CA Bates reading Flashcards
1
Q
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
A
Cerebral Cortex (1)
Central Nervous System Disorders
2
Q
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
A
Brainstem (2)
Central Nervous System Disorders
3
Q
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
A
Spinal Cord (3)
Central Nervous System Disorders
4
Q
Motor: Slowness of movement (bradykinesia), rigidity, and tremor
Sensory: Sensation not affected
DTR: normal or decreased
ex of cause: Parkinsonism
A
Subcortical Gray Matter: Basal Ganglia (4)
Central Nervous System Disorders
5
Q
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
A
Cerebellar
Central Nervous System Disorders
6
Q
Motor: Weakness and atrophy in a segmental or focal pattern; fasciculations
Sensory: Sensation intact
DTR: Decreased
ex of causes: Polio, amyotrophic lateral sclerosis
A
Anterior Horn Cell (1)
Peripheral Nervous System Disorders
7
Q
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
A
Spinal Roots and Nerves (2)
Peripheral Nervous System Disorders
8
Q
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
A
Peripheral Nerve—Mononeuropathy (3)
Peripheral Nervous System Disorders
9
Q
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
A
Peripheral Nerve—Polyneuropathy (4)
Peripheral Nervous System Disorders
10
Q
Motor: Fatigability more than weakness
Sensory: Sensation intact
DTR: Normal
ex of cause: Myasthenia gravis
A
Neuromuscular Junction (5)
Peripheral Nervous System Disorders
11
Q
Motor: Weakness usually more proximal than distal; fasciculations rare
Sensory: Sensation intact
DTR: Normal or decreased
ex of cause: Muscular dystrophy
A
Muscle (6)
Peripheral Nervous System Disorders
12
Q
Although there are many causes of coma, most can be classified as either (2 types)
A
structural or metabolic
13
Q
Arousal centers poisoned or critical substrates depleted
A
Toxic–Metabolic coma
14
Q
Lesion destroys or compresses brainstem arousal areas, either directly or secondary to more distant expanding mass lesions.
A
Structural coma
15
Q
Respiratory pattern:
If regular, may be normal or hyperventilation. If irregular, usually Cheyne-Stokes
A
Toxic–Metabolic coma
16
Q
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
A
Toxic–Metabolic coma
17
Q
Level of consciousness:
Changes after pupils change
A
Toxic–Metabolic coma
18
Q
causes: Uremia, hyperglycemia alcohol, drugs, liver failure hypothyroidism, hypoglycemia, anoxia, ischemia meningitis, encephalitis hyperthermia, hypothermia
A
Toxic–Metabolic coma
19
Q
respiratory pattern: Irregular, especially Cheyne-Stokes or ataxic breathing. Also with selected stereotypical patterns like “apneustic” respiration (peak inspiratory arrest) or central hyperventilation
A
Structural coma
20
Q
pupillary size and reaction: Unequal or unreactive to light (fixed)
A
Structural coma
21
Q
Midposition, fixed—suggests
A
midbrain compression
22
Q
Dilated, fixed—suggests
A
compression of CN III from herniation
23
Q
LOC: changes BEFORE pupils change
A
Structural coma
24
Q
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
A
structural coma
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.
size, equality, and light reactions
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.
Bilaterally small pupils (1–2.5 mm)
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.
Pinpoint pupils (
28
Midposition fixed pupils
Pupils that are in the midposition or slightly dilated (4–6 mm) and are fixed to light suggest structural damage in the midbrain
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.
Bilaterally fixed and dilated pupils
30
may be due to cocaine, amphetamine, LSD, or other sympathetic nervous system agonists.
Bilaterally large reactive pupils
31
warns of herniation of the temporal lobe, causing compression of the oculomotor nerve and midbrain.
A pupil that is fixed and another dilated
32
is most commonly seen in diabetic patients with infarction of CN III.
A single large pupil
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.
Oculocephalic Reflex (Doll’s Eye Movements)
34
In irritative lesions from epilepsy or early cerebral hemorrhage, the eyes _________ from the affected hemisphere.
Look away
35
In structural hemispheric lesions, the eyes _______________ in the affected hemisphere.
“look at the lesion”
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
midbrain or pons.
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.
oculocephalic
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.
Decorticate Rigidity (Abnormal Flexor Response)
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
hemiplegia (early)
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.
Decerebrate Rigidity (Abnormal Extensor Response)
41
A gait that lacks coordination, with reeling and instability, is called
may be due to cerebellar disease, loss of position sense, or intoxication
ataxic
42
Walk heel-to-toe in a straight line
may reveal an ataxia not previously obvious.
Tandem walking
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.
Walk on the toes, then on the heels
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.
Hop in place on each foot in turn (if the patient is not too ill)
45
difficulty suggests proximal weakness (extensors of the hip), weakness of the quadriceps (the extensor of the knee), or both.
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.
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.
Spastic Hemiparesis
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
Scissors Gait
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.
Steppage Gait
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).
Parkinsonian Gait
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.
Cerebellar Ataxia
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.
Sensory Ataxia
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
Spasiticity
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
Rigidity
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
Flaccidity
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
Paratonia
56
Marked floppiness indicates muscle ______ or _______ , usually from a disorder of the peripheral motor system.
hypotonia or flaccidity
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.
spasticity
58
is increased resistance throughout the range of movement and in both directions; it is not rate-dependent.
Rigidity
59
refers to weakness of one-half of the body
Hemiparesis
60
to paralysis of one-half of the body.
hemiplegia
61
means paralysis of the legs; quadriplegia means paralysis of all four limbs.
Paraplegia
62
With flexion and extension of the wrist or forearm, a superimposed rachetlike jerkiness is called
cogwheel rigidity
63
Tremors are rhythmic oscillatory movements, which may be roughly subdivided into three groups:
resting (or static) tremors,
postural tremors, and
intention tremors.
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.
Resting (Static) Tremors
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.
Postural Tremors
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.
Intention tremors
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.
Oral–Facial Dyskinesias
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.
tics
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.
Dystonia
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.
Athetosis
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.
Chorea
72
seen in peripheral nerve disease, from radial nerve damage, and in central nervous system disease, producing hemiplegia, seen in stroke or multiple sclerosis.
Weakness of extension
73
seen in cervical radiculopathy, de Quervain’s tenosynovitis, carpal tunnel syndrome, arthritis, and epicondylitis.
A weak grip
74
Weak finger abduction occurs in
ulnar nerve disorders.
75
Look for weak opposition of the thumb in ____________ such as ____________
median nerve disorders such as carpal tunnel syndrome
76
Symmetric weakness of the proximal muscles suggests a
myopathy
77
symmetric weakness of distal muscles suggests a
polyneuropathy
disorder of peripheral nerves
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.
Hyperactive reflexes (hyperreflexia)
79
scale for grading redflexes
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
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.
Hypoactive or absent reflexes (hyporeflexia)
81
Assessing patients with stroke involves three fundamental questions, based on a careful history and detailed physical examination
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?
82
ischemic brain injury begins with a central core of very low perfusion and often irreversible cell death.
acute ischemic stroke
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.
ischemic penumbra
acute ischemic stroke
84
most irreversible damage occurs in the first __________ after onset of symptoms,
3 to 6 hours
85
therapies targeted to the ______ window achieve the best outcomes, with recovery in up to 50% of patients in some studies.
3-hour
86
Contralateral leg weakness
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
87
Contralateral face, arm > leg weakness, sensory loss, field cut, aphasia (left MCA) or neglect, apraxia (right MCA)
Vascular Territory: Anterior circulation—middle cerebral artery (MCA)
Largest vascular bed for stroke
88
Contralateral motor or sensory deficit without cortical signs
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
89
Contralateral field cut
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.
90
Dysphagia, dysarthria, tongue/palate deviation and/or ataxia with crossed sensory/motor deficits (= ipsilateral face with contralateral body)
Vascular Territory: Posterior circulation—brainstem, vertebral, or basilar artery branches
91
Oculomotor deficits and/or ataxia with crossed sensory/motor deficits
Vascular territory: posterior circulation—basilar artery
Complete basilar artery occlusion—“locked-in syndrome” with intact consciousness but with inability to speak and quadriplegia
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
Vasodepressor or Vasovagal Syncope (the common faint)
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
Orthostatic (Postural) Hypotension (orthostatic)
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
Orthostatic (Postural) Hypotension (orthostatic)
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
Orthostatic (Postural) Hypotension (orthostatic)
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
Cough Syncope
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
Micturition Syncope
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
Cardiovascular Disorders
Arrhythmias
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.
Cardiovascular Disorders
Aortic Stenosis and Hypertrophic Cardiomyopathy
100
Mechanism: Sudden arrhythmia or decreased cardiac output
Precipitating Factors: Variable
Predisposing Factors: Coronary artery disease
Prodromal Manifestations: Ischemic chest pain; often none
Cardiovascular Disorders
Myocardial Infarction
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
Cardiovascular Disorders
Massive Pulmonary Embolism
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.
Disorders Resembling Syncope
Hypocapnia due to Hyperventilation
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
Disorders Resembling Syncope
Hypoglycemia
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
Disorders Resembling Syncope
Hysterical Fainting From Conversion Reaction
105
Seizures are classified into (2)
focal and generalized
106
Underlying causes should be identified as (3)
genetic, structural/metabolic, or unknown.
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.
Focal seizures
108
for each seizure type waht is consistent from one seizure to another?
ictal onset
109
some cases though there are more than one network, and more than one seizure type, but each individual seizure type has a consistent
site of onset
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
Focal Seizures Without Impairment of Consciousness or Awareness: With observable motor and autonomic symptoms
Jacksonian
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
Focal Seizures Without Impairment of Consciousness or Awareness: With observable motor and autonomic symptoms
Other motor
112
A “funny feeling” in the epigastrium, nausea, pallor, flushing, lightheadedness
Normal consciousness
Focal Seizures Without Impairment of Consciousness or Awareness: With observable motor and autonomic symptoms
with autonomic symptoms
113
Numbness, tingling; simple visual, auditory, or olfactory hallucinations such as flashing lights, buzzing, or odors
Normal consciousness
Focal Seizures Without Impairment of Consciousness or Awareness: With subjective sensory or psychic phenomena
114
Anxiety or fear; feelings of familiarity (déjà vu) or unreality; dreamy states; fear or rage; flashback experiences; more complex hallucinations
Normal consciousness
Focal Seizures Without Impairment of Consciousness or Awareness: With subjective sensory or psychic phenomena
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.
Focal Seizures With Impairment of Consciousness
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.
Focal Seizures That Become Generalized
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.
Generalized seizures
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.
tonic–clonic seizures
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.
Generalized Seizures
Tonic–Clonic (grand mal)
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
Generalized Seizures:
Absence
121
Sudden, brief, rapid jerks, involving the trunk or limbs. Associated with a variety of disorders
Postictal (post seizure) state: Variable
Generalized Seizures:
Myoclonic
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
Generalized Seizures:
Myoclonic Atonic (drop attack)
123
The movements may have personally symbolic significance and often do not follow a neuroanatomic pattern. Injury is uncommon.
Postictal (post seizure) state: Variable
Pseudoseizures:
May mimic seizures but are due to a conversion reaction (a psychological disorder)
124
Disorders of speech fall into three groups affecting:
(1) the voice,
(2) the articulation of words, and
(3) the production and comprehension of language.
125
refers to a loss of voice that accompanies disease affecting the larynx or its nerve supply.
Aphonia
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).
Dysphonia
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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.
Dysarthria
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refers to a disorder in producing or understanding language. It is often caused by lesions in the dominant cerebral hemisphere, usually the left.
Aphasia
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(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.
two common types of aphasia
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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
Wernicke’s Aphasia
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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
Broca’s Aphasia
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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).
Nystagmus
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observe for nystagmus only within the field of
full binocular vision.
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** picture of both eyes looking to the PATIENTS right ***
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Nystagmus on Right Lateral Gaze
Nystagmus Present (Right Lateral Gaze)
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Left-Beating Nystagmus—a Quick Jerk to the Left in Each Eye, Then a Slow Drift to the Right
Direction of the Quick and Slow Phases
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Nystagmus usually has both slow and fast movements, but is defined by its
fast phase
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if the eyes jerk quickly to the patient’s left and drift back slowly to the right, the patient is said to have
left-beating nystagmus.
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Occasionally, nystagmus consists only of coarse oscillations without quick and slow components. It is then said to be
pendular
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3 planes of movements for nystagmus
1. Horizontal Nystagmus
2. Vertical
3. Rotary
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It is the ____ of the movements, not the direction of the gaze, that defines this variable.
plane
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Facial weakness or paralysis may result either from (2)
(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.
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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
different effects on the upper part of the face.
go to page 757 in BATES... great pictures of this! :)
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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.
upper motor neurons
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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.
pathways from both sides of the cortex.
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____________ nerve damage to CN VII paralyzes the entire right side of the face, including the forehead.
Peripheral
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other symptoms with Peripheral Nerve damage of CN VII
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
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CN VII—Central Lesion
Closing eyes: right eye closes with slight weakness
flat right nasolabial fold
Raising eyebrows: right forehead wrinkled, eyebrow raised
right paralysis of lower face
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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.
The corticospinal tracts
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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.
basal ganglia system
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receives both sensory and motor input and coordinates motor activity, maintains equilibrium, and helps to control posture.
cerebellar system.
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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.
i know it is long.. but it is just for reading purposes
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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
AHA/ASA Stroke Attack Warning Signs
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Hypertension: Hypertension is the leading risk factor for both ischemic and hemorrhagic stroke. Individuals with blood pressure
Behavioral Risk Factors
for stokes
Primary Prevention for Ischemic Stoke
.... again i know it is long.... just read it
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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
Disease-Specific Risk Factors for strokes
Primary Prevention for Ischemic Stoke
.... again i know it is long.... just read it
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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.
Don’ts” When Assessing the Comatose Patient
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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
Mirgaines primary Headache
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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
tension primary headache
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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
Cluster Primary Headache
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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
Secondary Headaches:
Analgesic Rebound
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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
Headaches From Eye Disorders:
Errors of Refraction (farsightedness and astigmatism, but not nearsightedness)
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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
Headaches From Eye Disorders
Acute Glaucoma
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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
Headache From Sinusitis
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Process: Infection of the meninges surrounding the brain and spinal cord
Location: Generalized
Quality/Severity: Steady or throbbing, very severe
Onset: Fairly rapid, usually
Meningitis
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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
Subarachnoid Hemorrhage
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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
Brain Tumor
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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
Giant Cell (Temporal) Arteritis
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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
Postconcussion Headache
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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
Cranial Neuralgias :
Trigeminal Neuralgia (CNV)
