(17) Nervous System Tables Flashcards
1
Q
Tables 17-1 and 17-2 not done
A
p. 774-777
2
Q
Vasovagal Syncope (the common faint) & Vasodepressor Syncope: Mechanism
A
For vasovagal syncope: reflex withdrawal of sympathetic
tone and increased vagal tone causing drop in blood
pressure and heart rate
For vasodepressor syncope: same mechanism but no
vagal surge or drop in heart rate
Baroreflexes normal
3
Q
Vasovagal Syncope (the common faint) & Vasodepressor Syncope: Precipitating Factors
A
Strong emotion such as fear or
pain, prolonged standing, hot
humid environment
4
Q
Vasovagal Syncope (the common faint) & Vasodepressor Syncope: Predisposing Factors
A
Fatigue, hunger, preload reduction from
dehydration, diuretics, vasodilators
5
Q
Vasovagal Syncope (the common faint) & Vasodepressor Syncope: Prodromal Manifestations
A
Usually >10 s. Palpitations,
nausea, blurred vision, warmth,
pallor, diaphoresis, lightheadedness
6
Q
Vasovagal Syncope (the common faint) & Vasodepressor Syncope: Postural Associations
A
Usually occurs when
standing, at times
when sitting
7
Q
Vasovagal Syncope (the common faint) & Vasodepressor Syncope: Recovery
A
Prompt return of consciousness after lying down, but pallor, weakness, nausea, and slight confusion may persist for a time Most common type of syncope
8
Q
Orthostatic hypotension: definition
A
drop in SBP >20 or DBP >10 within 3 min of standing
9
Q
Orthostatic hypotension:
mechanism
A
Gravitationally mediated redistribution and pooling of
300–800 mL blood in the lower extremities and
splanchnic venous system, caused by decreased venous
return and an excessive fall in cardiac output, or by an
inadequate vasoconstrictor mechanism (with inadequate
release of norepinephrine)
Hypovolemia, a diminished blood volume insufficient to
maintain cardiac output and blood pressure
10
Q
Orthostatic hypotension:
precipitating factors
A
standing up
standing up after hemorrhage or dehydration
11
Q
Orthostatic hypotension:
predisposing factors
A
Aging; central and peripheral neuropathies:
Parkinson disease, multiple system atrophy;
Lewy body disease diabetes, amyloidosis;
antihypertensive vasodilator drugs; prolonged
bed rest
Bleeding from the GI tract or trauma, potent
diuretics, vomiting, diarrhea, polyuria
12
Q
Orthostatic hypotension:
prodromal manifestations
A
Lightheadedness, dizziness,
cognitive slowing, fatigue
Often none
Light-headedness and
palpitations (tachycardia) on
standing up
13
Q
Orthostatic hypotension:
postural associations
A
Occurs soon after
standing
Supine hypertension
is common
Occurs soon after
standing up
14
Q
Orthostatic hypotension:
recovery
A
Prompt return to normal when
lying down
Improves with volume repletion
15
Q
Cough Syncope:
mechanism
A
Neurally mediated, possibly from reflex vasodepressorbradycardia
response; cerebral hypoperfusion,
increased CSF pressure also proposed
16
Q
Cough Syncope:
precipitating factors
A
Severe paroxysm of coughing
17
Q
cough syncope:
predisposing factors
A
COPD, asthma, pulmonary hypertension.
Typically occurs in overweight middle-aged
patients
18
Q
cough syncope:
prodromal manifestations
A
Often none except for cough;
blurred vision, light-headedness
may occur
19
Q
cough syncope:
postural associations
A
May occur in any
position
20
Q
cough syncope:
recovery
A
Prompt return to normal after a
few seconds
21
Q
Micturition Syncope:
mechanism
A
Vasovagal response, sudden hypotension proposed
22
Q
Micturition Syncope:
precipitating factors
A
Emptying the bladder after
getting out of bed to void
23
Q
Micturition Syncope:
predisposing factors
A
Nocturia, usually in elderly or adult men
24
Q
Micturition Syncope:
prodromal manifestations
A
Often none
25
Micturition Syncope:
| postural associations
Commonly just after
(or during) voiding
after standing up
26
Micturition Syncope:
| recovery
Prompt return to normal
27
Table 17-3 Cardiovascular Disorders and Disorders Resembling Syncope not done
pg. 778-779
28
Focal Seizures
Focal seizures “are conceptualized as originating within networks limited to one hemisphere.
■ They may be discretely localized or more widely distributed.
■ Focal seizures may originate in subcortical structures.
■ For each seizure type, ictal onset is consistent from one seizure to another, with preferential propagation patterns that can
involve the contralateral hemisphere. In some cases, however, there is more than one network, and more than one seizure
type, but each individual seizure type has a consistent site of onset.
■ Focal seizures do not fall into any recognized set of natural causes.”
The distinction between simple partial and partial complex is eliminated, but clinicians are urged to recognize and describe
“impairment of consciousness/awareness or other dyscognitive features, localization, and progression of ictal events.”
29
Jacksonian seizures
clinical manifestations: tonic then clonic movements that start unilaterally in the hand, foot, or face and spread to other body parts on the same side
postictal state: normal consciousness
30
Focal Seizures without impairment of consciousness: other motor
clinical manifestations: Turning of the head and eyes to one side, or tonic and
clonic movements of an arm or leg without the
Jacksonian spread
postictal state: Normal consciousness
31
focal seizures without impairment of consciousness: with autonomic symptoms
clinical manifestations: A “funny feeling” in the epigastrium, nausea, pallor,
flushing, lightheadedness
postictal state: Normal consciousness
32
focal seizures w/o impairment of consciousness: with subjective sensory or psychic phenomena
clinical manifestations:
- Numbness, tingling; simple visual, auditory, or
olfactory hallucinations such as flashing lights,
buzzing, or odors
- Anxiety or fear; feelings of familiarity (déjà vu) or
unreality; dreamy states; fear or rage; flashback
experiences; more complex hallucinations
postictal state: Normal consciousness
33
focal seizures w/ impairment of consciousness
clinical manifestations: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
```
34
focal seizures that become generalized
clinical manifestations: Partial seizures that become generalized resemble
tonic–clonic seizures (see next page); the patient may
not recall the focal onset
```
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
```
35
Generalized Seizures and Pseudoseizures
Generalized seizures “are conceptualized as originating at 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.
■ Generalized seizures can be asymmetric.
■ They may begin with body movements, impaired consciousness, or both.
■ If onset of tonic–clonic seizures begins after age 30 yrs, suspect either a partial seizure that has become generalized or a
generalized seizure caused by a toxic or metabolic disorder.
Toxic and metabolic causes include withdrawal from alcohol or other sedative drugs, uremia, hypoglycemia, hyperglycemia,
hyponatremia, drug toxicity, and bacterial meningitis.
36
Tonic-Clonic (Grand-Mal) Seizures
clinical manifestations: The patient loses consciousness suddenly, sometimes
with a cry, and the body stiffens into tonic extensor
rigidity. Breathing stops, and the patient 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 State: Confusion, drowsiness, fatigue,
headache, muscular aching, and
sometimes the temporary
persistence of bilateral neurologic
deficits such as hyperactive reflexes
and Babinski responses. The
patient is amnestic about the
seizure and aura.
```
37
Absence Seizures
clinical manifestations: A sudden brief lapse of consciousness, with
momentary blinking, staring, or movements of the lips
and hands but no falling. Two subtypes are: typical
absence—lasts <10 s and stops abruptly; atypical
absence—may last >10 s.
Postictal State: No aura recalled. In typical
absence, a prompt return to
normal; in atypical absence, some
postictal confusion
38
Myoclonic Seizures
clinical manifestations: Sudden, brief, rapid jerks, involving the trunk or
limbs. Associated with a variety of disorders.
Postictal State: variable
39
Myoclonic Atonic (Drop Attack) Seizures
clinical manifestations: Sudden loss of consciousness with falling but no
movements. Injury may occur.
Postictal State: Either a prompt return to normal
or a brief period of confusion.
40
Pseudoseizures
may mimic seizures but are d/t a conversion disorder (Functional Neurologic Symptom Disorder in DSM-5)
clinical manifestations: The movements may have personally symbolic
significance and often do not follow a neuroanatomic
pattern. Injury is uncommon.
Postictal State: variable
41
Tremors
Tremors are rhythmic oscillatory movements, which may be roughly subdivided into three groups: resting (or static) tremors,
postural tremors, and intention tremors.
42
Resting (static) tremors
```
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.
```
43
postural tremors
```
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 often familial) tremor.
```
44
intention tremors
```
absent at rest, appear
with movement and often get worse as
the target gets closer. Causes include
cerebellar disorders such as multiple
sclerosis.
```
45
oral-facial dyskinesias
Oral–facial dyskinesias are arrhythmic, 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.
46
tics
Tics are brief, repetitive, stereotyped, coordinated movements
occurring at irregular intervals. Examples include repetitive
winking, grimacing, and shoulder shrugging. Causes include
Tourette syndrome and late effects of drugs such as
phenothiazines.
47
dystonia
Dystonic movements are similar to athetoid movements, but
often involve larger parts 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.
48
athetosis
Athetoid movements are 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.
49
chorea
Choreiform movements are 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 chorea (with rheumatic
fever) and Huntington disease
50
Table 17-6
pg.784
51
Table 17-7
pg. 785-6
52
Table 17-8
pg. 787
53
Table 17-9: Disordered of Muscle Tone
pg. 788
54
Spastic Hemiparesis
```
Seen in corticospinal tract lesions
that cause poor control of flexor
muscles during swing phase (for
example, from stroke).
■ Affected arm is flexed, immobile,
and held close to the side, with
elbow, wrists, and
interphalangeal joints flexed.
■ Affected leg extensors are
spastic; ankles are 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.
```
55
Steppage Gait
```
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, appearing to
be walking up stairs.
■ Patients cannot walk on their
heels.
■ Gait may involve one or both
legs.
■ Tibialis anterior and toe
extensors are weak.
```
56
Cerebellar Ataxia
```
Seen in disease of the cerebellum
or associated tracts.
■ Gait is staggering and unsteady,
with feet wide apart and
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
```
57
Sensory Ataxia
```
Seen in loss of position sense in
the legs from 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.
■ Patients watch the ground for
guidance when walking.
■ With eyes closed, patients cannot
stand steadily with feet together
(positive Romberg sign), and the
staggering gait worsens.
```
58
Scissors Gait
```
Seen in spinal cord disease, causing
bilateral lower extremity spasticity,
including adductor spasm.
■ 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, and there may be
compensating sway of the trunk
away from the side of the
advancing leg.
■ Scissoring is seen in all spasticity
disorders, most commonly
cerebral palsy.
```
59
Parkinsonian Gait
```
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
(anteropulsion or retropulsion).
```
60
Table 17-11
pg. 790
61
GCS Scale
```
Eye Opening
1- none
2- pain
3- speech
4- spontaneous
```
```
Motor Response
1- none (limbs flaccid)
2- extension
3- flexor response
4- withdrawal
5- localized pain
6- obeys commands
```
```
Verbal Response
1- none
2- incomprehensible (moans/groans)
3- inappropriate (no sustained sentences)
4- confused
5- oriented
```
62
pupils in comatose patients:
| small/pinpoint
Bilaterally small pupils (1–2.5 mm) 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.
Pinpoint pupils (<1 mm) 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.
63
pupils in comatose patients:
| mid position fixed
Pupils that are in the midposition or slightly dilated (4–6 mm)
and are fixed to light suggest structural damage in the
midbrain.
64
pupils in comatose patients:
| large
Bilaterally fixed and dilated pupils may be due to severe anoxia
and its sympathomimetic effects, as seen after cardiac arrest.
They may also result from atropine-like agents, phenothiazines,
or tricyclic antidepressants.
Bilaterally large reactive pupils may be due to cocaine,
amphetamine, LSD, or other sympathetic nervous system
agonists.
65
pupils in comatose patients:
| one large pupil
A pupil that is fixed and dilated warns of herniation of the
temporal lobe, causing compression of the oculomotor nerve
and midbrain. A single large pupil is commonly seen in
diabetic patients with infarction of CN III.
66
Decorticate Rigidity (abnormal Flexor Response) Posturing
In decorticate rigidity, 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.
67
Hemiplegia (early) Posturing
Sudden unilateral brain damage involving the
corticospinal tract may produce a hemiplegia
(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.
68
Decerebrate Rigidity (Abnormal Extensor Response) Posturing
In decerebrate rigidity, 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 may also arise
from severe metabolic disorders such as
hypoxia or hypoglycemia
