(17) Nervous System Flashcards

1
Q

Guiding Questions for Examination of the

Nervous System

A

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?

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2
Q

4 brain regions

A

the cerebrum, the diencephalon, the

brainstem, and the cerebellum.

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3
Q

Each cerebral hemisphere is subdivided into

A

frontal, parietal, temporal, and occipital lobes.

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4
Q

The central nervous system (CNS) of the brain is

A

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

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5
Q

Brain tissue may be

A

gray

white

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6
Q

Gray matter

A

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

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7
Q

White matter

A

consists of neuronal axons that are coated with
myelin. The myelin sheaths, which create the white color, allow nerve impulses
to travel more rapidly.

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8
Q

Thalamus

A

processes sensory impulses

and relays them to the cerebral cortex.

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9
Q

hypothalamus

A

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.

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10
Q

The internal capsule

A

is a white-matter structure where myelinated fibers converge

from all parts of the cerebral cortex and descend into the brainstem.

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11
Q

Brainstem

A

which connects the upper part of the brain with the spinal cord, has three sections:
the midbrain, the pons, and the medulla.

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12
Q

Consciousness relies on the interaction between

A

intact cerebral hemispheres and
a structure in the diencephalon and upper brainstem, the reticular activating
(arousal) system.

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13
Q

cerebellum,

A

which lies at the base of the brain, coordinates all movement and
helps maintain the body upright in space.

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14
Q

Spinal Cord

A

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.

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15
Q

Peripheral Nervous System

A

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

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16
Q

Cranial nerves

A

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).

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17
Q

Peripheral Nerves

A

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.

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18
Q

Cranial Nerve I

A

Olfactory - sense of smell

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19
Q

Cranial Nerve II

A

Optic - vision

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20
Q

Cranial Nerve III

A

Oculomotor Pupillary constriction, opening the eye (lid elevation), and most extraocular movements

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21
Q

Cranial Nerve IV

A

Trochlear Downward, internal rotation of the eye

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22
Q

Cranial Nerve V

A

Trigeminal Motor—temporal and masseter muscles (jaw clenching), lateral pterygoids (lateral jaw movement)

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23
Q

Cranial Nerve VI

A

Abducens Lateral deviation of the eye

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24
Q

Cranial Nerve VII

A

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

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Cranial Nerve VIII
Acoustic Hearing (cochlear division) and balance—(vestibular division)
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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)
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Cranial Nerve X
Vagus Motor—palate, pharynx, and larynx | Sensory—pharynx and larynx
28
Cranial Nerve XI
Spinal accessory | Motor—the sternocleidomastoid and upper portion of the trapezius
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Cranial Nerve XII
Hypoglossal Motor—tongue
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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.
31
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
32
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.
33
Principal Motor Pathways
Corticospinal (pyramidal) tract Basal Ganglia System Cerebellar System
34
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.
35
The cerebellar system.
The cerebellum receives both sensory and motor input and | coordinates motor activity, maintains equilibrium, and helps to control posture.
36
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
37
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. ```
38
When upper motor neuron systems are damaged above their crossover in the medulla, motor impairment develops on
the opposite or contralateral side
39
In damage below the crossover, motor impairment occurs on
the same or ipsilateral | side of the body.
40
In upper motor neuron lesions, muscle | tone is
increased and deep tendon | reflexes are exaggerated
41
Damage to the | lower motor neuron systems causes
ipsilateral weakness and paralysis, but in this case, muscle tone and reflexes are decreased or absent.
42
Disease of the basal ganglia system or cerebellar system causes
disability but not paralysis
43
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. ```
44
Cerebellar damage impairs
coordination, gait, | and equilibrium, and decreases muscle tone.
45
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
46
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.
47
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
48
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
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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
50
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.
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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
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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
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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
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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
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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.
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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.
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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?
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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.
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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
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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)
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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
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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
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Key Facts for Stroke Prevention and Patient Education
● Stroke affects nearly 800,000 Americans each year, including more than 600,000 suffering a first stroke, and accounts for about 1 in every 20 deaths. ● The total annual costs associated with stroke are estimated to be about $34 billion. ● Stroke prevalence and mortality are disproportionately higher in African Americans compared to whites: ● Prevalence, black versus white men: 4.2% versus 2.2%; black versus white women: 4.7% versus 2.5% ● Mortality per 100,000, black versus white men: 55 versus 36; black versus white women: 47 versus 36
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Stroke at a glance
● Although younger and middle-aged women have lower age-specific stroke incidence rates than men, rates increase with age so that women, who on average live longer than men, have an overall higher lifetime risk for stroke. Risk factors for women include autoimmune collagen vascular disease and history of preeclampsia, gestational diabetes, and pregnancy-induced hypertension. ● The prevalence of silent stroke, estimated to range from 6% to 28%, increases with age. ● Individuals with TIA have a 1-year mortality of ∼12%; 10-year risks for stroke and death from cardiovascular disease are 19% and 43%, respectively. ● Only 51% of the United States population is aware of the five stroke warning signs (see below) and would call 911 if they thought someone was having a stroke. ● Stroke outcomes improve significantly when thrombolytic therapy is given within 3 to 4.5 hours of symptom onset; however, only a minority of those suffering a stroke reaches an emergency room within this time window.
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Symptoms and signs of stroke depend on the vascular territory affected in the brain. The most common cause of ischemic symptoms is occlusion of the middle cerebral artery, which causes visual field cuts and contralateral hemiparesis and sensory deficits. Occlusion of the left middle cerebral artery often produces aphasia; and occlusion of the right middle cerebral artery, neglect or inattention to the opposite side of the body
a
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stroke warning signs
F Face Drooping—Does one side of the face droop or is it numb?53 Ask the person to smile. Is the person’s smile uneven? A Arm Weakness—Is one arm weak or numb? Ask the person to raise both arms. Does one arm drift downward? S Speech Difficulty—Is speech slurred? Is the person unable to speak or hard to understand? Ask the person to repeat a simple sentence, like “The sky is blue.” Is the sentence repeated correctly? T Time to call 9-1-1—If someone shows any of these symptoms, even if the symptoms go away, call 9-1-1 and get the person to the hospital immediately. Check the time so you’ll know when the first symptoms appeared Beyond FAST: Other important symptoms ● Sudden numbness or weakness of the leg, arm, or face ● Sudden confusion or trouble understanding ● Sudden trouble seeing in one or both eyes ● Sudden trouble walking, dizziness, loss of balance or coordination ● Sudden severe headache with no known cause
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Stroke - primary prevention
Recognizing that stroke and coronary heart disease share common cardiovascular risk factors and threats to health, in 2010, Healthy People 2020 and the AHA presented a new concept of “cardiovascular health” that encompasses seven health behaviors and health factors, and a new set of combined impact goals for the coming decade: By 2020, to improve the cardiovascular health of all Americans by 20%, while reducing deaths from cardiovascular disease and stroke by 20%.54 For primary prevention, target documented modifiable risk factors, detailed in the box below. Learn the indications for using aspirin in healthy and diabetic individuals.55,56 Optimal blood pressure control is essential for preventing hemorrhagic stroke. Additional risk factors for the most common cause of hemorrhagic stroke— ruptured aneurysms in the circle of Willis—include smoking, alcohol use, oral contraceptives, and family history in a first-degree relative
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Stroke Risk Factors—Primary Prevention | of Ischemic Stroke: Documented and Modifiable Risk Factors
Hypertension Hypertension is the leading risk factor for both ischemic and hemorrhagic stroke. Pharmacologic reduction of blood pressure significantly reduces stroke risk, particularly among African Americans and older adults. Smoking Smoking is associated with doubling the risk of ischemic stroke and a 2- to 4-fold increased risk of subarachnoid hemorrhage. Smoking cessation rapidly reduces the risk of stroke, but never to the level of never-smokers. Dyslipidemia Statin treatment reduces the risk of all strokes by about 20% for patients with or at risk for atherosclerotic cardiovascular disease. Diabetes Stroke risk is doubled with diabetes and 20% of diabetic patients will die of stroke. Good blood pressure control and statin therapy reduce stroke risk in diabetic patients. Weight Obesity increases the risk of ischemic stroke by 64%. Diet and nutrition Dietary factors affect stroke risk primarily by elevating blood pressure. Decreasing salt and saturated fat intake and diets emphasizing fruits, vegetables, nuts, and low-fat dairy products may reduce stroke risk. Physical inactivity Moderate exercise, like brisk walking for 150 minutes a week or 30 minutes on most days, improves cardiovascular health. Alcohol use Alcohol use has a direct dose-dependent effect on the risk of hemorrhagic stroke. Heavy alcohol use increases the risk for all types of stroke due to effects on hypertension, hypercoagulable states, cardiac arrhythmias, and reduced cerebral blood flow.
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Stroke Risk Factors—Primary Prevention | of Ischemic Stroke: Disease-Specific Risk Factors
Atrial fibrillation Valvular (rheumatic) and nonvalvular atrial fibrillation increases risk of stroke between 2- to 7-fold and 17-fold, respectively, compared to the general population. Antiplatelet agents and anticoagulants can reduce the risk for ischemic stroke. When considering antithrombotic therapy, experts recommend individual risk stratification into high-, moderate-, and low-risk groups to balance risk of stroke against risk of bleeding. CHADS2 is a commonly used scoring system based on Congestive heart failure, Hypertension, Age ≥75 years, Diabetes, and prior Stroke/TIA. The CHA2DS2-VASc, which adds an age category of 65 to 74 years, female sex, and vascular disease to the scoring system, improves risk stratification for individuals estimated as low or moderate risk with CHADS2 Carotid artery disease The estimated prevalence of clinically important carotid artery stenosis in the United States population over age 65 years is 1%. Medical therapy, including statins, antiplatelet agents, treatment of diabetes and hypertension, and smoking cessation, has reduced the risk of stroke in individuals with asymptomatic carotid artery stenosis to less than 2% annually. Experts recommend carotid endarterectomy for selected asymptomatic patients with carotid artery stenosis >60%— provided that the surgeon and center have very low perioperative risks for stroke and mortality. Obstructive sleep apnea Sleep apnea is an independent risk factor for stroke, particularly in men. Stroke risk increases with increasing sleep apnea severity as measured by the number of respiratory events (cessation or air flow reduction) per hour. Sleep apnea is usually treated with continuous positive airway pressure (CPAP), though its effectiveness for reducing stroke risk is unknown
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Screening for Asymptomatic Carotid Artery Stenosis.
Carotid duplex ultrasound accurately and safely detects significant carotid artery stenosis and is widely used for evaluating symptomatic patients. Although asymptomatic carotid artery stenosis is a stroke risk, it accounts for only a small proportion of ischemic strokes. Based on a systematic review, the U.S. Preventive Services Task Force (USPSTF) recommended against screening for asymptomatic carotid artery stenosis in the general adult population (grade D).57 The USPSTF found no evidence that ultrasound screening reduced the risk for ipsilateral stroke.58 Given that the population prevalence of asymptomatic carotid artery stenosis is only 1%, screening would lead to many false-positive results. Furthermore, treating asymptomatic patients incurs risks for strokes, death, and other harms.
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TIA and Stroke: secondary presentation
For the patient who has already suffered TIA or stroke, focus on: identifying the underlying cause including noncardiac emboli, cardiac emboli, and carotid artery stenosis; reducing cardiovascular risk factors, including inactivity, hyperlipidemia, poorly controlled diabetes or hypertension, smoking, and heavy alcohol consumption; and identifying the most appropriate interventions for secondary prevention including antiplatelet agents, anticoagulants, and carotid revascularization.59 Strokes in young adults often have a different set of causes—patent foramen ovale and less commonly, carotid or vertebral/basilar artery dissection, hypercoagulable states, or cocaine and illicit drug use
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reducing risk of diabetic peripheral neuropathy
Diabetes causes several types of peripheral neuropathy.62 Maintaining optimal glycemic control can prevent or delay the onset of neuropathy, particularly from type I diabetes. ■ Distal symmetric sensorimotor polyneuropathy. This is the most common type of diabetic neuropathy. It is slowly progressive, often asymptomatic, and a risk factor for ulcerations, arthropathy, and amputation. Symptomatic patients report burning electrical pain in the lower extremities, usually at night. ■ Autonomic dysfunction, mononeuropathies, and polyradiculopathies, including diabetic amyotrophy, which initially causes unilateral thigh pain and proximal lower extremity weakness. Diabetic patients should have their feet examined regularly for neuropathy, including testing pinprick sensation, ankle reflexes, vibration perception (with a 128-Hz tuning fork) and plantar light touch sensation (with a Semmes-Weinstein monofilament), as well as checking for skin breakdown, poor circulation, and musculoskeletal abnormalities. 63 The monofilament test involves pressing the perpendicular monofilament against the skin at the great toe and metatarsals until it bends (Fig. 17-8), or against the dorsal arch if without calluses; the test is positive if the patient cannot feel the monofilament.
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Herpes Zoster Vaccination
Herpes zoster, which results from reactivation of latent varicella (chicken pox) virus infection within the sensory ganglia, usually causes painful unilateral vesicular rashes in a dermatomal distribution.64 The lifetime risk of herpes zoster infection is about one in three, and is higher for women than for men. Up to one in four adults experience complications following infection, including postherpetic neuralgia (persistent pain in the area of the rash), bacterial skin infections, ophthalmic complications, cranial and peripheral neuropathies, encephalitis, pneumonitis, and hepatitis.65 Herpes zoster risk is increased in immunocompromised conditions including cancer, HIV, bone marrow or organ transplantation, and immunosuppressive therapies. Increasing age is also strongly associated with developing both herpes zoster infection and postherpetic neuralgia. The herpes zoster vaccine effectively reduces the short-term risks for zoster and postherpetic neuralgia in adults ≥50 years.66 The Advisory Committee on Immunization Practices (ACIP) currently recommends routinely offering onetime vaccination for adults ≥60 years; the Federal Drug Administration has approved the vaccine for adults ≥50 years. Because the long-term efficacy of the herpes zoster vaccine is uncertain, the ACIP is re-evaluating the best age to administer the vaccine and the need for revaccination
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Detecting Delirium
Delirium, a multifactorial syndrome, is an acute confusional state marked by sudden onset, fluctuating course, inattention, and at times changing levels of consciousness. Risk for developing delirium depends on both predisposing conditions which increase susceptibility and the immediate precipitating factors. About one third of older adults experience delirium during hospitalizations on medical services; rates are even higher following major elective surgeries. Intensive care unit admissions are associated with a high incidence of delirium regardless of age. Even though delirium is associated with poor patient outcomes, more than 50% of cases are undetected. The Confusional Assessment Method (CAM) algorithm, displayed below, is recommended for screening at-risk patients. The CAM instrument can quickly and accurately detect delirium at the bedside67; a CAM severity (CAM-S) measure can be used to predict risks for death and nursing home placement.68 The National Institutes of Health (NIH) have issued guidelines for preventing delirium that emphasize multicomponent interventions by interdisciplinary teams targeting key clinical precipitants
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The Confusion Assessment Method (CAM) | Diagnostic Algorithm
1. Acute change in mental status and fluctuating course ● Is there evidence of an acute change in cognition from baseline? ● Does the abnormal behavior fluctuate during the day? 2. Inattention ● Does the patient have difficulty focusing attention? 3. Disorganized thinking ● Does the patient have rambling or irrelevant conversations, unclear or illogical flow of ideas, or unpredictable switching from subject to subject? 4. Abnormal level of consciousness ● Is the patient anything besides alert—hyperalert, lethargic, stuporous, or comatose?
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Dementia
Dementia is characterized by declines in memory and cognitive ability that interfere with activities of daily living.70,71 The most common types are Alzheimer disease (affecting 5 million Americans over age 65 years), vascular dementia, Lewy body dementia, and frontotemporal dementia.70,72 Diagnosing dementia requires exclusion of delirium and depression. Teasing out agerelated changes in cognition from mild cognitive impairment is also challenging. Less than 2% of patients with dementia have potentially reversible causes, such as hypothyroidism, medication side effects, normal pressure hydrocephalus, or major depression. A meta-analysis identified potentially modifiable risk factors for developing Alzheimer disease, including physical inactivity, depression, smoking, midlife hypertension, midlife obesity, cognitive inactivity or low educational attainment, and diabetes.73 However, a 2011 NIH review concluded “currently, no evidence of even moderate scientific quality exists to support the association of any modifiable factors . . . with reduced risk for Alzheimer disease.”74 The USPSTF did not find convincing evidence that pharmacologic or nonpharmacologic interventions could benefit patients with mild to moderate cognitive impairment.75 Consequently, the USPSTF issued an I statement (insufficient evidence) regarding screening for cognitive impairment
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Depression.
Depression is more common in individuals with significant medical conditions, including several neurologic disorders—dementia, epilepsy, multiple sclerosis, and Parkinson disease—and is also underdiagnosed. Two screening questions, with an area under the receiver operating curve (ROC) of 0.93, can accurately identify major depressive disorders: “Have you been feeling down, depressed, or hopeless (depressed mood)?” and, “Have you felt little interest or pleasure in doing things (anhedonia)?”76 Be sure to assess suicidality and the possibility of bipolar disorder in depressed patients.
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Neuro: important areas of examination
● Mental status—see Chapter 5, Behavior and Mental Status ● CNs I through XII ● Motor system: muscle bulk, tone, and strength; coordination, gait, and stance ● Sensory system: pain and temperature, position and vibration, light touch, discriminative sensation ● Deep tendon, abdominal, and plantar reflexes
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four important questions that govern your neurologic evaluation
■ Does the patient have neurologic disease? ■ If so, what is the localization of the lesion(s)? Are your findings symmetric? ■ What is the pathophysiology of the process? ■ What is the preliminary differential diagnosis?
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Whether you conduct a comprehensive or | screening neuro examination, organize your thinking into five categories:
(1) mental status, speech, and language; (2) CNs; (3) the motor system; (4) the sensory system; and (5) reflexes
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CN I (Olfactory) exam
Test the sense of smell by presenting the patient with familiar nonirritating odors. First, make sure that each nasal passage is patent by compressing one side of the nose and asking the patient to sniff through the other. Then ask the patient to close both eyes. Occlude one nostril and test smell in the other with substances like cloves, coffee, soap, or vanilla. Avoid noxious odors like ammonia that might stimulate CN V. Ask the patient to identify each odor. Test smell on the other side. Normally the patient perceives odors on each side and identifies them correctly.
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CN II (Optic) exam
Test visual acuity. Inspect the optic fundi with your ophthalmoscope, paying special attention to the optic discs. Test the visual fields by confrontation. Test each eye separately, and both eyes together. Occasionally, in stroke patients, for example, patients will complain of partial loss of vision, and testing of both eyes reveals a visual field defect, an abnormality in peripheral vision such as homonymous hemianopsia. Testing only one eye would miss this finding.
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CN II (Optic) and III (Oculomotor) exam
Inspect the size and shape of the pupils, and compare one side with the other. Anisocoria, or a difference of >0.4 mm in the diameter of one pupil compared to the other, is seen in up to 38% of healthy individuals. Test the pupillary reactions to light. Also check the near response (p. 230), which tests pupillary constriction (pupillary constrictor muscle), convergence (medial rectus muscles), and accommodation of the lens (ciliary muscle).
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Cranial Nerves III, IV, and VI—Oculomotor, Trochlear, and Abducens exam
Test the extraocular movements in the six cardinal directions of gaze, and look for loss of conjugate movements in any of the six directions, which causes diplopia. Ask the patient which direction makes the diplopia worse and inspect the eye closely for asymmetric deviation of movement. Determine if the diplopia is monocular or binocular by asking the patient to cover one eye, then the other. Check convergence of the eyes. Identify any nystagmus, an involuntary jerking movement of the eyes with quick and slow components. Note the direction of gaze in which it appears, the plane of the nystagmus (horizontal, vertical, rotary, or mixed), and the direction of the quick and slow components. Nystagmus is named for the direction of the quick component. Ask the patient to fix his or her vision on a distant object and observe if the nystagmus increases or decreases. Look for ptosis (drooping of the upper eyelids). A slight difference in the width of the palpebral fissures is a normal variant in approximately one third of patients
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Cranial Nerve V—Trigeminal exam
Motor. While palpating the temporal and masseter muscles in turn, ask the patient to firmly clench the teeth (Figs. 17-9 and 17-10). Note the strength of muscle contraction. Ask the patient to open and move the jaw from side to side Sensory. After explaining what you plan to do, test the forehead, cheeks, and chin on each side for pain sensation in the circled areas in Figure 17-11. The patient’s eyes should be closed. Use a suitable sharp object such as a pin or cotton swab. You can create a sharp wood splinter by breaking or twisting a cotton swab. To avoid transmitting infection, use a new object for each patient. While testing, occasionally substitute the blunt end for the point as a contrasting stimulus. Ask the patient to report whether each stimulus is “sharp” or “dull” and to compare sides. If you detect sensory loss, confirm it by testing temperature sensation. Two test tubes, filled with hot and ice-cold water, are the traditional stimuli. You can also use a tuning fork, which usually feels cool, and make it warm or cool with running water. Dry it, then touch the skin and ask the patient to identify “hot” or “cold.” Then test for light touch, using a fine wisp of cotton. Ask the patient to respond whenever you touch the skin. Corneal Reflex. Test the corneal reflex. Ask the patient to look up and away from you and approach from the opposite side, out of the patient’s line of vision. Avoiding the eyelashes, lightly touch the cornea (not just the conjunctiva) with a fine wisp of cotton (Fig. 17-12). If the patient is apprehensive touching the conjunctiva first may be helpful Inspect for blinking of both eyes, the normal reaction to this stimulus. The sensory limb of this reflex is carried in CN V, and the motor response in CN VII on both sides. Contact lenses interfere with this testing
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CN VII (Facial) exam
Inspect the face both at rest and during conversation with the patient. Note any asymmetry, often visible in the nasolabial folds, and observe any tics or other abnormal movements. Ask the patient to: 1. Raise both eyebrows. 2. Frown. 3. Close both eyes tightly so that you cannot open them. Test muscular strength by trying to open them, as illustrated in Figure 17-13. 4. Show both upper and lower teeth. 5. Smile. 6. Puff out both cheeks. Cranial Nerve VIII—Acoustic and Vestibular. Assess hearing with the whispered voice test. Ask the patient to repeat numbers whispered into one ear while blocking or rubbing your fingers next to the contralateral ear. If hearing loss is present, determine if the loss is conductive, from impaired “air through ear” transmission, or sensorineural, from damage to the cochlear branch of CN VIII. Test for air and bone conduction, using the Rinne test, and lateralization, using the Weber test. Specific tests of the vestibular function of CN VIII are rarely included in the typical neurologic examination. Consult textbooks of neurology or otolaryngology as the need arises.
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Cranial Nerves IX and X—Glossopharyngeal and Vagus. exam
Listen to the patient’s voice. Is it hoarse, or does it have a nasal quality? Is there difficulty in swallowing? Ask the patient to say “ah” or to yawn as you watch the movements of the soft palate and the pharynx. The soft palate normally rises symmetrically, the uvula remains in the midline, and each side of the posterior pharynx moves medially, like a curtain. The slightly curved uvula seen occasionally as a normal variation should not be mistaken for a uvula deviated by a lesion of CN IX or X. Warn the patient that you are going to test the gag reflex, which some patients may refuse. This reflex consists of elevation of the tongue and soft palate and constriction of the pharyngeal muscles. Stimulate the back of the throat lightly on each side in turn and observe the gag reflex. This reflex is diminished in many normally healthy people.
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Cranial Nerve XI—Spinal Accessory. exam
Standing behind the patient, look for atrophy or fasciculations in the trapezius muscles, and compare one side with the other. Fasciculations are fine flickering irregular movements in small groups of muscle fibers. Ask the patient to shrug both shoulders upward against your hands (Fig. 17-14). Note the strength and contraction of the trapezii Ask the patient to turn his or her head to each side against your hand (Fig. 17-15). Observe the contraction of the opposite sternocleidomastoid (SCM) muscle and note the force of the movement against your hand
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Cranial Nerve XII—Hypoglossal
Listen to the articulation of the patient’s words. This depends on CNs V, VII, IX, and X, as well as XII. Inspect the patient’s tongue as it lies on the floor of the mouth. Look for any atrophy or fasciculations. Some coarser restless movements are normal. Then, with the patient’s tongue protruded, look for asymmetry, atrophy, or deviation from the midline. Ask the patient to move the tongue from side to side, and note the symmetry of the movement. In ambiguous cases, ask the patient to push the tongue against the inside of each cheek in turn as you palpate externally for strength
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Muscle Tone exam
When a normal muscle with an intact nerve supply is relaxed voluntarily, it maintains a slight residual tension known as muscle tone. This is best assessed by feeling the muscle’s resistance to passive stretch. Persuade the patient to relax. Hold one hand with yours and, while supporting the elbow, flex and extend the patient’s fingers, wrist, and elbow, and put the shoulder through a moderate range of motion. With practice, you can combine these actions into a single smooth movement. On each side, note muscle tone—the resistance offered to your movements. Tense patients may show increased resistance. With repeated practice, you will learn the feel of normal resistance. If you suspect decreased resistance, hold the forearm and shake the hand loosely back and forth. Normally the hand moves back and forth freely but is not completely floppy. If resistance is increased, determine if it varies as you move the limb or persists throughout the range of movement and in both directions, for example, during both flexion and extension. Feel for any jerkiness in the resistance. To assess muscle tone in the legs, support the patient’s thigh with one hand, grasp the foot with the other, and flex and extend the patient’s knee and ankle on each side. Note the resistance to moving the limb
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Scale for Grading Muscle Strength
Muscle strength is graded on a 0 to 5 scale: 0 —No muscular contraction detected 1 —A barely detectable flicker or trace of contraction 2 —Active movement of the body part with gravity eliminated 3 —Active movement against gravity 4 —Active movement against gravity and some resistance 5 — Active movement against full resistance without evident fatigue. This is normal muscle strength.
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Muscle Strength exam
Normal strength varies widely, so your standard of normal should allow for factors like age, sex, and muscular training. The patient’s dominant side is usually slightly stronger than the nondominant side, though differences can be hard to detect. Keep this difference in mind as you compare sides. Test muscle strength by asking the patient to actively resist your movement. Remember that a muscle is strongest when shortest, and weakest when longest. Give the patient the advantage as you try to overcome the resistance and judge true the muscle’s true strength. Some patients give way during tests of muscle strength due to pain, misunderstanding of the test, an effort to help the examiner, conversion disorder, or malingering. If the muscles are too weak to overcome resistance, test them against gravity alone or with gravity eliminated. When the forearm rests in a pronated position, for example, dorsiflexion at the wrist can be tested against gravity alone. When the forearm is midway between pronation and supination, extension at the wrist can be tested with gravity eliminated. Finally, if the patient fails to move the body part, observe or palpate for weak muscular contraction Many clinicians make further distinctions by adding plus or minus signs toward the stronger end of this scale. Thus, 4+ indicates good but not full strength, while 5− means a trace of weakness. Methods for testing individual major muscle groups are described in the text that follows. The spinal root innervations and the muscles affected are shown in parentheses. To localize lesions in the spinal cord or the PNS more precisely, consult texts of neurology for specialized additional testing
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``` Test flexion (C5, C6—biceps and brachioradialis) and extension (C6, C7, C8—triceps) at the elbow by ```
having the patient pull and push against your hand
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Test extension at the wrist (C6, C7, C8, radial nerve— extensor carpi radialis longus and brevis) by
``` asking the patient to make a fist and resist as you press down (Fig. 17-22). Or ask the patient to extend the forearms with fingers straight and palms up, then press the palms downward. ```
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Test the grip (C7, C8, T1).
Ask the patient to squeeze two of your fingers as hard as possible and not let them go (Fig. 17-23). To avoid getting hurt by strong grips, place your own middle finger on top of your index finger. Normally it should be difficult for you to pull your fingers from the patient’s grip. Test both grips simultaneously with the patient’s arms extended or in the lap to help compare the right handgrip with the left
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Test finger abduction (C8, T1, ulnar nerve).
Position the patient’s hand with palm down and fingers spread. Instruct the patient to prevent you from moving any fingers as you try to force them together
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Test opposition of the thumb (C8, T1, median nerve).e
Ask the patient to touch the | tip of the little finger with the thumb, against your resistanc
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You may already have assessed muscle strength of the trunk during other segments of the examination, namely:
■ Flexion, extension, and lateral bending of the spine | ■ Thoracic expansion and diaphragmatic excursion during respiration
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Test flexion at the hip (L2, L3, L4—iliopsoas) by
placing your hand on the patient’s mid-thigh and asking the patient to raise the leg against your hand
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Test adduction at the hips (L2, L3, L4—adductors).
Place your hands firmly on the | bed between the patient’s knees. Ask the patient to bring both legs together
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Test abduction at the hips (L4, L5, S1—gluteus medius and minimus).
Place your hands firmly outside the patient’s knees. Ask the patient to spread both legs against your hands
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Test extension at the hips (S1—gluteus maximus).
Have the patient push the mid | posterior thigh down against your hand
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Test extension at the knee (L2, L3, L4—quadriceps).
Support the knee in flexion and ask the patient to straighten the leg against your hand (Fig. 17-27). The quadriceps is the strongest muscle in the body, so expect a forceful response
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Test flexion at the knee (L4, L5, S1, S2—hamstrings)
Position the patient’s leg so that the knee is flexed with the foot resting on the bed. Tell the patient to keep the foot down as you try to straighten the leg (Fig. 17-28)
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Test foot dorsiflexion (mainly L4, L5—tibialis anterior) and plantar flexion (mainly S1—gastrocnemius, soleus) at the ankle by
asking the patient to pull up and push down against your hand (Figs. 17-29 and 17-30). Heel and toe walk also assess foot dorsiflexion and plantar flexion, respectively
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Coordination of muscle movement requires four areas of the | nervous system to function in an integrated way
■ The motor system, for muscle strength ■ The cerebellar system (also part of the motor system), for normal rhythmic movement and steady posture ■ The vestibular system, for balance and for coordinating eye, head, and body movements ■ The sensory system, for position sense
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To assess coordination, observe the patient performing
■ Rapid alternating movements ■ Point-to-point movements ■ Gait and other related body movements ■ Standing in specified ways
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Rapid alternating movements: arms
Show the patient how to strike one hand on the thigh, raise the hand, turn it over, and then strike the back of the hand down on the same place. Urge the patient to repeat these alternating movements as rapidly as possible (Fig. 17-31). Observe the speed, rhythm, and smoothness of the movements. Repeat with the other hand. The nondominant hand may perform less well. Show the patient how to tap the distal joint of the thumb with the tip of the index finger, again as rapidly as possible (Fig. 17-32). Again, observe the speed, rhythm, and smoothness of the movements. The nondominant side often performs less well
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Rapid alternating movements: legs
Ask the patient to tap the ball of each foot in turn as quickly as possible on your hand or the floor. Note any slowness or awkwardness. Normally the feet do not perform as well as the hands
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point-to-point movements: arms
Finger-to-Nose Test. Ask the patient to touch your index finger and then his or her nose alternately several times. Move your finger so that the patient has to change directions and extend the arm fully to reach your finger. Observe the accuracy and smoothness of movement, and watch for any tremor. Now hold your finger in one place so that the patient can touch it with one arm and finger outstretched. Ask the patient to raise the arm overhead and lower it again to touch your finger. After several repeats, ask the patient to close both eyes and try several more times. Repeat on the other side. Normally the patient touches the examiner’s finger successfully with eyes open or closed. These maneuvers test position sense and the function of both the labyrinth of the inner ear and the cerebellum.
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point-to-point movements: legs
Heel-to-Shin Test. Ask the patient to place one heel on the opposite knee, then run it down the shin to the big toe. Observe this movement for smoothness and accuracy. Repetition with the patient’s eyes closed tests for position sense. Repeat on the other side.
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Gait exam
``` Ask the patient to: ■ Walk across the room or down the hall, then turn and come back. Observe posture, balance, swinging of the arms, and movements of the legs. Normally balance is intact, the arms swing symmetrically at the sides, and turns are smooth. ■ Walk heel-to-toe in a straight line— called tandem walking (Fig. 17-33). ■ Walk on the toes, then on the heels— this tests plantar flexion and dorsiflexion of the ankles as well as balance ■ Hop in place on each foot in turn (if the patient is not too ill)—this tests proximal and distal muscle strength in the legs and requires both normal position sense and cerebellar function. ■ Do a shallow knee bend, first on one leg, then on the other (Fig. 17-34). Steady the patient if you think the patient might fall. ■ Or alternatively, rise from a sitting position without arm support and step up on a sturdy stool—if the patient is unsteady, neurologically impaired, or frail these tests are more suitable than hopping or knee bends ```
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Stance exams
Romberg | Pronator Drift
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The Romberg Test
This is mainly a test of position sense. The patient should first stand with feet together and eyes open and then close both eyes for 30 to 60 seconds without support. Note the patient’s ability to maintain an upright posture. Normally any swaying is mi
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Test for Pronator Drift.
The patient should stand for 20 to 30 seconds with eyes closed and both arms held straight forward with palms up (Fig. 17-35). Normally patients hold this arm position well. If necessary, patients can be tested in the sitting position. Next, instruct the patient to keep the arms out and eyes shut and tap the arms briskly downward. The arms normally return smoothly to the horizontal position. This response requires muscular strength, coordination, and good position sense.
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To evaluate the sensory system, you will test several kinds of sensation
■ Pain and temperature (spinothalamic tracts) ■ Position and vibration (posterior columns) ■ Light touch (both of these pathways) ■ Discriminative sensations, which depend on some of the above sensations but also involve the cortex
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Tips for Detecting Sensory Deficits
● Compare symmetric areas on the two sides of the body, including the arms, legs, and trunk. ● For pain, temperature, and touch sensation, compare distal to proximal areas of the extremities. Scatter the stimuli to sample most of the dermatomes and major peripheral nerves (see pp. 756–757). One suggested pattern is to include: ● both shoulders (C4) ● the inner and outer aspects of the forearms (C6 and T1) ● the thumbs and little fingers (C6 and C8) ● the fronts of both thighs (L2) ● the medial and lateral aspects of both legs (L4 and L5) ● the little toes (S1) ● the medial aspect of each buttock (S3) ● For vibration and position sensation, test the fingers and toes first. If these are normal, you may safely assume that more proximal areas are also be normal. ● Vary the pace of your testing so that the patient does not merely respond to your repetitive rhythm. ● When you detect an area of sensory loss or hypersensitivity, map out its boundaries in detail. Stimulate first at a point of reduced sensation, then in progressive steps until the patient reports a change to normal sensation. An example is shown here.
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pain exam
Use a sharp safety pin, the stick portion of a broken cotton swab, or other suitable tool. Occasionally, substitute the blunt end for the point. Ask the patient, “Is this sharp or dull?” or, when making comparisons, “Does this feel the same as this?” Apply the lightest pressure needed for the stimulus to feel sharp; avoid heavy pricks that draw blood. To prevent transmitting a bloodborne infection, discard the pin or other device safely. Do not reuse it on another person
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temperature exam
Testing skin temperature is often omitted if pain sensation is normal. If there are sensory deficits, use two test tubes filled with hot and cold water, or a tuning fork heated or cooled by running water. Touch the skin and ask the patient to identify “hot” or “cold.”
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light touch exam
With a fine wisp of cotton, touch the skin lightly, avoiding pressure. Ask the patient to respond whenever a touch is felt, and to compare one area with another. Avoid testing calloused skin, which is normally relatively insensitive.
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Vibration exam
Use a relatively low-pitched tuning fork of 128 Hz. Tap it on the heel of your hand and place it firmly over a distal interphalangeal joint of the patient’s finger, then over the interphalangeal joint of the big toe (Fig. 17-37). Ask what the patient feels. If you are not sure whether the patient is feeling pressure or vibration, ask the patient to tell you when the vibration stops. Then touch the tuning fork to stop it from vibrating and confirm this change with the patient. If vibration sense is impaired, proceed to more proximal bony prominences (e.g., wrist, elbow; medial malleolus, shin, patella, anterior superior iliac spine, spinous processes, and clavicles).
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Proprioception (Joint Position | Sense) exam
Grasp the patient’s big toe, holding it by its sides between your thumb and index finger, then pull it away from the other toes (Fig. 17-38). This prevents extraneous tactile stimuli from affecting testing. Demonstrate “up” and “down” as you move the patient’s toe clearly upward and downward. Then, with the patient’s eyes closed, ask the patient to say “up” or “down” when moving the large toe in a small arc Repeat the test several times on each side. If position sense is impaired, move proximally to test the ankle joint. In a similar fashion, test position in the fingers, moving proximally, if indicated, to the metacarpophalangeal joints, wrist, and elbow
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Discriminative Sensations exams
``` Stereognosis Number Identification (Graphesthesia) Two-point discrimination Point localization Extinction ```
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Stereognosis.
``` refers to the ability to identify an object by feeling it. Place a familiar object such as a coin, paper clip, key, pencil, or cotton ball, in the patient’s hand and ask the patient to tell you what it is. Normally a patient will manipulate it skillfully and identify it correctly within 5 seconds. Asking the patient to distinguish “heads” from “tails” on a coin is a sensitive test of stereognosis. ```
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Number identification (graphesthesia).
``` If arthritis or other conditions prevent the patient from manipulating an object well enough to identify it, test the ability to identify numbers. With the blunt end of a pen or pencil, draw a large number in the patient’s palm (Fig. 17-39). A normally abled person can identify most such numbers ```
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Two-point discrimination
Using the two ends of an opened paper clip, or two pins, touch a finger pad in two places simultaneously (Fig. 17-40). Alternate the double stimulus irregularly with a one-point touch. Be careful not to cause pain. Find the minimal distance at which the patient can discriminate one from two points (normally <5 mm on the finger pads). This test may be used on other parts of the body, but normal distances vary widely from one body region to another.
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Point Localization
Briefly touch a point on the patient’s skin. Then ask the patient to open both eyes and point to the place touched. Normally a person can do so accurately
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Extinction
Stimulate one side or simultaneously stimulate corresponding areas on both sides of the body. Ask where the patient feels your touch. Normally both stimuli are felt
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Scale for Grading Reflexes
4 - Very brisk, hyperactive, with clonus (rhythmic oscillations between flexion and extension) 3 - Brisker than average; possibly but not necessarily indicative of disease 2 - Average; normal 1 - Somewhat diminished; low normal 0 - Reflex absent
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Muscle Stretch Reflexes
Eliciting the muscle stretch reflexes requires special handling of the reflex hammer. Select a properly weighted reflex hammer, and learn the different uses of the pointed end and the flat end. For example, the pointed end is useful for striking small areas, such as your finger as it overlies the biceps tendon. Test the reflexes as follows: ■ Encourage the patient to relax, then position the limbs properly and symmetrically. Hold the reflex hammer loosely between your thumb and index finger so that it swings freely in an arc within the limits set by your palm and other fingers (Fig. 17-45). ■ With your wrist relaxed, strike the tendon briskly using a rapid wrist movement. Your strike should be quick and direct, not glancing. Note the speed, force, and amplitude of the reflex response and grade the response using the scale below. Always compare the response of one side with the other. Reflexes are usually graded on a 0 to 4 scale Reflex response depends partly on the force of your strike on the tendon. Use only enough force to provoke a definite response. Differences between sides are usually easier to detect than symmetric changes on both sides. Symmetrically increased, diminished, or even absent reflexes can be normal.
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Reinforcement Exam
If the patient’s reflexes are symmetrically diminished or absent, use reinforcement, a technique involving isometric contraction of other muscles for up to 10 seconds that may increase reflex activity. To reinforce the arm reflexes, for example, ask the patient to clench his or her teeth or to squeeze both knees together. If leg reflexes are diminished or absent, ask the patient to lock fingers and pull one hand against the other. Tell the patient to pull just before you strike the patellar or Achilles tendon (Fig. 17-46).
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The Biceps Reflex (C5, C6).
The patient’s elbow should be partially flexed and the forearm pronated with palm down. Place your thumb or finger firmly on the biceps tendon. Aim the strike with the reflex hammer directly through your digit toward the biceps tendon (Figs. 17-47 and 17-48). Observe flexion at the elbow, and watch for and feel the contraction of the biceps muscle.
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The Triceps Reflex (C6, C7).
The patient may be sitting or supine. Flex the patient’s arm at the elbow, with palm toward the body, and pull it slightly across the chest. Strike the triceps tendon with a direct blow directly behind and just above the elbow (Figs. 17-49 and 17-50). Watch for contraction of the triceps muscle and extension at the elbow. If you have difficulty getting the patient to relax, try supporting the upper arm. Ask the patient to let the arm go limp, as if it were “hung up to dry.” Then strike the triceps tendon (Fig. 17-51).
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The Brachioradialis Reflex (C5, C6).
The patient’s hand should rest on the abdomen or the lap, with the forearm partly pronated. Strike the radius with the point or flat edge of the reflex hammer, about 1 to 2 inches above the wrist (Fig. 17-52). Watch for flexion and supination of the forearm
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The Quadriceps (Patellar) Reflex (L2, L3, L4).
The patient may be either sitting or lying down as long as the knee is flexed. Briskly tap the patellar tendon just below the patella (Fig. 17-53). Note contraction of the quadriceps with extension at the knee. Placing your hand on the patient’s anterior thigh lets you feel this reflex. There are two options for examining the supine patient. Supporting both knees at once allows you to assess small differences between quadriceps reflexes by repeatedly testing one reflex and then the other (Fig. 17-54). If supporting both legs is uncomfortable for you or the patient, you can place your supporting arm under the patient’s leg (Fig. 17-55). Some patients find it easier to relax with this method.
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The Achilles (Ankle) Reflex (Primarily S1).
If the patient is sitting, partially dorsiflex the foot at the ankle. Persuade the patient to relax. Strike the Achilles tendon, and watch and feel for plantar flexion at the ankle (Fig. 17-56). Also note the speed of relaxation after muscular contraction When the patient is lying down, flex one leg at both hip and knee and rotate it externally so that the lower leg rests across the opposite shin. Then dorsiflex the foot at the ankle and strike the Achilles tendon (Fig. 17-57).
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Clonus.
If the reflexes seem hyperactive, test for ankle clonus. Support the knee in a partly flexed position. With your other hand, dorsiflex and plantar flex the foot a few times while encouraging the patient to relax, then sharply dorsiflex the foot and maintain it in dorsiflexion (Fig. 17-58). Look and feel for rhythmic oscillations between dorsiflexion and plantar flexion. Normally the ankle does not react to this stimulus. There may be a few clonic beats if the patient is tense or has exercised. Other joints may display clonus. A sharp downward displacement of the patella, for example, may elicit patellar clonus in the extended knee.
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The Abdominal Reflexes.
``` Test the abdominal reflexes by lightly but briskly stroking each side of the abdomen, above (T8, T9, T10) and below (T10, T11, T12) the umbilicus in the directions illustrated (Fig. 17-59). Use a key, the wooden end of a cottontipped applicator, or a tongue blade twisted and split longitudinally. Note the contraction of the abdominal muscles and movement of the umbilicus toward the stimulus. If obesity or previous abdominal surgery masks the abdominal reflexes, retract the patient’s umbilicus away from the side being tested with your finger and feel for the muscular contraction ```
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The Plantar Response (L5, S1).
With a key or the wooden end of an applicator stick, stroke the lateral aspect of the sole from the heel to the ball of the foot, curving medially across the ball (Fig. 17-60). Use the lightest stimulus needed to provoke a response, but increase firmness if necessary. Closely observe movement of the big toe, normally plantar flexion Some patients withdraw from this stimulus by flexing the hip and the knee. Hold the ankle, if necessary, to complete your observation. At times it is difficult to distinguish withdrawal from a Babinski response
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The Anal Reflex
Using a broken applicator stick or pinprick, lightly scratch the anus on both sides. Watch for reflex contraction of the external anal sphincter. Detection of the reflex contraction is facilitated by placing a gloved finger in the anus during testing
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Meningeal Signs
Test for these important signs whenever you suspect | meningeal inflammation from meningitis or subarachnoid hemorrhage
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Neck Mobility/Nuchal Rigidity
First, make sure there is no injury or fracture to the cervical vertebrae or cervical cord. In trauma settings, this often requires radiologic evaluation. Then, with the patient supine, place your hands behind the patient’s head and flex the neck forward, if possible until the chin touches the chest. Normally the neck is supple, and the patient can easily bend the head and neck forward
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Brudzinski Sign.
As you flex the neck, watch the hips and knees in reaction | to your maneuver. Normally they should remain relaxed and motionless.
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Kernig Sign.
Flex the patient’s leg at both the hip and the knee, and then slowly extend the leg and straighten the knee (Fig. 17-62). Discomfort behind the knee during full extension is normal but should not produce pain
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Lumbosacral Radiculopathy: Straight-Leg Raise
If the patient has low back pain that radiates down the thigh and leg, commonly called sciatica if in the sciatic nerve distribution, test straight-leg raising on each side in turn. Place the patient in the supine position. Raise the patient’s relaxed and straightened leg, flexing the thigh at the hip (Fig. 17-63). Some examiners first raise the patient’s leg with the knee flexed, then extend the leg. Assess the degree of elevation at which pain occurs, the quality and distribution of the pain, and the effects of foot dorsiflexion. Tightness or discomfort in the buttocks or hamstrings is common during these maneuvers and should not be interpreted as “radiating pain” or a positive test. In addition, be sure to examine motor and sensory function and reflexes at the lumbosacral levels.
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Asterixis.
Asterixis suggests metabolic encephalopathy in patients whose mental functions are impaired. Asterixis is caused by abnormal function of the diencephalic motor centers that regulate agonist and antagonist muscle tone and maintain posture Ask the patient to “stop traffic” by extending both arms, with hands cocked up and fingers spread (Fig. 17-64). Watch for 1 to 2 minutes, coaxing the patient as necessary to maintain this position.
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Winging of the Scapula.
When the shoulder muscles seem weak or atrophic, inspect for scapular winging. Ask the patient to extend both arms and push against your hand or against a wall (Fig. 17-65). Observe the scapulae. Normally they lie close to the thorax In very thin but normal people, the scapulae may appear “winged” even when the musculature is intact.
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The Stuporous or Comatose Patient.
Coma, a state of impaired arousal and awareness, signals a potentially life-threatening event affecting the two hemispheres, the brainstem, or both. Accurate assessment is critical.102–107 Although the arousal and awareness functions are interrelated, “a change in one is not always associated with a similar change in the other.”102 Arousal occurs in the ascending reticular activating system of the brainstem which projects through the thalamus to several areas of the cortex, which “processes, integrates, and gives context to the information provided to it thus generating awareness. Injury to any of these areas or their connections can result in impaired consciousness.” The usual sequence of history, physical examination, and laboratory evaluation does not apply. Instead, you must: ■ First assess and stabilize the ABCs (airway, breathing, and circulation) ■ Establish the patient’s level of consciousness ■ Perform the neurologic examination. Identify any focal or asymmetric findings and determine if the cause of impaired consciousness is structural or metabolic. ■ Interview relatives, friends, or witnesses to establish the speed of onset and duration of unconsciousness, any warning symptoms, precipitating factors, or previous episodes, and the premorbid appearance and behavior of the patient. Any history of past medical and psychiatric illnesses is also important
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“Don’ts” When Assessing the Comatose Patient
● Don’t dilate the pupils, the single most important clue to the underlying cause of coma (structural vs. metabolic). ● Don’t flex the neck if there is any question of trauma to the head or neck. Immobilize the cervical spine and get an x-ray first to rule out fractures of the cervical vertebrae that could compress and damage the spinal cord.
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LOC: techniques and patient response
``` Alertness: Speak to the patient in a normal tone of voice - The alert patient opens the eyes, looks at you, and responds fully and appropriately to stimuli (arousal intact) ``` ``` Lethargy: Speak to the patient in a loud voice. For example, call the patient’s name or ask “How are you?” - The patient appears drowsy but opens the eyes and looks at you, responds to questions, and then falls asleep ``` ``` Obtundation: Shake the patient gently as if awakening a sleeper - The obtunded patient opens the eyes and looks at you but responds slowly and is somewhat confused. Alertness and interest in the environment are decreased ``` ``` Stupor: Apply a painful stimulus. For example, pinch a tendon, rub the sternum, or roll a pencil across a nail bed. (No stronger stimuli needed!) - The stuporous patient arouses from sleep only after painful stimuli. Verbal responses are slow or even absent. The patient lapses into an unresponsive state when the stimulus ceases. There is minimal awareness of self or the environment ``` ``` Coma: Apply repeated painful stimuli - A comatose patient remains unarousable with eyes closed. There is no evident response to inner need or external stimuli ```
151
Neuro eval: respirations
Observe the rate, rhythm, and pattern of respiration. Because neural structures that govern breathing in the cortex and brainstem overlap with those that govern consciousness, abnormalities of respiration often occur in coma.
152
Neuro eval: pupils
Observe the size and equality of the pupils and test their reaction to light. The presence or absence of the light reaction is one of the most important signs distinguishing structural from metabolic causes of coma. The light reaction often remains intact in metabolic coma
153
Neuro eval: ocular movement
Observe the position of the eyes and eyelids at rest. Check for horizontal deviation of the eyes to one side (gaze preference). When the oculomotor pathways are intact, the eyes look straight ahead
154
Neuro eval: Oculocephalic Reflex (Doll’s Eye Movements).
This reflex helps assess brainstem function in the comatose patient. Holding the upper eyelids open so that you can see the eyes, turn the head quickly, first to one side and then to the other (Fig. 17-67). Make sure the patient has no neck injury before performing this test. In a comatose patient with an intact brainstem, as the head is turned in one direction, the eyes move toward the opposite side (the doll’s eye movements). In Figure 17-68, for example, the patient’s head has been turned to the right; her eyes have moved to the left. Her eyes still seem to gaze at the camera. The doll’s eye movements are intact
155
Neuro eval: Oculovestibular Reflex (with Caloric Stimulation)
If the oculocephalic reflex is absent and you seek further testing of brainstem function, test the oculovestibular reflex. Note that this test is usually not performed in an awake patient Make sure the eardrums are intact and the ear canals clear. Elevate the patient’s head to 30° to perform the test accurately. Place a kidney basin under the ear to catch any water that spills over. With a large syringe, inject ice water through a small catheter that is lying in (but not plugging) the ear canal. Watch for deviation of the eyes in the horizontal plane. You may need to use up to 120 mL of ice water to elicit a response. In the comatose patient with an intact brainstem, the eyes drift toward the irrigated ear. Repeat on the opposite side, waiting 3 to 5 minutes if necessary for the first response to disappear.
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Posture
Observe the patient’s posture. If there is no spontaneous movement, you may need to apply a painful stimulus (see p. 769). Classify the resulting pattern of movement as: ■ Normal–avoidant—the patient purposefully pushes the stimulus away or withdraws. ■ Stereotypic—the stimulus evokes abnormal postural responses of the trunk and extremities. ■ Flaccid paralysis or no response
157
Muscle Tone exam
Test muscle tone by grasping each forearm near the wrist and raising it to a vertical position. Note the position of the hand, which is usually only slightly flexed at the wrist (Fig. 17-70). Then lower the arm to about 12 or 18 inches off the bed and drop it. Watch how it falls. A normal arm drops somewhat slowly. Support the patient’s flexed knees. Then extend one leg at a time at the knee and let the leg fall (Fig. 17-72). Compare the speed with which each leg falls. Flex both legs so that the heels rest on the bed and then release them. The normal leg returns slowly to its original extended position