potentials, cannot be seen but can be
recorded with EMG. Weakness leads to delayed or reduced recruit-
ment of motor units, with fewer than normal activated at a particular
discharge frequency.
Neuromuscular Junction Weakness Disorders of the neuro-
muscular junction produce weakness of variable degree and distribu-
tion. The number of muscle fibers that are activated varies over time,
depending on the state of rest of the neuromuscular junctions. Strength
Muscle spindle
(intrafusal fibers)
FIGURE 24-2 Lower motor neurons are divided into ` and f types. The larger α
motor neurons are more numerous and innervate the extrafusal muscle fibers of
the motor unit. Loss of α motor neurons or disruption of their axons produces lower
motor neuron weakness. The smaller, less numerous γ motor neurons innervate
the intrafusal muscle fibers of the muscle spindle and contribute to normal tone
and stretch reflexes. The α motor neuron receives direct excitatory input from
corticomotoneurons and primary muscle spindle afferents. The α and γ motor
neurons also receive excitatory input from other descending upper motor neuron
pathways, segmental sensory inputs, and interneurons. The α motor neurons
receive direct inhibition from Renshaw cell interneurons, and other interneurons
indirectly inhibit the α and γ motor neurons. A muscle stretch (tendon) reflex
requires the function of all the illustrated structures. A tap on a tendon stretches
muscle spindles (which are tonically activated by γ motor neurons) and activates
the primary spindle afferent neurons. These neurons stimulate the α motor neurons
in the spinal cord, producing a brief muscle contraction, which is the familiar tendon
reflex.
is influenced by preceding activity of the affected muscle. In myasthe-
nia gravis, for example, sustained or repeated contractions of affected
muscle decline in strength despite continuing effort (Chap. 440). Thus,
fatigable weakness is suggestive of disorders of the neuromuscular
junction, which cause functional loss of muscle fibers due to failure of
their activation.
Myopathic Weakness Myopathic weakness is produced by a
decrease in the number or contractile force of muscle fibers acti-
vated within motor units. With muscular dystrophies, inflammatory
myopathies, or myopathies with muscle fiber necrosis, the number of
muscle fibers is reduced within many motor units. On EMG, the size
of each motor unit action potential is decreased, and motor units must
be recruited more rapidly than normal to produce the desired power.
Some myopathies produce weakness through loss of contractile force
of muscle fibers or through relatively selective involvement of type II
(fast) fibers. These myopathies may not affect the size of individual
motor unit action potentials and are detected by a discrepancy between
the electrical activity and force of a muscle.
Psychogenic Weakness Weakness may occur without a recog-
nizable organic basis. It tends to be variable, inconsistent, and with a
pattern of distribution that cannot be explained on a neuroanatomic
basis. On formal testing, antagonists may contract when the patient is
supposedly activating the agonist muscle. The severity of weakness is
out of keeping with the patient’s daily activities.
■ DISTRIBUTION OF WEAKNESS
Hemiparesis Hemiparesis results from an upper motor neuron
lesion above the midcervical spinal cord; most such lesions are above
the foramen magnum. The presence of other neurologic deficits helps
localize the lesion. Thus language disorders, for example, point to a
cortical lesion. Homonymous visual field defects reflect either a corti-
cal or a subcortical hemispheric lesion. A “pure motor” hemiparesis of
the face, arm, and leg often is due to a small, discrete lesion in the pos-
terior limb of the internal capsule, cerebral peduncle in the midbrain,
or upper pons. Some brainstem lesions produce “crossed paralyses,”
consisting of ipsilateral cranial nerve signs and contralateral hemipa-
resis (Chap. 426). The absence of cranial nerve signs or facial weak-
ness suggests that a hemiparesis is due to a lesion in the high cervical
spinal cord, especially if associated with Brown-Séquard syndrome,
consisting of loss of joint position and vibration sense on the side of
the weakness, and loss of pain and temperature sense on the opposite
side (Chap. 442).
Acute or episodic hemiparesis usually results from focal structural
lesions, particularly vascular etiologies, rapidly expanding lesions, or
an inflammatory process. Subacute hemiparesis that evolves over days
or weeks may relate to subdural hematoma, infectious or inflamma-
tory disorders (e.g., cerebral abscess, fungal granuloma or meningitis,
parasitic infection, multiple sclerosis, sarcoidosis), or primary or meta-
static neoplasms. AIDS may present with subacute hemiparesis due to
toxoplasmosis or primary central nervous system (CNS) lymphoma.
Chronic hemiparesis that evolves over months usually is due to a neo-
plasm or vascular malformation, a chronic subdural hematoma, or a
degenerative disease.
Investigation of hemiparesis (Fig. 24-3) of acute origin usually starts
with a CT scan of the brain and laboratory studies. If the CT is normal,
or in subacute or chronic cases of hemiparesis, MRI of the brain and/or
cervical spine (including the foramen magnum) is performed, depend-
ing on the clinical accompaniments.
Paraparesis Acute paraparesis is caused most commonly by an
intraspinal lesion, but its spinal origin may not be recognized initially
if the legs are flaccid and areflexic. Usually, however, there is sensory
loss in the legs with an upper level on the trunk; a dissociated sensory
loss (loss of pain and temperature but not touch, position, and vibra-
tion sense) suggestive of a central cord syndrome; or hyperreflexia in
the legs with normal reflexes in the arms (Chap. 442). Imaging the
DISTRIBUTION OF WEAKNESS
Hemiparesis Paraparesis Quadriparesis Monoparesis Distal
Alert
UMN signs LMN signs* Yes No UMN signs
Cerebral signs
Yes No
UMN signs LMN signs*
EMG and NCS
UMN pattern LMN pattern
Anterior horn,
Brain CT
or MRI
† Spinal MRI
‡
root, or peripheral
nerve disease
* or signs of myopathy
†
If no abnormality detected, consider spinal MRI.
‡
If no abnormality detected, consider myelogram or brain MRI.
FIGURE 24-3 An algorithm for the initial workup of a patient with weakness. CT, computed tomography; EMG, studies to determine the level of muscle
electromyography; LMN, lower motor neuron; MRI, magnetic resonance imaging; NCS, nerve conduction studies; enzymes and electrolytes and with EMG
UMN, upper motor neuron.
spinal cord (Fig. 24-3) may reveal compressive lesions, infarction (pro- 167
prioception usually is spared), arteriovenous fistulas or other vascular
anomalies, or transverse myelitis (Chap. 442).
Diseases of the cerebral hemispheres that produce acute parapare-
sis include anterior cerebral artery ischemia (shoulder shrug also is
affected), superior sagittal sinus or cortical venous thrombosis, and
acute hydrocephalus.
Paraparesis may also result from a cauda equina syndrome, for
example, after trauma to the low back, a midline disk herniation, or
an intraspinal tumor. The sphincters are commonly affected, whereas
hip flexion often is spared, as is sensation over the anterolateral thighs.
CHAPTER 24 Neurologic Causes of Weakness and Paralysis
Rarely, paraparesis is caused by a rapidly evolving anterior horn cell
disease (such as poliovirus or West Nile virus infection), peripheral
neuropathy (such as Guillain-Barré syndrome; Chap. 447), or myop-
athy (Chap. 449).
Subacute or chronic spastic paraparesis is caused by upper motor
neuron disease. When associated with lower-limb sensory loss and
sphincter involvement, a chronic spinal cord disorder should be con-
sidered (Chap. 442). If hemispheric signs are present, a parasagittal
meningioma or chronic hydrocephalus is likely. The absence of spas-
ticity in a long-standing paraparesis suggests a lower motor neuron or
myopathic etiology.
Investigations typically begin with spinal MRI, but when upper
motor neuron signs are associated with drowsiness, confusion, sei-
zures, or other hemispheric signs, brain MRI should also be performed,
sometimes as the initial investigation. Electrophysiologic studies are
diagnostically helpful when clinical findings suggest an underlying
neuromuscular disorder.
Quadriparesis or Generalized Weakness Generalized weakness
may be due to disorders of the CNS or the motor unit. Although the terms
often are used interchangeably, quadriparesis is commonly used when
an upper motor neuron cause is suspected, and generalized weakness is
used when a disease of the motor units is likely. Weakness from CNS
disorders usually is associated with changes in consciousness or cognition
and accompanied by spasticity, hyperreflexia, and sensory disturbances.
Most neuromuscular causes of generalized
weakness are associated with normal men-
tal function, hypotonia, and hypoactive
muscle stretch reflexes. The major causes
of intermittent weakness are listed in
Proximal Restricted Table 24-2. A patient with generalized
fatigability without objective weakness
may have chronic fatigue syndrome
(Chap. 450).
ACUTE QUADRIPARESIS Quadriparesis
LMN signs* with onset over minutes may result from
disorders of upper motor neurons (such
as from anoxia, hypotension, brainstem or
cervical cord ischemia, trauma, and sys-
temic metabolic abnormalities) or muscle
(electrolyte disturbances, certain inborn
errors of muscle energy metabolism, tox-
ins, and periodic paralyses). Onset over
hours to weeks may, in addition to these
disorders, be due to lower motor neu-
ron disorders such as Guillain-Barré syn-
Myopathic pattern
drome (Chap. 447).
In obtunded patients, evaluation
Muscle or begins with a CT or MRI scan of the
neuromuscular brain. If upper motor neuron signs are
junction disease present but the patient is alert, the initial
test is usually an MRI of the cervical
cord. If weakness is lower motor neu-
ron, myopathic, or uncertain in origin,
the clinical approach begins with blood
and nerve conduction studies.
 168
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
PART 2
a. Transient ischemic attacks of the brainstem
b. Transient global cerebral ischemia
c. Multiple sclerosis
5. Lack of voluntary effort
Cardinal Manifestations and Presentation of Diseases
a. Anxiety
b. Pain or discomfort
c. Somatization disorder
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 sub-
dural hematomas, and various metabolic, toxic, and infectious disor-
ders. 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, evalua-
tion 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 usu-
ally be distinguished clinically, and imaging is directed first at the clin-
ically 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 impair-
ment 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 indi-
cated. 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 sug-
gests lower motor neuron or peripheral nerve disease. Acute distal
lower-limb weakness results occasionally from an acute toxic polyneu-
ropathy 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 weak-
ness 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 dis-
ease, 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 fre-
quently 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 sym-
metric weakness with fatigue is characteristic of neuromuscular junc-
tion 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 Ner-
vous System, 4th ed. Edinburgh, Saunders, 2000.
25 Numbness, Tingling,
and Sensory Loss
Stephen L. Hauser
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,
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 periph-
eral or central sensory pathway. The nature and severity of the abnor-
mal 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 unno-
ticed 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 abnor-
mal 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 stim-
ulus, 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 exami-
nation 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 opti-
mally 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
deformation of the skin or stretch of muscles). Each type of receptor 169
has its own set of sensitivities to specific stimuli, size and distinctness
of receptive fields, and adaptational qualities.
Afferent peripheral nerve fibers conveying somatosensory informa-
tion 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, temper-
CHAPTER 25 Numbness, Tingling, and Sensory Loss
ature 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 syn-
apse 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 pri-
mary sensation (pain, touch, vibration, joint position, and thermal
sensation) (Table 25-1). The examiner must depend on patient
responses, and this complicates interpretation. Further, examina-
tion 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 exam-
iner 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
 170
Leg
Trunk Post-central
cortex

Arm
Thalamus

Face
PART 2

Internal
capsule
Ventral
Cardinal Manifestations and Presentation of Diseases

posterolateral
nucleus of
thalamus

MIDBRAIN

Principal sensory PONS

nucleus of V
Medial lemniscus

Nucleus of
funiculus gracilis
Nucleus of
funiculus cuneatus MEDULLA
Spinothalamic tract
Nucleus of
spinal tract V
Posterior column
fibers

SPINAL CORD

Spinothalamic tract

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.)

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 recep-
tors respond to each. Touch usually is tested with a wisp of cotton,

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 Large and small Lem, also D and SpTh
naked endings
Vibration Tuning fork, 128 Hz Mechanoreceptors, especially pacinian Large Lem, also D
corpuscles
Joint position Passive movement of specific Joint capsule and tendon endings, Large Lem, also D
joints muscle spindles
Abbreviations: D, diffuse ascending projections in ipsilateral and contralateral anterolateral columns; Lem, posterior column and lemniscal projection, ipsilateral; SpTh,
spinothalamic projection, contralateral.
 171
I
Greater
Lesser n. } occipital nerves

II Great auricular n.
Great auricular n.

III Ant. cut. n. of neck

Ant. cut. n. of neck
C5
C6 T1 Supraclavicular n’s.
Supraclavicular n’s. T2
Post.
Axillary n. 3
Axillary n. cut.
T2 (circumflex) 4
(circumflex) rami Lat. Med. cut. n. of arm
Ant. 3 5
of cut. & intercostobrachial n.
4 Med. cut. n. of arm 6
Post cut. n. of arm thor.rami

CHAPTER 25 Numbness, Tingling, and Sensory Loss

cut. 5 & intercostobrachial n. 7
Lower lat. cut. n. of arm Lat. (from radial n.) n’s.
6 8
(from radial n.) rami Post. cut. n. of forearm
9
7 Lower 10 (from radial n.)
of L1
cut. 8 Lat. cut. of arm 11
thor. (from radial n.) 12 Med. Lat. cut. n. of forearm
9 Med. cut. n. (from musculocut n.)
Lat. cut. of forearm of forearm S1 cut. n.
(from musculocut. n.) n’s. 10 Post. rami of
rami of
11 Iliohypo- lumbar sacral forearm Radial n.
12 gastric n. & coccygeal n’s.
Iliohypo- Radial n.
Ilio- Ulnar n.
gastric n.
inguinal n. Inf. med.
Median n. cluneal n. Inf. lat.
Femoral Genital
branch branch of cluneal n’s.
of genito- genitofem. Inf. med. n. of thigh Median n.
femoral n. n.
Ulnar n.
(lumbo-inguinal n.) Obturator n.
Dorsal n. of penis Post cut. n. of thigh
Lat. cut. n. of thigh
Intermed. & med. cut. n’s. Scrotal branch of perineal n. Med. cut. n. of thigh
of thigh (from femoral n.) (from femoral n.)
Lat. cut. n.of calf
Obturator n. (from common femoral n.)
Saphenous n. Lat. plantar n.
(from femoral n.) Lat. cut. n. of calf Saphenous n. Med.
(from common peroneal n.) plantar n. Lat.
(from femoral n.) plantar n.
Superficial
peroneal
Superficial peroneal n. n.
(from common peroneal n.)
Deep peroneal n. Superficial peroneal n. Saphenous n.
(from common peroneal n.) (from common peroneal n.) Sural n. (from tibial n.) Calcanean branches
of tibial & sural n’s. Sural n.

Sural n. Calcanean branches of

Med. & lat. plantar n’s.
(from posttibial n.) (from tibial n.) sural & tibial n’s.

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.)

C2
minimizing pressure on the skin. In general, it is better to avoid
testing touch on hairy skin because of the profusion of the sensory
C3
endings that surround each hair follicle. The patient is tested with
C3 the eyes closed and should respond as soon as the stimulus is per-
C4
T2 C4
ceived, indicating its location.
C5
T2
T4 Joint position testing is a measure of proprioception. With the
T4 T6 patient’s eyes closed, joint position is tested in the distal inter-
T6 T8
T2
C5
phalangeal joint of the great toe and fingers. The digit is held
T8 T10 by its sides, distal to the joint being tested, and moved passively
T1 T10 T12 T1 while more proximal joints are stabilized—the patient indicates the
C6 L1
L
L3 2
C6 change in position or direction of movement. If errors are made,
T12
S1 C8 more proximal joints are tested. A test of proximal joint position
S2
C7 C8
L1
sense, primarily at the shoulder, is performed by asking the patient
S5 S4
S3 C7 to bring the two index fingers together with arms extended and
L2 eyes closed. Normal individuals can do this accurately, with errors
of 1 cm or less.
L3
S2
The sense of vibration is tested with an oscillating tuning fork
L3 that vibrates at 128 Hz. Vibration is tested over bony points, begin-
L4
ning 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
L5 L4
the hands, it is tested dorsally at the distal phalanx of the fingers. If
L5
abnormalities are found, more proximal sites should be examined.
Vibratory thresholds at the same site in the patient and the exam-
iner may be compared for control purposes.
S1
L5
S1
CORTICAL SENSATION
The most commonly used tests of cortical function are two-point
FIGURE 25-3 Distribution of the sensory spinal roots on the surface of the body discrimination, touch localization, and bilateral simultaneous stim-
(dermatomes). (Reproduced with permission from D Sinclair: Mechanisms of ulation, and tests for graphesthesia and stereognosis. Abnormalities
Cutaneous Sensation. Oxford, UK, Oxford University Press, 1981 through PLS Clear.)
 172
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 nor-
mal individual can distinguish about a 3-mm separation of points.
PART 2
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. Bilat-
eral simultaneous stimulation at analogous sites (e.g., the dorsum of
both hands) can be carried out to determine whether the percep-
Cardinal Manifestations and Presentation of Diseases
tion 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. Quan-
titative 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 evalu-
ate 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 ace-
tazolamide. 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 one-
half 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 abnor-
malities are readily mapped and generally have discrete boundaries
(Figs. 25-2 and 25-3). Root (“radicular”) lesions frequently are accom-
panied 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 terri-
tory 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 pres-
ent, 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 pin-
prick 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 dis-
sociation. Sensory dissociation may occur also with spinal cord lesions
(Chap. 442). Large-fiber polyneuropathies are characterized by vibra-
tion 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-length-
dependent 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 involve-
ment 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
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 medul-
lary 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 ante-
rior parietal region. If abrupt in onset, the lesion is likely to be due to
a small stroke (lacunar infarction), particularly if localized to the thal-
amus. 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 con-
tralateral hemineglect, hemi-inattention, and a tendency not to use the
affected hand and arm. On cortical sensory testing (e.g., two-point dis-
crimination, 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 symp-
tom 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; sei-
zures may be transient, lasting only for seconds, or persist for an hour
or more. Focal motor features may supervene, often becoming general-
ized with loss of consciousness and tonic-clonic jerking.
Psychogenic Symptoms Sensory symptoms may have a psycho-
genic basis. Such symptoms may be generalized or have an anatomic
boundary that is difficult to explain neurologically, for example, cir-
cumferentially 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 mid-
line splitting of impaired vibration, pinprick, or light touch apprecia-
tion; variability or poor reproducibility of sensory deficits; or normal
performance of tasks requiring sensory input that is seemingly abnor-
mal 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. Symp-
tomatic treatment of acute and chronic pain is discussed in Chap. 13.
Dysesthesias, when severe and persistent, may respond to anticonvul-
sants (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 173
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.
CHAPTER 26 Gait Disorders, Imbalance, and Falls
26 Gait Disorders,
Imbalance, and Falls
Jessica M. Baker
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 pos-
tural 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 gener-
ators 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 depen-
dent 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 per-
turbation. Forward motion of the center of mass provides propulsive
force for stepping, but failure to maintain the center of mass within sta-
bility limits results in falls. The anatomic substrate for dynamic balance
has not been well defined, but the vestibular nucleus and midline cere-
bellum 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 environ-
ment, 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