CA Bates reading

Question 1

Motor: Chronic contralateral corticospinal-type weakness and spasticity. Flexion is stronger than extension in the arm, plantar flexion is stronger than dorsiflexion in the foot, and the leg is externally rotated at the hip.

Sensory: Contralateral sensory loss in the limbs and trunk on the same side as the motor deficits

DTR: increases

Ex of cause: cortical stroke

Answer 1

Cerebral Cortex (1)

Central Nervous System Disorders

Question 2

MOtor Weakness and spasticity as above, plus cranial nerve deficits such as diplopia (from weakness of the extraocular muscles) and dysarthria

Sensory: Variable; no typical sensory findings

DTR: increased

ex of cause: Brainstem stroke, acoustic neuroma

Answer 2

Brainstem (2)

Central Nervous System Disorders

Question 3

MOTor: Weakness and spasticity as above, but often affecting both sides (when cord damage is bilateral), causing paraplegia or quadriplegia depending on the level of injury

Sensory:Dermatomal sensory deficit on the trunk bilaterally at the level of the lesion, and sensory loss from tract damage below the level of the lesion

DTR: increased

ex of cause: Trauma, causing cord compression

Answer 3

Spinal Cord (3)

Central Nervous System Disorders

Question 4

Motor: Slowness of movement (bradykinesia), rigidity, and tremor

Sensory: Sensation not affected

DTR: normal or decreased

ex of cause: Parkinsonism

Answer 4

Subcortical Gray Matter: Basal Ganglia (4)

Central Nervous System Disorders

Question 5

Motor: Hypotonia, ataxia, and other abnormal movements, including nystagmus, dysdiadochokinesis, and dysmetria

Sensory: Sensation not affected

DTR: normal or decreased

ex of cause: Cerebellar stroke, brain tumor

Answer 5

Cerebellar

Central Nervous System Disorders

Question 6

Motor: Weakness and atrophy in a segmental or focal pattern; fasciculations

Sensory: Sensation intact

DTR: Decreased

ex of causes: Polio, amyotrophic lateral sclerosis

Answer 6

Anterior Horn Cell (1)

Peripheral Nervous System Disorders

Question 7

Motor: Weakness and atrophy in a root-innervated pattern; sometimes with fasciculations

Sensory: Corresponding dermatomal sensory deficits

DTR: decreased

examples of cause: Herniated cervical or lumbar disc

Answer 7

Spinal Roots and Nerves (2)

Peripheral Nervous System Disorders

Question 8

Motor: Weakness and atrophy in a peripheral nerve distribution; sometimes with fasciculations

Sensory: Sensory loss in the pattern of that nerve

DTR: decreased

ex of cause: trauma

Answer 8

Peripheral Nerve—Mononeuropathy (3)

Peripheral Nervous System Disorders

Question 9

Motor: Weakness and atrophy more distal than proximal; sometimes with fasciculations

Sensory: Sensory deficits, commonly in stocking-glove distribution

DTR: decreased

Ex of cause:Peripheral polyneuropathy of alcoholism, diabetes

Answer 9

Peripheral Nerve—Polyneuropathy (4)

Peripheral Nervous System Disorders

Question 10

Motor: Fatigability more than weakness

Sensory: Sensation intact

DTR: Normal

ex of cause: Myasthenia gravis

Answer 10

Neuromuscular Junction (5)

Peripheral Nervous System Disorders

Question 11

Motor: Weakness usually more proximal than distal; fasciculations rare

Sensory: Sensation intact

DTR: Normal or decreased

ex of cause: Muscular dystrophy

Answer 11

Muscle (6)

Peripheral Nervous System Disorders

Question 12

Although there are many causes of coma, most can be classified as either (2 types)

Answer 12

structural or metabolic

Question 13

Arousal centers poisoned or critical substrates depleted

Answer 13

Toxic–Metabolic coma

Question 14

Lesion destroys or compresses brainstem arousal areas, either directly or secondary to more distant expanding mass lesions.

Answer 14

Structural coma

Question 15

Respiratory pattern:

If regular, may be normal or hyperventilation. If irregular, usually Cheyne-Stokes

Answer 15

Toxic–Metabolic coma

Question 16

Pupillary size and reaction:
Equal, reactive to light. If pinpoint from opiates or cholinergics, you may need a magnifying glass to see the reaction.

May be unreactive if fixed and dilated from anticholinergics or hypothermia

Answer 16

Toxic–Metabolic coma

Question 17

Level of consciousness:

Changes after pupils change

Answer 17

Toxic–Metabolic coma

Question 18

causes: Uremia, hyperglycemia alcohol, drugs, liver failure hypothyroidism, hypoglycemia, anoxia, ischemia meningitis, encephalitis hyperthermia, hypothermia

Answer 18

Toxic–Metabolic coma

Question 19

respiratory pattern: Irregular, especially Cheyne-Stokes or ataxic breathing. Also with selected stereotypical patterns like “apneustic” respiration (peak inspiratory arrest) or central hyperventilation

Answer 19

Structural coma

Question 20

pupillary size and reaction: Unequal or unreactive to light (fixed)

Answer 20

Structural coma

Question 21

Midposition, fixed—suggests

Answer 21

midbrain compression

Question 22

Dilated, fixed—suggests

Answer 22

compression of CN III from herniation

Question 23

LOC: changes BEFORE pupils change

Answer 23

Structural coma

Question 24

Example of cause: Epidural, subdural, or intracerebral hemorrhage; cerebral infarct or embolus; tumor, abscess; brainstem infarct, tumor, or hemorrhage; cerebellar infarct, hemorrhage, tumor, or abscess

Answer 24

structural coma

Question 25

Pupillary ____, ______, and ______ help to assess the cause of coma and to determine the region of the brain that is impaired.

Remember that unrelated pupillary abnormalities, including miotic drops for glaucoma or mydriatic drops for a better view of the ocular fundi, may have preceded the coma.

Answer 25

size, equality, and light reactions

Question 26

suggest damage to the sympathetic pathways in the hypothalamus, or metabolic encephalopathy, a diffuse failure of cerebral function that has many causes, including drugs. Light reactions are usually normal.

Answer 26

Bilaterally small pupils (1–2.5 mm)

Question 27

suggest a hemorrhage in the pons, or the effects of morphine, heroin, or other narcotics. The light reactions may be seen with a magnifying glass.

Answer 27

Pinpoint pupils (

Question 28

Midposition fixed pupils

Answer 28

Pupils that are in the midposition or slightly dilated (4–6 mm) and are fixed to light suggest structural damage in the midbrain

Question 29

may be due to severe anoxia and its sympathomimetic effects, as seen after cardiac arrest. They may also result from atropinelike agents, phenothiazines, or tricyclic antidepressants.

Answer 29

Bilaterally fixed and dilated pupils

Question 30

may be due to cocaine, amphetamine, LSD, or other sympathetic nervous system agonists.

Answer 30

Bilaterally large reactive pupils

Question 31

warns of herniation of the temporal lobe, causing compression of the oculomotor nerve and midbrain.

Answer 31

A pupil that is fixed and another dilated

Question 32

is most commonly seen in diabetic patients with infarction of CN III.

Answer 32

A single large pupil

Question 33

This reflex helps to assess brainstem function in a 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. Make sure the patient has no neck injury before performing this test.

Answer 33

Oculocephalic Reflex (Doll’s Eye Movements)

Question 34

In irritative lesions from epilepsy or early cerebral hemorrhage, the eyes _________ from the affected hemisphere.

Answer 34

Look away

Question 35

In structural hemispheric lesions, the eyes _______________ in the affected hemisphere.

Answer 35

“look at the lesion”

Question 36

In a comatose patient with absence of doll’s eye movements ( the ability to move both eyes to one side) is lost, suggesting a lesion of the

Answer 36

midbrain or pons.

Question 37

If the _________ reflex is absent and you seek further assessment of brainstem function, test the oculovestibular reflex. Note that this test is almost never performed in an awake patient.

Answer 37

oculocephalic

Question 38

the upper arms are flexed tight to the sides with elbows, wrists, and fingers flexed. The legs are extended and internally rotated. The feet are plantar flexed. This posture implies a destructive lesion of the corticospinal tracts within or very near the cerebral hemispheres. When unilateral, this is the posture of chronic spastic hemiplegia.

Answer 38

Decorticate Rigidity (Abnormal Flexor Response)

Question 39

Sudden unilateral brain damage involving the corticospinal tract may produce a _________ (one-sided paralysis), which is flaccid early in its course. Spasticity will develop later. The paralyzed arm and leg are slack. They fall loosely and without tone when raised and dropped to the bed. Spontaneous movements or responses to noxious stimuli are limited to the opposite side. The leg may lie externally rotated. One side of the lower face may be paralyzed, and that cheek puffs out on expiration. Both eyes may be turned away from the paralyzed side

Answer 39

hemiplegia (early)

Question 40

the jaws are clenched and the neck is extended. The arms are adducted and stiffly extended at the elbows, with forearms pronated, wrists and fingers flexed. The legs are stiffly extended at the knees, with the feet plantar flexed. This posture may occur spontaneously or only in response to external stimuli such as light, noise, or pain. It is caused by a lesion in the diencephalon, midbrain, or pons, although severe metabolic disorders such as hypoxia or hypoglycemia may also produce it.

Answer 40

Decerebrate Rigidity (Abnormal Extensor Response)

Question 41

A gait that lacks coordination, with reeling and instability, is called

may be due to cerebellar disease, loss of position sense, or intoxication

Answer 41

ataxic

Question 42

Walk heel-to-toe in a straight line

may reveal an ataxia not previously obvious.

Answer 42

Tandem walking

Question 43

sensitive tests, respectively, for plantar flexion and dorsiflexion of the ankles, as well as for balance.

may reveal distal muscular weakness in the legs. Inability to heel-walk is a sensitive test for corticospinal tract damage.

Answer 43

Walk on the toes, then on the heels

Question 44

involves the proximal muscles of the legs as well as the distal ones and requires both good position sense and normal cerebellar function

difficultly may be due to weakness, lack of position sense, or cerebellar dysfunction.

Answer 44

Hop in place on each foot in turn (if the patient is not too ill)

Question 45

difficulty suggests proximal weakness (extensors of the hip), weakness of the quadriceps (the extensor of the knee), or both.

Answer 45

Difficulty in doing a shallow knee bend:

Do a shallow knee bend, first on one leg, then on the other. Support the patient’s elbow if you think the patient is in danger of falling.

Question 46

Seen in corticospinal tract lesion in stroke, causing poor control of flexor muscles during swing phase. Affected arm is flexed, immobile, and held close to the side, with elbow, wrists, and interphalangeal joints flexed. Affected leg extensors spastic; ankle plantar-flexed and inverted. Patients may drag toe, circle leg stiffly outward and forward (circumduction), or lean trunk to contralateral side to clear affected leg during walking.

Answer 46

Spastic Hemiparesis

Question 47

Seen in spinal cord disease, causing bilateral lower extremity spasticity, including adductor spasm, and abnormal proprioception. Gait is stiff. Patients advance each leg slowly, and the thighs tend to cross forward on each other at each step. Steps are short. Patients appear to be walking through water. Scissoring is seen in all spasticity disorders, most commonly cerebral palsy

Answer 47

Scissors Gait

Question 48

Seen in foot drop, usually secondary to peripheral motor unit disease. Patients either drag the feet or lift them high, with knees flexed, and bring them down with a slap onto the floor, thus appearing to be walking up stairs. They cannot walk on their heels. The steppage gait may involve one or both legs. Tibialis anterior and toe extensors are weak.

Answer 48

Steppage Gait

Question 49

Seen in the basal-ganglia defects of Parkinson disease. Posture is stooped, with flexion of head, arms, hips, and knees. Patients are slow getting started. Steps are short and shuffling, with involuntary hastening (festination). Arm swings are decreased, and patients turn around stiffly—“all in one piece.” Postural control is poor (retropulsion).

Answer 49

Parkinsonian Gait

Question 50

Seen in disease of the cerebellum or associated tracts. Gait is staggering, unsteady, and wide based, with exaggerated difficulty on turns. Patients cannot stand steadily with feet together, whether eyes are open or closed. Other cerebellar signs are present such as dysmetria, nystagmus, and intention tremor.

Answer 50

Cerebellar Ataxia

Question 51

Seen in loss of position sense in the legs (with polyneuropathy or posterior column damage). Gait is unsteady and wide based (with feet wide apart). Patients throw their feet forward and outward and bring them down, first on the heels and then on the toes, with a double tapping sound. They watch the ground for guidance when walking. With eyes closed, they cannot stand steadily with feet together (positive Romberg sign), and the staggering gait worsens.

Answer 51

Sensory Ataxia

Question 52

Location of lesion:Upper motor neuron or corticospinal tract systems

Description: Increased muscle tone (hypertonia) that is rate dependent. Tone is greater when passive movement is rapid, and less when passive movement is slow. Tone is also greater at the extremes of the movement arc. During rapid passive movement, initial hypertonia may give way suddenly as the limb relaxes. This spastic “catch” and relaxation is known as “clasp-knife” resistance.

Common Cause: Stroke, especially late or chronic stage

Answer 52

Spasiticity

Question 53

Location of lesion:Basal ganglia system

Description: Increased resistance that persists throughout the movement arc, independent of rate of movement, is called lead-pipe rigidity. With flexion and extension of the wrist or forearm, a superimposed rachetlike jerkiness is called cogwheel rigidity.

Common cause: Parkinsonism

Answer 53

Rigidity

Question 54

Location of lesion: Lower motor neuron system at any point from the anterior horn cell to the peripheral nerves

Description: Loss of muscle tone (hypotonia), causing the limb to be loose or floppy. The affected limbs may be hyperextensible or even flail-like. Flaccid muscles are also weak.

Common cause: Guillain-Barré syndrome; also initial phase of spinal cord injury (spinal shock) or stroke

Answer 54

Flaccidity

Question 55

Location of lesion: Both hemispheres, usually in the frontal lobes

Description:Sudden changes in tone with passive range of motion. Sudden loss of tone that increases the ease of motion is called mitgehen (moving with). Sudden increase in tone making motion more difficult is called gegenhalten (holding against).

Common cause: Dementia

Answer 55

Paratonia

Question 56

Marked floppiness indicates muscle ______ or _______ , usually from a disorder of the peripheral motor system.

Answer 56

hypotonia or flaccidity

Question 57

velocity-dependent increased tone that worsens at the extremes of range.

seen in central corticospinal tract diseases, is rate-dependent, increasing with rapid movement.

Answer 57

spasticity

Question 58

is increased resistance throughout the range of movement and in both directions; it is not rate-dependent.

Answer 58

Rigidity

Question 59

refers to weakness of one-half of the body

Answer 59

Hemiparesis

Question 60

to paralysis of one-half of the body.

Answer 60

hemiplegia

Question 61

means paralysis of the legs; quadriplegia means paralysis of all four limbs.

Answer 61

Paraplegia

Question 62

With flexion and extension of the wrist or forearm, a superimposed rachetlike jerkiness is called

Answer 62

cogwheel rigidity

Question 63

Tremors are rhythmic oscillatory movements, which may be roughly subdivided into three groups:

Answer 63

resting (or static) tremors,

postural tremors, and

intention tremors.

Question 64

These tremors are most prominent at rest and may decrease or disappear with voluntary movement. Illustrated is the common, relatively slow, fine, pill-rolling tremor of parkinsonism, about 5 per second.

Answer 64

Resting (Static) Tremors

Question 65

These tremors appear when the affected part is actively maintaining a posture. Examples include the fine rapid tremor of hyperthyroidism, the tremors of anxiety and fatigue, and benign essential (and sometimes familial) tremor.

Answer 65

Postural Tremors

Question 66

, absent at rest, appear with movement and often get worse as the target gets closer. Causes include disorders of cerebellar pathways, as in multiple sclerosis, or any other disease of the cerebellum.

Answer 66

Intention tremors

Question 67

are rhythmic, repetitive, bizarre movements that chiefly involve the face, mouth, jaw, and tongue: grimacing, pursing of the lips, protrusions of the tongue, opening and closing of the mouth, and deviations of the jaw.

The limbs and trunk are involved less often.

These movements may be a late complication of psychotropic drugs such as phenothiazines, termed tardive (late) dyskinesias. They also occur in long-standing psychoses, in some elderly individuals, and in some edentulous persons.

Answer 67

Oral–Facial Dyskinesias

Question 68

brief, repetitive, stereotyped, coordinated movements occurring at irregular intervals. Examples include repetitive winking, grimacing, and shoulder shrugging. Causes include Tourette’s syndrome and drugs such as phenothiazines and amphetamines.

Answer 68

tics

Question 69

similar to athetoid movements, but often involve larger portions of the body, including the trunk. Grotesque, twisted postures may result. Causes include drugs such as phenothiazines, primary torsion dystonia, and as illustrated, spasmodic torticollis.

Answer 69

Dystonia

Question 70

slower and more twisting and writhing than choreiform movements, and have a larger amplitude. They most commonly involve the face and the distal extremities. Athetosis is often associated with spasticity. Causes include cerebral palsy.

Answer 70

Athetosis

Question 71

brief, rapid, jerky, irregular, and unpredictable. They occur at rest or interrupt normal coordinated movements. Unlike tics, they seldom repeat themselves. The face, head, lower arms, and hands are often involved. Causes include Sydenham’s chorea (with rheumatic fever) and Huntington’s disease.

Answer 71

Chorea

Question 72

seen in peripheral nerve disease, from radial nerve damage, and in central nervous system disease, producing hemiplegia, seen in stroke or multiple sclerosis.

Answer 72

Weakness of extension

Question 73

seen in cervical radiculopathy, de Quervain’s tenosynovitis, carpal tunnel syndrome, arthritis, and epicondylitis.

Answer 73

A weak grip

Question 74

Weak finger abduction occurs in

Answer 74

ulnar nerve disorders.

Question 75

Look for weak opposition of the thumb in ____________ such as ____________

Answer 75

median nerve disorders such as carpal tunnel syndrome

Question 76

Symmetric weakness of the proximal muscles suggests a

Answer 76

myopathy

Question 77

symmetric weakness of distal muscles suggests a

Answer 77

polyneuropathy

disorder of peripheral nerves

Question 78

__________ are seen in central nervous system lesions along the descending corticospinal tract. Look for associated upper motor neuron findings of weakness, spasticity, or a positive Babinski sign.

Answer 78

Hyperactive reflexes (hyperreflexia)

Question 79

scale for grading redflexes

Answer 79

4+: very brisk, hyperactive, with clonus (rhythmic oscillations between flection and extension)

3+: brisker than average, possibly but not necessarily indicative of disease

2+: average, normal

1+: somewhat diminished, low normal

0: no response

Question 80

seen in diseases of spinal nerve roots, spinal nerves, plexuses, or peripheral nerves. Look for associated findings of lower motor unit disease, namely weakness, atrophy, and fasciculations.

Answer 80

Hypoactive or absent reflexes (hyporeflexia)

Question 81

Assessing patients with stroke involves three fundamental questions, based on a careful history and detailed physical examination

Answer 81

What brain area and related vascular territory explain the patient’s findings?
Is the stroke ischemic or hemorrhagic?
If ischemic, is the mechanism thrombus or embolus?

Question 82

ischemic brain injury begins with a central core of very low perfusion and often irreversible cell death.

Answer 82

acute ischemic stroke

Question 83

This core is surrounded by an_____________ of metabolically disturbed cells that are still potentially viable, depending on restoration of blood flow and duration of ischemia.

Answer 83

ischemic penumbra

acute ischemic stroke

Question 84

most irreversible damage occurs in the first __________ after onset of symptoms,

Answer 84

3 to 6 hours

Question 85

therapies targeted to the ______ window achieve the best outcomes, with recovery in up to 50% of patients in some studies.

Answer 85

3-hour

Question 86

Contralateral leg weakness

Answer 86

Vascular Territory: Anterior circulation—anterior cerebral artery (ACA)

Includes stem of Circle of Willis connecting internal carotid artery to ACA, and the segment distal to ACA and its anterior choroidal branch

Question 87

Contralateral face, arm > leg weakness, sensory loss, field cut, aphasia (left MCA) or neglect, apraxia (right MCA)

Answer 87

Vascular Territory: Anterior circulation—middle cerebral artery (MCA)

Largest vascular bed for stroke

Question 88

Contralateral motor or sensory deficit without cortical signs

Answer 88

Vascular Territory: Subcortical circulation*—lenticulostriate deep penetrating branches of MCA

Small vessel subcortical lacunar infarcts in internal capsule, thalamus, or brainstem. Four common syndromes: pure motor hemiparesis; pure sensory hemianesthesia; ataxic hemiparesis; clumsy hand—dysarthria syndrome

Question 89

Contralateral field cut

Answer 89

Vascular Territory: Posterior circulation—posterior cerebral artery (PCA)

Includes paired vertebral and basilar artery, paired posterior cerebral arteries. Bilateral PCA infarction causes cortical blindness but preserved pupillary light reaction.

Question 90

Dysphagia, dysarthria, tongue/palate deviation and/or ataxia with crossed sensory/motor deficits (= ipsilateral face with contralateral body)

Answer 90

Vascular Territory: Posterior circulation—brainstem, vertebral, or basilar artery branches

Question 91

Oculomotor deficits and/or ataxia with crossed sensory/motor deficits

Answer 91

Vascular territory: posterior circulation—basilar artery

Complete basilar artery occlusion—“locked-in syndrome” with intact consciousness but with inability to speak and quadriplegia

Question 92

Mechanism: Sudden peripheral vasodilatation, especially in the skeletal muscles, without a compensatory rise in cardiac output. Heart rate then blood pressure fall. Often slow onset, slow offset.

Precipitating Factors:A strong emotion such as fear or pain

Predisposing Factors: Fatigue, hunger, a hot humid environment

Prodromal Manifestations: Restlessness, weakness, pallor, nausea, salivation, sweating, yawning

Answer 92

Vasodepressor or Vasovagal Syncope (the common faint)

Question 93

Mechanism: Inadequate vasoconstrictor reflexes in both arterioles and veins, with resultant venous pooling, decreased cardiac output, and low blood pressure

Precipitating Factors: Standing up

Predisposing Factors: Central and peripheral neuropathies: Parkinson disease, Shy-Drager syndrome; Lewy body disease diabetes, amyloidosis; antihypertensive vasodilator drugs; prolonged bed rest

Prodromal Manifestations: Often none

Answer 93

Orthostatic (Postural) Hypotension (orthostatic)

Question 94

Mechanism: Hypovolemia, a diminished blood volume insufficient to maintain cardiac output and blood pressure, especially in the upright position

Precipitating Factors: Standing up after hemorrhage or dehydration

Predisposing Factors: Central and peripheral neuropathies: Parkinson disease, Shy-Drager syndrome; Lewy body disease diabetes, amyloidosis; antihypertensive vasodilator drugs; prolonged bed rest

Answer 94

Orthostatic (Postural) Hypotension (orthostatic)

Question 95

Predisposing Factors: Bleeding from the GI tract or trauma, potent diuretics, vomiting, diarrhea, polyuria

Prodromal Manifestations: Light-headedness and palpitations (tachycardia) on standing up

Answer 95

Orthostatic (Postural) Hypotension (orthostatic)

Question 96

Mechanism:Neurally mediated, possible vagal stimulation

Precipitating Factors: Severe paroxysm of coughing

Predisposing Factors: Chronic bronchitis in a muscular man

Prodromal Manifestations: Often none except for cough

Answer 96

Cough Syncope

Question 97

Mechanism: Vasovagal stimulation

Precipitating Factors: Emptying the bladder after getting out of bed to void

Predisposing Factors: Nocturia, usually in elderly or adult men

Prodromal Manifestations: Often none

Answer 97

Micturition Syncope

Question 98

Mechanism: Decreased cardiac output from cardiac ischemia, ventricular arrhythmias, prolonged QT syndrome, persistent bradycardia, infrafascicular block. Often sudden onset; sudden offset.

Precipitating Factors: A sudden change in rhythm

Predisposing Factors: Heart disease, aging decrease tolerance of abnormal rhythms.

Prodromal Manifestations: Often none

Answer 98

Cardiovascular Disorders

Arrhythmias

Question 99

Mechanism: Vascular resistance falls with exercise, but cardiac output cannot rise due to outflow obstruction.

Precipitating Factors: Exercise

Predisposing Factors: Cardiac disorders

Prodromal Manifestations: Often none. Onset is sudden.

Answer 99

Cardiovascular Disorders

Aortic Stenosis and Hypertrophic Cardiomyopathy

Question 100

Mechanism: Sudden arrhythmia or decreased cardiac output

Precipitating Factors: Variable

Predisposing Factors: Coronary artery disease

Prodromal Manifestations: Ischemic chest pain; often none

Answer 100

Cardiovascular Disorders

Myocardial Infarction

Question 101

Mechanism: Sudden hypoxia or decreased cardiac output

Precipitating Factors: Variable, including prolonged bed rest and clotting disorders

Predisposing Factors: Deep vein thrombosis, bedrest hypercoagulable states (SLE; cancer), protein S or C deficiency, antithrombin III deficiency. Estrogen therapy

Prodromal Manifestations: Dyspnea, pleuritic chest pain

Answer 101

Cardiovascular Disorders

Massive Pulmonary Embolism

Question 102

Mechanism: Constriction of cerebral blood vessels secondary to hypocapnia induced by hyperventilation

Precipitating Factors: Anxiety, panic disorder

Predisposing Factors: Anxiety

Prodromal Manifestations: Dyspnea, palpitations, chest discomfort, numbness and tingling of the hands and around the mouth lasting for several minutes. Consciousness is often maintained.

Answer 102

Disorders Resembling Syncope

Hypocapnia due to Hyperventilation

Question 103

Mechanism: Insufficient glucose to maintain cerebral metabolism; secretion of epinephrine contributes to symptoms. True syncope is uncommon.

Precipitating Factors: Variable, including fasting

Predisposing Factors: Insulin therapy and a variety of metabolic disorders

Prodromal Manifestations: Sweating, tremor, palpitations, hunger, headache, confusion, abnormal behavior, coma

Answer 103

Disorders Resembling Syncope

Hypoglycemia

Question 104

Mechanism: The symbolic expression of an unacceptable idea through body language. Skin color and vital signs may be normal; sometimes with bizarre and purposive movements; occurrence in the presence of other people.

Precipitating Factors: Stressful situation

Predisposing Factors: Hysterical personality traits

Prodromal Manifestations: Variable

Answer 104

Disorders Resembling Syncope

Hysterical Fainting From Conversion Reaction

Question 105

Seizures are classified into (2)

Answer 105

focal and generalized

Question 106

Underlying causes should be identified as (3)

Answer 106

genetic, structural/metabolic, or unknown.

Question 107

“are conceptualized as originating within networks limited to one hemisphere. They may be discretely localized or more widely distributed. they may originate in subcortical structures.

Answer 107

Focal seizures

Question 108

for each seizure type waht is consistent from one seizure to another?

Answer 108

ictal onset

Question 109

some cases though there are more than one network, and more than one seizure type, but each individual seizure type has a consistent

Answer 109

site of onset

Question 110

Tonic and then clonic movements that start unilaterally in the hand, foot, or face and spread to other body parts on the same side

Normal consciousness

Answer 110

Focal Seizures Without Impairment of Consciousness or Awareness: With observable motor and autonomic symptoms

Jacksonian

Question 111

Turning of the head and eyes to one side, or tonic and clonic movements of an arm or leg without the Jacksonian spread

Normal consciousness

Answer 111

Focal Seizures Without Impairment of Consciousness or Awareness: With observable motor and autonomic symptoms

Other motor

Question 112

A “funny feeling” in the epigastrium, nausea, pallor, flushing, lightheadedness

Normal consciousness

Answer 112

Focal Seizures Without Impairment of Consciousness or Awareness: With observable motor and autonomic symptoms

with autonomic symptoms

Question 113

Numbness, tingling; simple visual, auditory, or olfactory hallucinations such as flashing lights, buzzing, or odors

Normal consciousness

Answer 113

Focal Seizures Without Impairment of Consciousness or Awareness: With subjective sensory or psychic phenomena

Question 114

Anxiety or fear; feelings of familiarity (déjà vu) or unreality; dreamy states; fear or rage; flashback experiences; more complex hallucinations

Normal consciousness

Answer 114

Focal Seizures Without Impairment of Consciousness or Awareness: With subjective sensory or psychic phenomena

Question 115

The seizure may or may not start with the autonomic or psychic symptoms outlined above. Consciousness is impaired, and the person appears confused. Automatisms include automatic motor behaviors such as chewing, smacking the lips, walking about, and unbuttoning clothes; also more complicated and skilled behaviors such as driving a car.

Postictal state: The patient may remember initial autonomic or psychic symptoms (which are then termed an aura), but is amnesic for the rest of the seizure. Temporary confusion and headache may occur.

Answer 115

Focal Seizures With Impairment of Consciousness

Question 116

Partial seizures that become generalized resemble tonic–clonic seizures (see next page). Unfortunately, the patient may not recall the focal onset, and observers may overlook it.

Postictal state: As in a tonic–clonic seizure, described on the next page. Two attributes indicate a partial seizure that has become generalized: (1) the recollection of an aura, and (2) a unilateral neurologic deficit during the postictal period.

Answer 116

Focal Seizures That Become Generalized

Question 117

“are conceptualized as originating as some point within, and rapidly engaging, bilaterally distributed networks….that include cortical and subcortical structures, but do not necessarily include the entire cortex… the location and lateralization are not consistent from one seizure to another.

can be asymmetric.

They may begin with body movements, impaired consciousness, or both.

Answer 117

Generalized seizures

Question 118

begin after age 30, suspect either a partial seizure that has become generalized or a general seizure caused by a toxic or metabolic disorder. Toxic and metabolic causes include withdrawal from alcohol or other sedative drugs, uremia, hypoglycemia, hyperglycemia, hyponatremia, and bacterial meningitis.

Answer 118

tonic–clonic seizures

Question 119

The person loses consciousness suddenly, sometimes with a cry, and the body stiffens into tonic extensor rigidity. Breathing stops, and the person becomes cyanotic. A clonic phase of rhythmic muscular contraction follows. Breathing resumes and is often noisy, with excessive salivation. Injury, tongue biting, and urinary incontinence may occur.

Postictal (post seizure) state: Confusion, drowsiness, fatigue, headache, muscular aching, and sometimes the temporary persistence of bilateral neurologic deficits such as hyperactive reflexes and Babinski responses. The person has amnesia for the seizure and recalls no aura.

Answer 119

Generalized Seizures

Tonic–Clonic (grand mal)

Question 120

A sudden brief lapse of consciousness, with momentary blinking, staring, or movements of the lips and hands but no falling. Two subtypes are recognized. Typical absences last less than 10 second and stop abruptly. Atypical absences may last more than 10 second.

Postictal (post seizure) state: No aura recalled. In petit mal absences, a prompt return to normal; in atypical absences, some postictal confusion

Answer 120

Generalized Seizures:

Absence

Question 121

Sudden, brief, rapid jerks, involving the trunk or limbs. Associated with a variety of disorders

Postictal (post seizure) state: Variable

Answer 121

Generalized Seizures:

Myoclonic

Question 122

Sudden loss of consciousness with falling but no movements. Injury may occur.

Postictal (post seizure) state: Either a prompt return to normal or a brief period of confusion

Answer 122

Generalized Seizures:

Myoclonic Atonic (drop attack)

Question 123

The movements may have personally symbolic significance and often do not follow a neuroanatomic pattern. Injury is uncommon.

Postictal (post seizure) state: Variable

Answer 123

Pseudoseizures:

May mimic seizures but are due to a conversion reaction (a psychological disorder)

Question 124

Disorders of speech fall into three groups affecting:

Answer 124

(1) the voice,
(2) the articulation of words, and
(3) the production and comprehension of language.

Question 125

refers to a loss of voice that accompanies disease affecting the larynx or its nerve supply.

Answer 125

Aphonia

Question 126

refers to less severe impairment in the volume, quality, or pitch of the voice. For example, a person may be hoarse or only able to speak in a whisper. Causes include laryngitis, laryngeal tumors, and a unilateral vocal cord paralysis (CN X).

Answer 126

Dysphonia

Question 127

refers to a defect in the muscular control of the speech apparatus (lips, tongue, palate, or pharynx). Words may be nasal, slurred, or indistinct, but the central symbolic aspect of language remains intact. Causes include motor lesions of the central or peripheral nervous system, parkinsonism, and cerebellar disease.

Answer 127

Dysarthria

Question 128

refers to a disorder in producing or understanding language. It is often caused by lesions in the dominant cerebral hemisphere, usually the left.

Answer 128

Aphasia

Question 129

(1) Wernicke’s, a fluent (receptive) aphasia, and (2) Broca’s, a nonfluent (or expressive) aphasia.

There are other less-common kinds of aphasia, which are distinguished by differing responses on the specific tests listed. Neurologic consultation is usually indicated.

Answer 129

two common types of aphasia

Question 130

Qualities of Spontaneous Speech: Fluent; often rapid, voluble, and effortless. Inflection and articulation are good, but sentences lack meaning and words are malformed (paraphasias) or invented (neologisms). Speech may be totally incomprehensible

Word Comprehension: Impaired

Reputation: Impaired

Naming: Impaired

Reading Comprehension: Impaired

Writing: Impaired

Location of Lesion: Posterior superior temporal lobe

Answer 130

Wernicke’s Aphasia

Question 131

Qualities of Spontaneous Speech: Nonfluent; slow, with few words and laborious effort. Inflection and articulation are impaired but words are meaningful, with nouns, transitive verbs, and important adjectives. Small grammatical words are often dropped.

Word Comprehension: Fair to good

Reputation: Impaired

Naming: Impaired, though the patient recognizes objects

Reading Comprehension: Fair to good

Writing: Impaired

Location of Lesion: Posterior inferior frontal lobe

Answer 131

Broca’s Aphasia

Question 132

rhythmic oscillation of the eyes, analogous to a tremor in other parts of the body.

It has multiple causes, including impairment of vision in early life, disorders of the labyrinth and the cerebellar system, and drug toxicity.

occurs normally when a person watches a rapidly moving object (e.g., a passing train).

Answer 132

Nystagmus

Question 133

observe for nystagmus only within the field of

Answer 133

full binocular vision.

Question 134

** picture of both eyes looking to the PATIENTS right ***

Answer 134

Nystagmus on Right Lateral Gaze
Nystagmus Present (Right Lateral Gaze)

Question 135

Left-Beating Nystagmus—a Quick Jerk to the Left in Each Eye, Then a Slow Drift to the Right

Answer 135

Direction of the Quick and Slow Phases

Question 136

Nystagmus usually has both slow and fast movements, but is defined by its

Answer 136

fast phase

Question 137

if the eyes jerk quickly to the patient’s left and drift back slowly to the right, the patient is said to have

Answer 137

left-beating nystagmus.

Question 138

Occasionally, nystagmus consists only of coarse oscillations without quick and slow components. It is then said to be

Answer 138

pendular

Question 139

3 planes of movements for nystagmus

Answer 139

1. Horizontal Nystagmus
2. Vertical
3. Rotary

Question 140

It is the ____ of the movements, not the direction of the gaze, that defines this variable.

Answer 140

plane

Question 141

Facial weakness or paralysis may result either from (2)

Answer 141

(1) a peripheral lesion of CN VII, the facial nerve, anywhere from its origin in the pons to its periphery in the face, or
(2) a central lesion involving the upper motor neuron system between the cortex and the pons.

Question 142

A peripheral lesion of CN VII, exemplified here by a Bell’s palsy, is compared with a central lesion, exemplified by a left hemispheric cerebrovascular accident. These can be distinguished by their

Answer 142

different effects on the upper part of the face.

go to page 757 in BATES… great pictures of this! :)

Question 143

The lower part of the face normally is controlled by _______________ located on only one side of the cortex—the opposite side.

Left hemispheric damage to these pathways, as in a stroke, paralyzes the right lower face.

Answer 143

upper motor neurons

Question 144

he upper face, however, is controlled by ______________

Even though the upper motor neurons on the left are destroyed, others on the right remain, and the right upper face continues to function fairly well.

Answer 144

pathways from both sides of the cortex.

Question 145

____________ nerve damage to CN VII paralyzes the entire right side of the face, including the forehead.

Answer 145

Peripheral

Question 146

other symptoms with Peripheral Nerve damage of CN VII

Answer 146

Closing eyes: right eye does not close; eyeball rolls up

flat nasolabial fold on pts right side

Raising eyebrows: forehead not wrinkled on pts right; eyebrow not raised on right

paralysis of lower face on right

Question 147

CN VII—Central Lesion

Answer 147

Closing eyes: right eye closes with slight weakness

flat right nasolabial fold

Raising eyebrows: right forehead wrinkled, eyebrow raised

right paralysis of lower face

Question 148

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.

originate in the motor cortex of the brain. 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 cranial nerves are termed corticobulbar.

Answer 148

The corticospinal tracts

Question 149

his 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.

Answer 149

basal ganglia system

Question 150

receives both sensory and motor input and coordinates motor activity, maintains equilibrium, and helps to control posture.

Answer 150

cerebellar system.

Question 151

Stroke at a Glance: Key Facts for Prevention and Patient Education

–> Stroke affects 7,000,000 Americans at a cost of $40 billion annually.

–> Stroke prevalence and mortality are disproportionately higher in African Americans, compared to whites:

–> Prevalence, black vs. white men: 4.5% vs. 2.4%; black vs. white women 4.4% vs. 3.3%

–> Mortality per 100,000, black vs. white men—67 vs. 40; black vs. white women—55 vs. 40

(Cardiovascular disease, including stroke, is the greatest contributor to the 6-year disparity in life expectancy for African Americans compared to whites. Other contributing factors include a higher prevalence of hypertension, diabetes, left ventricular hypertrophy, and income and insurance gaps.)

–> The prevalence of silent stroke increases progressively from 11% between ages 55 and 64 to 43% after age 85.

–> Individuals with TIA have a 1-year mortality of ~12%, and a 10-year risk of stroke and death from cardiovascular disease of 19% and 43%.

–> Women ages 45 to 54 are twice as likely as men to report previous stroke. Midlife risk factors now include autoimmune collagen vascular disease and history of preeclampsia, gestational diabetes, and pregnancy-induced hypertension.

–> Public awareness of stroke warning signs is improving, but only 17% of the U. S. population are aware of correct warning signs and would call 911 if they thought someone was having a stroke.

–> Stroke outcomes markedly improve if therapy is given within 3 hours of onset of symptoms; however, the median emergency room arrival time from symptom onset is 3 to 6 hours.

–> Physician awareness of warning signs, risk factors, and prevention remains insufficient.

Answer 151

i know it is long.. but it is just for reading purposes

Question 152

1. Sudden numbness or weakness of the face, arm, or leg
2. Sudden confusion, trouble speaking or understanding
3. Sudden trouble seeing in one or both eyes
4. Sudden trouble walking, dizziness, or loss of balance or coordination
5. Sudden severe headache

Answer 152

AHA/ASA Stroke Attack Warning Signs

Question 153

Hypertension: Hypertension is the leading risk factor for both ischemic and hemorrhagic stroke. Individuals with blood pressure

Answer 153

Behavioral Risk Factors
for stokes

Primary Prevention for Ischemic Stoke

…. again i know it is long…. just read it

Question 154

Atrial fibrillation:
Valvular (rheumatic) and nonvalvular atrial fibrillation increases risk of stroke 5- and 17-fold, respectively, compared to controls. Risk for ischemic stroke with warfarin therapy and aspirin therapy are ~68% and ~20%, but individual risk levels are variable. 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. Patients with atrial fibrillation at highest risk are those with additional stroke risk factors: prior TIA or stroke, hypertension, diabetes, poor left ventricular function, rheumatic mitral valve disease, and women over age 75.

Carotid artery disease:
The prevalence of atherosclerotic carotid artery disease of the extracranial carotid arteries in the U.S. population over age 65 is 1%. Medical therapy in individuals with asymptomatic carotid artery stenosis of 60% to 70% has improved, with an annual stroke rate of 1% annually. Experts recommend risk factor reduction and medical therapy, reserving endarterectomy and stenting for highly selected individuals. In 2007, the U.S. Preventive Services Task Force recommended against screening the general population due to lack of evidence that use of duplex ultrasonography reduces stroke

Answer 154

Disease-Specific Risk Factors for strokes

Primary Prevention for Ischemic Stoke

…. again i know it is long…. just read it

Question 155

Don’t dilate the pupils, the single most important clue to the underlying cause of coma (structural vs. metabolic), and

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.

Answer 155

Don’ts” When Assessing the Comatose Patient

Question 156

Process: Neuronal dysfunction, possibly of brainstem origin, involving low serotonin, spreading cortical depression and trigemino-vascular activation. Types: with aura; without aura; variants.

Location: Unilateral in ~70%; bifrontal or global in ~30%

Quality/Severity: Throbbing or aching, variable in severity.

Onset: Fairly rapid, reaching a peak in 1–2 hours

Duration: 4–72 hours

Course: Peak incidence early to mid-adolescence; prevalence is ~6% in men and ~15% in women. Recurrent—usually monthly, but weekly in ~10%

Associated Factors: Nausea, vomiting, photophobia, phonophobia, aura in 30%, either visual (flickering, zig-zagging lines), motor (paresthesias of hand, arm, or face, or language dysfunction).

Aggregate or provoke: Alcohol, certain foods, or stress may provoke; also menses, high altitude; aggravated by noise and bright light

Relieving Factors: Quiet, dark room; sleep; sometimes transient relief from pressure on the involved arter

Answer 156

Mirgaines primary Headache

Question 157

Process: Unclear—possibly heightened CNS pain sensitivity. Involves pericranial muscle tenderness. Etiology also unclear.

Location: Usually bilateral; may be generalized or localized to the back of the head and upper neck or to the frontotemporal area

Quality/Severity: Steady; pressing or tightening;nonthrobbing. Mild to moderate intensity

Onset: Gradual

Duration: 30 minutes to 7 days

Course: Episodic; may be chronic; Annual prevalence ~40%

Associated Factors: Sometimes photophobia, phonophobia; nausea absent

Aggregate or provoke: Sustained muscle tension, as in driving or typing

Relieving Factors: Possibly massage, relaxation

Answer 157

tension primary headache

Question 158

Process: Unclear—possibly hypothalamic then trigemino-autonomic activation.

Location: Unilateral, usually behind or around the eye or temple

Quality/Severity: Deep, continuous, severe

Onset: Abrupt; peaks within minutes

Duration: Up to 3 hours

Course: Episodic, clustered in time, with several each day for 4–8 weeks and then relief for 6–12 months; prevalence

Answer 158

Cluster Primary Headache

Question 159

Process: Withdrawal of medication

Location: Previous headache pattern

Quality/Severity:

Onset: Variable

Duration: Variable

Course: Depends on frequency of “mini-withdrawals”

Associated factors: Depends on prior headache pattern

Factors that aggravate or provoke: Fever, carbon monoxide, hypoxia, withdrawal of caffeine, other headache triggers

Factors that relieve: Depends on cause

Answer 159

Secondary Headaches:

Analgesic Rebound

Question 160

Process: Probably the sustained contraction of the extraocular muscles, and possibly of the frontal, temporal, and occipital muscles

Location: Around and over the eyes; may radiate to the occipital area

Quality/Severity: Steady, aching, dull

Onset: gradual

Duration:Variable

Course: Variable

Associated factors: Eye fatigue, “sandy” sensations in the eyes, redness of the conjunctiva

Factors that aggravate or provoke: Prolonged use of the eyes, particularly for close work

Factors that relieve: Rest of the eyes

Answer 160

Headaches From Eye Disorders:

Errors of Refraction (farsightedness and astigmatism, but not nearsightedness)

Question 161

Process: Sudden increase in intraocular pressure

Location: In and around one eye

Quality/Severity: Steady, aching, often severe

Onset: Often rapid

Duration: Variable, may depend on treatment

Course: Variable, may depend on treatment

Associated factors: Diminished vision, sometimes nausea and vomiting

Factors that aggravate or provoke: Sometimes provoked by drops that dilate the pupils

Answer 161

Headaches From Eye Disorders

Acute Glaucoma

Question 162

Process: Mucosal inflammation of the paranasal sinuses

Location: Usually above the eye (frontal sinus) or over the maxillary sinus

Quality/Severity: Aching or throbbing, variable in severity; consider possible migraine

Onset: Variable

Duration: Often several hours at a time, recurring over days or longer

Course: Often recurrent in a repetitive daily pattern

Associated factors: Local tenderness, nasal congestion, discharge, and fever

Factors that aggravate or provoke: May be aggravated by coughing, sneezing, or jarring the head

Factors that relieve: Nasal decongestants, antibiotics

Answer 162

Headache From Sinusitis

Question 163

Process: Infection of the meninges surrounding the brain and spinal cord

Location: Generalized

Quality/Severity: Steady or throbbing, very severe

Onset: Fairly rapid, usually

Answer 163

Meningitis

Question 164

Process: Bleeding, most often from a ruptured intracranial aneurysm

Location: Generalized

Quality/Severity: Very severe, “the worst of my life”

Onset: Usually abrupt, severe with prodromal symptoms

Duration: Variable, usually days

Course: A persistent headache in an acute illness

Associated factors: Nausea, vomiting, possibly loss of consciousness, neck pain

Factors that relieve: Subspecialty treatments

Answer 164

Subarachnoid Hemorrhage

Question 165

Process: Displacement of or traction on pain-sensitive arteries and veins or pressure on nerves

Location: Varies with the location of the tumor

Quality/Severity: Aching, steady, variable in intensity

Onset: Variable

Duration: Often brief

Course: Often intermittent but progressive

Factors that aggravate or provoke: May be aggravated by coughing, sneezing, or sudden movements of the head

Factors that relieve: Subspecialty treatments

Answer 165

Brain Tumor

Question 166

Process: Vasculitis from cell-mediated immune response to elastic lamina of artery

Location: Localized near the involved artery, most often the temporal, but also the occipital; age related

Quality/Severity: Throbbing, generalized, persistent; often severe

Onset: Gradual or rapid

Duration: Variable

Course: Recurrent or persistent over weeks to months

Associated factors: Tenderness of the adjacent scalp; fever (in ~50%), fatigue, weight loss; new headache (~60%), jaw claudication (~50%), visual loss or blindness (~15%–20%), polymyalgia rheumatica (~50%)

Factors that aggravate or provoke: Movement of neck and shoulders

Answer 166

Giant Cell (Temporal) Arteritis

Question 167

Process: Follows acceleration-deceleration traumatic brain injury

Location: May be localized to the injured area, but not necessarily

Quality/Severity: Generalized, dull, aching, constant; may have features of tension and migraine headaches

Onset: Within 7 days of the injury up to 3 months

Duration: Weeks, months, or even years

Course: Tends to diminish over time

Associated factors: Poor concentration, problems with memory, vertigo, irritability, restlessness, fatigue

Factors that aggravate or provoke: Mental and physical exertion, straining, stooping, emotional excitement, alcohol

Factors that relieve: Rest; medication

Answer 167

Postconcussion Headache

Question 168

Process: Compression of CN V, often by aberrant loop of artery or vein, usually near entry to pons

Location: Cheek, jaws, lips, or gums; trigeminal nerve divisions 2 and 3 > 1

Quality/Severity: Shocklike, stabbing, burning; severe

Onset: Abrupt, paroxysmal

Duration: Each jab lasts seconds but recurs at intervals of seconds or minutes

Course: May last for months, then disappear for months, but often recurs. It is uncommon at night.

Associated factors: Exhaustion from recurrent pain

Factors that aggravate or provoke: Touching certain areas of the lower face or mouth; chewing, talking, brushing teeth

Factors that relieve: Medication; neurovascular decompression

Answer 168

Cranial Neuralgias :

Trigeminal Neuralgia (CNV)