(17) Nervous System Flashcards
Guiding Questions for Examination of the
Nervous System
Does the patient have neurologic disease?
● If so, what is the localization of the lesion or lesions? Are your findings symmetric?
● What is the pathophysiology of abnormal findings?
● What is the preliminary differential diagnosis?
4 brain regions
the cerebrum, the diencephalon, the
brainstem, and the cerebellum.
Each cerebral hemisphere is subdivided into
frontal, parietal, temporal, and occipital lobes.
The central nervous system (CNS) of the brain is
a vast network of interconnecting
nerve cells, or neurons, consisting of cell bodies and their axons—single long
fibers that conduct impulses to other parts of the nervous system
Brain tissue may be
gray
white
Gray matter
consists of aggregations of neuronal
cell bodies. It rims the surfaces of the cerebral hemispheres, forming the
cerebral cortex.
Deep in the brain lie additional clusters of gray matter (Fig. 17-2). These include
the basal ganglia, which affect movement, and the thalamus and the hypothalamus
structures in the diencephalon
White matter
consists of neuronal axons that are coated with
myelin. The myelin sheaths, which create the white color, allow nerve impulses
to travel more rapidly.
Thalamus
processes sensory impulses
and relays them to the cerebral cortex.
hypothalamus
maintains homeostasis and regulates temperature, heart rate, and blood pressure. The hypothalamus
affects the endocrine system and governs emotional behaviors such as anger and
sexual drive. Hormones secreted in the hypothalamus act directly on the pituitary
gland.
The internal capsule
is a white-matter structure where myelinated fibers converge
from all parts of the cerebral cortex and descend into the brainstem.
Brainstem
which connects the upper part of the brain with the spinal cord, has three sections:
the midbrain, the pons, and the medulla.
Consciousness relies on the interaction between
intact cerebral hemispheres and
a structure in the diencephalon and upper brainstem, the reticular activating
(arousal) system.
cerebellum,
which lies at the base of the brain, coordinates all movement and
helps maintain the body upright in space.
Spinal Cord
Below the medulla, the CNS extends into
the elongated spinal cord, encased within the bony vertebral column
and terminating at the first or second lumbar vertebra. The cord
provides a series of segmental relays with the periphery, serving as a
conduit for information flow to and from the brain. The motor and
sensory nerve pathways relay neural signals that enter and exit the
cord through posterior and anterior nerve roots and the spinal and
peripheral nerves.
The spinal cord is divided into segments: cervical, from C1 to C8;
thoracic, from T1 to T12; lumbar, from L1 to L5; sacral, from S1 to
S5; and coccygeal (Fig. 17-3). The spinal cord is thickest in the
cervical segment, which contains nerve tracts to and from both the
upper and lower extremities.
Note that the spinal cord is not as long as the vertebral canal. The
lumbar and sacral roots travel the longest intraspinal distance and
fan out like a horse’s tail at L1–L2, giving rise to the term cauda
equina. To avoid injury to the spinal cord, most lumbar punctures
are performed at the L3–L4 or L4–L5 vertebral interspaces.
Peripheral Nervous System
The peripheral nervous system (PNS) consists of both CNs and peripheral
nerves that project to the heart, visceral organs, skin, and limbs.
It controls the somatic nervous system, which regulates muscle movements
and response to the sensations of touch and pain, and the
autonomic nervous system that connects to internal organs and generates
autonomic reflex responses. The autonomic nervous system
consists of the sympathetic nervous system, which “mobilizes organs
and their functions during times of stress and arousal, and the parasympathetic
nervous system, which
Cranial nerves
Twelve pairs of special nerves called cranial nerves
(CNs) emerge from the cranial vault through skull foramina and canals to
structures in the head and neck. They are numbered sequentially with Roman
numerals in rostral to caudal order as they arise from the brain. CNs III through
XII arise from the diencephalon and the brainstem, as illustrated in Figure 17-4.
CNs I and II are actually fiber tracts emerging from the brain. Some CNs are
limited to general motor and/or sensory functions, whereas others are specialized,
serving smell, vision, or hearing (I, II, VIII).
Peripheral Nerves
The PNS includes spinal and peripheral nerves
that carry impulses to and from the cord. A total of 31 pairs of spinal nerves
attach to the spinal cord: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and
1 coccygeal. Each nerve has an anterior (ventral) root containing motor fibers,
and a posterior (dorsal) root containing sensory fibers. The anterior and posterior
roots merge to form a short spinal nerve, <5 mm long. Spinal nerve fibers
commingle with similar fibers from other levels in plexuses outside the cord,
from which peripheral nerves emerge. Most peripheral nerves contain both sensory
(afferent) and motor (efferent) fibers.
Cranial Nerve I
Olfactory - sense of smell
Cranial Nerve II
Optic - vision
Cranial Nerve III
Oculomotor Pupillary constriction, opening the eye (lid elevation), and most extraocular movements
Cranial Nerve IV
Trochlear Downward, internal rotation of the eye
Cranial Nerve V
Trigeminal Motor—temporal and masseter muscles (jaw clenching), lateral pterygoids (lateral jaw movement)
Cranial Nerve VI
Abducens Lateral deviation of the eye
Cranial Nerve VII
Facial Motor—facial movements, including those of facial expression, closing the eye, and closing the mouth
Sensory—taste for salty, sweet, sour, and bitter substances on the anterior two thirds of the tongue and
sensation from the ear
Cranial Nerve VIII
Acoustic Hearing (cochlear division) and balance—(vestibular division)
Cranial Nerve IX
Glossopharyngeal
Motor—pharynx
Sensory—posterior portions of the eardrum and ear canal, the pharynx, and the posterior tongue, including
taste (salty, sweet, sour, bitter)
Cranial Nerve X
Vagus Motor—palate, pharynx, and larynx
Sensory—pharynx and larynx
Cranial Nerve XI
Spinal accessory
Motor—the sternocleidomastoid and upper portion of the trapezius
Cranial Nerve XII
Hypoglossal Motor—tongue
Like the brain, the spinal cord contains:
both gray matter and white matter
(Fig. 17-5). The gray matter consists of aggregations of nerve cell nuclei and
dendrites that are surrounded by white tracts of nerve fibers connecting the brain
to the PNS. Note the butterfly appearance of the gray matter nuclei and their
anterior and posterior horns.
Motor Pathways
Motor pathways are complex avenues that extend from upper motor neurons
through long white matter tracts to synapses with lower motor neurons, and continue
to the periphery through peripheral nerve structures. Upper motor neurons,
or nerve cell bodies, lie in the motor strip of the cerebral cortex and in
several brainstem nuclei; their axons synapse with motor nuclei in the brainstem
(for CNs) and in the spinal cord (for peripheral nerves). Lower motor neurons
have cell bodies in the spinal cord, termed anterior horn cells; their axons transmit
impulses through the anterior roots and spinal nerves into peripheral nerves,
terminating at the neuromuscular junction.
Three kinds of motor pathways impinge on the anterior horn cells: the corticospinal
tract, the basal ganglia system, and the cerebellar system. Additional pathways
originating in the brainstem mediate flexor and extensor tone in limb
movement and posture, most notably in coma
The corticospinal (pyramidal) tract.
The corticospinal tracts mediate voluntary
movement and integrate skilled, complicated, or delicate movements by stimulating
selected muscular actions and inhibiting others. They also carry
impulses that inhibit muscle tone, the slight tension maintained by normal
muscle even when it is relaxed. The corticospinal tracts originate in the motor
cortex of the brain (Fig. 17-6). Motor fibers travel down into the lower
medulla, where they form an anatomical structure resembling a pyramid.
There, most of these fibers cross to the opposite or contralateral side of the
medulla, continue downward, and synapse with anterior horn cells or with
intermediate neurons. Tracts synapsing in the brainstem with motor nuclei
of the CNs are termed corticobulbar.
Principal Motor Pathways
Corticospinal (pyramidal) tract
Basal Ganglia System
Cerebellar System
The basal ganglia system.
This exceedingly complex system includes motor
pathways between the cerebral cortex, basal ganglia, brainstem, and spinal
cord. It helps to maintain muscle tone and to control body movements, especially
gross automatic movements such as walking.
The cerebellar system.
The cerebellum receives both sensory and motor input and
coordinates motor activity, maintains equilibrium, and helps to control posture.
All of these higher motor pathways affect
movement only through the lower motor
neuron systems, sometimes called the
“final common pathway.” Any movement,
whether initiated voluntarily in the
cortex, “automatically” in the basal ganglia,
or reflexly via the sensory receptors,
must ultimately be translated into action
by the anterior horn cells. A lesion in any
of these areas will affect movement or
reflex activity
a
When the corticospinal tract is damaged or destroyed, its functions are reduced or
lost:
below the level of injury
The affected limb becomes weak or paralyzed, and skilled, complicated, or delicate movements are performed poorly when compared with gross movements.
When
upper motor neuron systems are damaged
above their crossover in the
medulla, motor impairment develops on
the opposite or contralateral side
In
damage below the crossover, motor
impairment occurs on
the same or ipsilateral
side of the body.
In upper motor neuron lesions, muscle
tone is
increased and deep tendon
reflexes are exaggerated
Damage to the
lower motor neuron systems causes
ipsilateral
weakness and paralysis, but in
this case, muscle tone and reflexes are
decreased or absent.
Disease of the basal ganglia system or cerebellar system causes
disability but not paralysis
Damage to the basal ganglia system produces changes in
muscle tone (most often an increase), disturbances in posture and gait, a slowness or lack of spontaneous and automatic movements termed bradykinesia, and various involuntary movements.
Cerebellar damage impairs
coordination, gait,
and equilibrium, and decreases muscle tone.
Sensory
impulses then travel to the sensory cortex of
the brain via one of two pathways:
the spinothalamic
tract, consisting of smaller sensory
neurons with unmyelinated or thinly myelinated
axons, and the posterior columns, which
have larger neurons with heavily myelinated
axons
Sensory impulses participate in:
reflex activity,
conscious sensation, locate
body position in space, and help regulate
internal autonomic functions such as blood
pressure, heart rate, and respiration.
A complex system of sensory receptors relays
impulses from
skin, mucous membranes,
muscles, tendons, and viscera that travel
through peripheral projections into the posterior
root ganglia, where a second projection
of the ganglia directs impulses centrally
into the spinal cord
The peripheral component of the smallfiber
spinothalamic tract arises in free nerve
endings in the skin that register pain, temperature,
and crude touch. Within one or two
spinal segments from their entry into the
cord, these fibers pass into the posterior
horn and synapse with secondary neurons.
The secondary neurons then cross to the
opposite side and pass upward into the
thalamus.
In the posterior column system, the peripheral large-fiber projections of the dorsal root
ganglia transmit the sensations of vibration, proprioception, kinesthesia, pressure, and
fine touch from skin and joint position receptors to the dorsal root ganglia, where they
travel through central projections in the posterior columns to second-order sensory
neurons in the medulla. Fibers projecting from the secondary neurons cross to the
opposite side at the medullary level and continue on to the thalamus.
At the thalamic level, the general quality of sensation is perceived (e.g., pain, cold,
pleasant, unpleasant), but not fine distinctions. For full perception, a third group
of sensory neurons sends impulses from the thalamus to the sensory cortex of the
brain. Here, stimuli are localized and higher-order discriminations are made.
Lesions at different points in the sensory pathways produce different kinds of
sensory loss. Patterns of sensory loss, together with their associated motor findings,
help you locate the causative lesions. A lesion in the sensory cortex may not
impair the perception of pain, touch, and position, for example, but does impair
finer discrimination. A patient with this lesion cannot appreciate the size, shape,
or texture of an object by feeling it and therefore cannot identify it. Loss of position
and vibration sense, with preservation of other sensations, points to disease
of the posterior columns, whereas loss of all sensations from the waist down,
together with paralysis and hyperactive reflexes in the legs, indicates severe
transverse damage to the spinal cord. Crude and light touch are often preserved
despite partial damage to the cord because impulses originating on one side of
the body travel up both sides of the cord.
just to read
Dermatone
the band of skin innervated by the sensory
root of a single spinal nerve. Knowledge and testing of dermatomes are valuable
when localizing a lesion to a specific spinal cord segment
READ: Spinal Reflexes: The Muscle Stretch response
The muscle stretch reflexes are relayed over structures of both the CNS and PNS.
Since the tendons are not the primary structures involved, the term muscle stretch
reflexes is more precise than the commonly used deep tendon reflexes. Recall that
a reflex is an involuntary stereotypical response that may involve as few as two
neurons, one afferent (sensory) and one efferent (motor), across a single synapse.
The muscle stretch reflexes in the arms and legs are such monosynaptic reflexes.
They illustrate the simplest unit of sensory and motor function. Other reflexes
are polysynaptic, involving interneurons interposed between sensory and motor
neurons.
To elicit a muscle stretch reflex, briskly tap the tendon of a partially stretched
muscle. For the reflex to occur, all components of the reflex arc must be intact:
sensory nerve fibers, spinal cord synapse, motor nerve fibers, neuromuscular
junction, and muscle fibers. Tapping the tendon activates special sensory fibers
in the partially stretched muscle, triggering a sensory impulse that travels to the
spinal cord via a peripheral nerve. The stimulated sensory fiber synapses directly
with the anterior horn cell innervating the same muscle. When the impulse
crosses the neuromuscular junction, the muscle suddenly contracts, completing
the reflex arc.
Because each muscle stretch reflex involves specific spinal segments, together
with their sensory and motor fibers, an abnormal reflex helps you locate a pathologic
lesion. Learn the segmental levels of the muscle stretch reflexes. You can
remember them easily by their numerical sequence in ascending order from
ankle to triceps: S1, L2–L4, C5–C6, C6–C7.
Muscle Stretch Reflexes
Ankle Reflex - sacral 1 primarily
Knee reflex - lumbar 2, 3-4
Supinator (brachioradialis) reflex- C5,6
Biceps reflex - C 5,6
Triceps reflex - C 6,7
Reflexes may be initiated by stimulating skin as well as muscle. Stroking the skin of
the abdomen, for example, produces a localized muscular twitch. Superficial (cutaneous)
reflexes and their corresponding spinal segments include the following
Abdominal reflexes: upper - T8,9,10
Abdominal reflexes: lower- T 10,11,12
Cremasteric reflex - L 1,2
Plantar responses - L5, S1
Anal reflex - S2, 3-4
Neuro: common or concerning symptoms
● Headache
● Dizziness or vertigo
● Weakness (generalized, proximal, or distal)
● Numbness, abnormal or absent sensation
● Fainting and blacking out (near-syncope and syncope)
● Seizures
● Tremors or involuntary movements
Headache
Headaches have many causes, ranging from benign to life
threatening, and always warrant thorough assessment. Neurologic causes such
as subarachnoid hemorrhage, meningitis, or mass lesions are especially ominous.
The careful clinician pays close attention to the history and a detailed neurologic
examination.
Always assess the severity of the headache and its location, duration, and any
associated symptoms such as double vision, visual changes, weakness, or loss of
sensation. Does the headache get worse with coughing, sneezing, or sudden
head movements, which can alter intracranial pressure dynamics? Is there fever,
stiff neck, or a parameningeal focus like ear, sinus, or throat infection that may
signal meningitis?10
An atypical presentation of the patient’s usual migraine may be suspicious for
stroke, especially in women using hormonal contraceptives.19–22
Always look for unusual headache warning signs, such as sudden onset “like a
thunderclap,” onset after age 50 years, and associated symptoms such as fever
and stiff neck. Examine for papilledema and focal neurologic signs
Dizziness or Vertigo
As you learned in Chapter 7, Head and Neck,
dizziness and light-headedness are common, somewhat vague, complaints that
prompt a more specific history and neurologic examination, with emphasis on
detection of nystagmus and focal neurologic signs. Especially in older patients,
ask about medications.
Does the patient feel faint or about to fall or pass out (presyncope)? Or unsteady
and off balance (disequilibrium or ataxia)? Or is there true vertigo, a spinning sensation
within the patient or of the surroundings? If there is true vertigo, establish
the time course of symptoms, which helps distinguish among the different types
of peripheral vestibular disorders.
If there are localizing symptoms or signs like double vision (diplopia), difficulty
forming words (dysarthria), or problems with gait or balance (ataxia), investigate
the central causes of vertigo.
Weakness
Weakness is another common symptom with many causes
which bears careful investigation. It is important to clarify what the patient
means—fatigue, apathy, drowsiness, or actual loss of strength. True motor
weakness can arise from the CNS, a peripheral nerve, the neuromuscular
junction, or a muscle. Time course and location are especially relevant. Is the
onset sudden, gradual or subacute, or chronic, over a long period of time?
What areas of the body are involved? Is the weakness generalized, or focal to
the face or a limb? Does it involve one side of the body or both sides? What
movements are affected? As you listen to the patient’s story, identify the patterns
below:
■ Proximal—in the shoulder and/or hip girdle, for example
■ Distal—in the hands and/or feet
■ Symmetric—in the same areas on both sides of the body
■ Asymmetric—types of weakness include focal, in a portion of the face or
extremity; monoparesis, in an extremity; paraparesis, in both lower extremities;
and hemiparesis, in one side of the body
To identify proximal weakness, ask about difficulty with movements such as
combing hair, reaching up to a shelf, getting up out of a chair, or climbing stairs.
Does the weakness get worse with repetition and improve after rest (suggesting
myasthenia gravis)? Are there associated sensory or other symptoms?
To identify distal weakness, ask about hand strength when opening a jar or using
scissors or a screwdriver, or problems tripping when walking.
Numbness, Abnormal or Absent Sensation
In a patient who
reports numbness, ask the patient to be more precise. Is there tingling like “pins
and needles,” which are altered sensations called paresthesias, distorted sensations
(dysesthesias), or is sensation reduced or completely absent?
In dysesthesias, light touch or pinprick, for example, may cause a burning or
irritating sensation.
Establish the pattern of sensory loss. Is there a stocking-glove distribution? Are
sensory deficits patchy, nondermatomal, and occurring in more than one limb?
Fainting and Blacking out (near syncope and syncope)
Patient
reports of fainting or “passing out” are common and warrant a meticulous history
to guide management and possible hospital admission.36 Begin by finding out
whether the patient has actually lost consciousness. Did the patient hear
external noise or voices throughout the episode, feel light-headed or weak, but
fail to actually lose consciousness, consistent with near syncope or presyncope? Or
did the patient actually experience complete loss of consciousness, a more
serious symptom representing true syncope, defined as a sudden but temporary
loss of consciousness and postural tone from transient global hypoperfusion of
the brain?
Elicit a complete description of the event. What was the patient doing when the
episode occurred? Was the patient standing, sitting, or lying down? Were there
any triggers or warning symptoms? How long did the episode last? Could voices
still be heard? Importantly, were onset and offset slow or fast? Were there any
palpitations? Is there a history of heart disease, which has a sensitivity for a cardiac
cause of more than 95% (with a specificity of ∼45%)?36
Try to interview any witnesses. Consider the possibility of a seizure based on
the features described in the following section, especially if the onset was
abrupt and without warning.
seizures
Patients may report “spells” or fainting that raises suspicion of
seizure, a sudden excessive electrical discharge from cortical neurons. Seizures
may be symptomatic, with an identifiable cause, or idiopathic. A careful history
is important to rule out other causes of loss of consciousness and acute
symptomatic seizures that have discernible explanations.
If there is more than one seizure, consider epilepsy, defined as two or more seizures
that are not provoked by other illnesses or circumstances.38,39 The incidence
of epilepsy in the United States is 3%; in more than 60% to 70% of affected
patients, no cause is identified.
Epilepsy does not always involve loss of consciousness, depending on the type.
It is usually classified as generalized or partial, based on the location in the cortex
of the initial seizure focus. If available, ask a witness how the patient looked
before, during, and after the episode. Was there any seizure-like movement of
the arms or legs? Any incontinence of the bladder or bowel? What about any
drowsiness or impaired memory after the event suggestive of a postictal state?
Ask about age at onset, frequency, change in frequency or symptom pattern, and
use of medications, alcohol, or illicit drugs. Check for any history of head injury
Tremors or involuntary movements
Tremor, “a rhythmic oscillatory
movement of a body part resulting from the contraction of opposing muscle
groups,” is the most common movement disorder.41,42 It may be an isolated finding
or part of a neurologic disorder. Ask about any tremor, shaking, or body movements
that the patient seems unable to control. Does the tremor occur at rest? Does it get
worse with voluntary intentional movement or with sustained postures?
Distinct from these symptoms is restless legs syndrome, present in 6% to 12% of
the U.S. population, described as an unpleasant sensation in the legs, especially
at night, that gets worse with rest and improves with movement of the symptomatic
limb(s)
Neuro:
Important Topics for health promotion and counseling
● Preventing stroke and transient ischemic attack
● Carotid artery screening
● Reducing risk of peripheral neuropathy
● Herpes zoster vaccination
● Detecting the “three D’s”: delirium, dementia, and depression
preventing stroke and TIA
Stroke is a
sudden neurologic deficit caused by cerebrovascular ischemia (87%) or
hemorrhage (13%). Hemorrhagic strokes may be intracerebral (10% of all strokes)
or subarachnoid (3% of all strokes). Stroke is the fourth leading cause of death
in the United States and a leading cause of long-term disability.47
The American Heart Association (AHA) and the American Stroke Association
(ASA) have established tissue-based definitions for ischemic stroke and transient
ischemic attack (TIA) that have important implications for assessing and preventing
strokes.48 These definitions encourage early neurodiagnostic imaging
following a TIA and risk stratification for subsequent stroke.
■ Ischemic stroke is “an infarction of CNS tissue” that may be symptomatic or
silent. “Symptomatic ischemic strokes are manifest by clinical signs of focal
or global cerebral, spinal, or retinal dysfunction caused by CNS infarction.
A silent stroke is a documented CNS infarction that was asymptomatic.”
■ TIA is now defined as “a transient episode of neurological dysfunction caused
by focal brain, spinal cord, or retinal ischemia, without acute infarction.” The
AHA/ASA guidelines recommend neurodiagnostic imaging within 24 hours
of symptom onset and routine noninvasive imaging of the carotid and intracranial
vessels.
TIAs are a major risk factor for stroke, which occurs in 3% to 10% of patients
within 2 days and in 9% to 17% within 90 days.47 Short-term stroke risk is highest
in those with age 60 years and older, diabetes, focal symptoms of weakness
or impaired speech, and a TIA lasting more than 10 minutes. One population-based
study found a combined risk for recurrent TIA/stroke/and death of 25% within
the 3 months following a TIA.50
