Chapter 2 - Higher congitive function
Questions
Define the following terms:
agnosia,
agnosagnosia,
apraxia,
receptive
aphasia,
expressive
aphasia,
global
aphasia,
alexia,
agraphia,
dysinhibition,
dysnomia,
paraphasic,
paratonia,
perseveration.
Agnosia is the inability to recognize what something is despite being
able to perceive it. This can be visual, auditory or tactile.
Agnosagnosia is the inability to recognize a particular deficit (for
example that one is paralyzed).
Apraxia is the inability to synthesize a complex motor pattern despite
having the strength and coordination to perform it.
Receptive aphasia is the inability to understand language (written or
verbal).
Expressive aphasia is the inability to synthesize language (written or
verbal).
Global aphasia is the inability to either understand or to synthesize
language (written or verbal).
Alexia is the inability to read.
Agraphia is the inability to write.
Dysinhibition is the appearance of responses that are normally
suppressed. In the context of higher cognitive functions, it is the
return of more primitive reflexes or behavior patterns that are
normally suppressed by "higher areas" of the brain (often the frontal
lobe).
Dysnomia is the inability to name objects.
Paraphasic errors include substituting words that have inappropriate
meaning, although the words sound somewhat similar or start with the
same sounds. This often happens with receptive aphasias.
Paratonia is an involuntary, irregular resistance to passive movement
(it feels like the patient is assisting in movement when they are not
attempting to).
Perseveration is repeating motions (or responses) when it is
inappropriate to do so.
2-1. Name some
cerebral cortical functions that are well localized and unilateral.
Answer 2-1. Well localized, unilateral cortical functions include:
somatic sensation, voluntary motor function (especially of hands), expressive
language, receptive language, attention to the contralateral world (neglect),
understanding of what is wrong (agnosagnosia), vision.
2-2. Name some
cerebral cortical functions that are well localized and represented bilaterally.
Answer 2-2. Well-localized and bilateral cortical functions: hearing,
short term memory, frontal lobe functions (mood, behavior, emotional
control, motivation, executive functions), visuospatial function
(parietal lobe)
2-3. Name some
cerebral cortical functions that are diffusely represented in the cerebral
cortex.
Answer 2-3. Diffuse cerebral cortical functions: long term memory, self
and species preservation functions (including many behavioral functions.
2-4. Damage to
which cerebral cortex produces aphasia?
Answer 2-4. Aphasia is lateralized to the dominant hemisphere
2-5. What can you
say about the ability to write in patients with aphasia?
Answer 2-5. Patients with aphasia will write and read the same way that
they speak and comprehend speech, respectively.
2-6. What can you
say about the ability of a patient with expressive, receptive, or global aphasia
to repeat complex phrases?
Answer 2-6. Patients with expressive, receptive or global aphasia will
be unable to repeat complex phrases.
2-7. What can you
say about the ability of a patient with transcortical aphasia to repeat complex
phrases?
Answer 2-7. Patients with transcortical aphasia will be able to repeat
although they may not be able to name objects that are presented to
them or to understand language.
2-8. What problems
will a patient with a transcortical aphasia have?
Answer 2-8. Transcortical aphasia: will be able to repeat complex
phrases but will either be unable to understand complex statements or
commands (transcortical receptive) or be unable to come up with names
for objects (transcortical motor).
2-9. What are the
characteristics of the patient with an expressive aphasia (Broca's)?
Answer 2-9. Epressive aphasia: Broca's area, nonfluent, frustrated,
dysnomic, can read and understand speech, telegraphic speech.
2-10. What are
the characteristics of the patient with a receptive aphasia (Wernicke's)?
Answer 2-10. Receptive aphasia: Wernicke's area, fluent, not
frustrated, dysnomic, can't read or understand complex speech.
2-11. What is
the most common lesion to produce alexia without agraphia (can write but can't
read)?
Answer 2-11. Damage to the dominant occipital lobe and splenium of
corpus callosum can produce alexia without agraphia (can write but
can't read).
2-12. What area
is involved in immediate recall (for example of a phone number)?
Answer 2-12. Immediate recall is a frontal lobe effect (give back a
phone number).
2-13. What area
is involved in short-term memory?
Answer 2-13. Short-term memory is a hippocampal function (minutes to hours).
2-14. Where is
long-term memory stored?
Answer 2-14. Long-term memory is stored diffusely (only lost if large
and diffuse areas are damaged).
2-15. What are
"executive functions" and where are they primarily located?
Answer 2-15. Executive functions in dorsolateral prefronal part of
frontal lobes - these include sequencing, planning, immediate recall,
abstractions.
2-16. Where are
the areas involved in most of emotional control and "personality"?
Answer 2-16. The orbital and medial frontal (and anterior cingulate)
cortex are involved in emotional control.
2-17. Damage to
which hemisphere is more likely to produce depression? Which will more likely
produce mania?
Answer 2-17. Left frontal damage often produces depression; right
frontal may lead to mania.
2-18. Neglect
of one side of the world is most commonly due to damage to what area?
Answer 2-18. The parietal lobe is responsible for attention to
contralateral world (damage produces neglect) and knowledge of deficits.
2-19. Agnosagnosia
most often results from damage to what area?
Answer 2-19. Agnosagnosia, a lack of recognition of problems, is due to
damage to the parietal lobe (especially the non-dominant side).
2-20. What "primitive
responses" would be expected to be uncovered by damage to the frontal lobes?
Answer 2-20. disinhibited glabellar, snout, suck, palmomental and
grasp reflexes.
2-21. Paratonia
is a sign of what?
Answer 2-21. Paratonia results from diffuse cortical dysfunction (some
degree may be normal).
2-22. What would
you expect to see in the patient with a split corpus callosum?
Answer 2-22. Corpus callosum lesions may prevent information from
transferring from one hemisphere to the other. The "left hand does not
know what right hand is doing."
2-23. The neocortex
provides inhibitory modulation of what four basic drives?
Answer 2-23. Feeding, fighting, fleeing and procreation (the four F's).
2-24. What is
the clinical term used to describe diffuse hemispheric disease (one word)?
Answer 2-24. Dementia.
2-25. What are
the clinical signs of advanced dementia?
Answer 2-25. Loss of cognitive, intellectual functions in more than one
sphere of function.
2-26. What regressive
reflexes emerge with loss of cortical inhibition?
Answer 2-26. Dysinhibition of glabellar response, palmomental reflex,
grasp reflex, suck reflex, rooting reflex, snout reflex and loss of
nuchocephalic reflex.
2-27. What
are the functions of the limbic areas of the brain?
Answer 2-27. Self and species preservation functions, the "four
F's" and emotional reactivity.
2-28. Of 100 people,
how many will have significant R hemispheric representation of speech functions?
Of these, how many will have bilateral speech representation?
Answer 2-28. 1% right dominant and 2% mixed.
2-29. What percentage
of R-handed people are L-hemisphere dominant for speech?
Answer 2-29. About 99.9%.
2-30. What percentage
of L-handed people are L-hemisphere dominant for speech?
Answer 2-30. About 70%.
2-31. Below what
age can speech function be recovered if the dominant hemisphere is damaged?
Answer 2-31. Age four.
2-32. What are
dysfunctions of speech called? What is a complete loss of speech called?
Answer 2-32. Dysphonia (if hoarseness due to mechanical problems in
larynx), dysarthria (if due to problems with cranial nerves or
cerebellum) or aphasia (this is actually a language problem, not just
speech problem). Dysphasia is incomplete, aphasia complete loss of
language function.
2-33. A patient
with verbal language dysfunction, homonymous hemianopsia, right visual field deficit
and little motor deficit most likely has what type of dysphasia?
Answer 2-33. Receptive (Wernicke's) - this is because Wernicke's area
is closer to the parietal lobe (and the optic radiations).
2-34. A patient
with verbal language dysfunction, marked hemimotor and hemisensory deficit,
and no visual abnormality most likely has what type of dysphasia?
Answer 2-34. Expressive (Broca's) - this is because Broca's area is
closer to the motor cortex.
2-35. Where is
Broca's area located? Where is Wernicke's area located? Name the fasciculus
that links the two of them.
Answer 2-35. Broca's - Inferior frontal lobe, just anterior to motor
cortex and near Sylvian fissure; Wernicke's - posterior part of
superior temporal gyrus; the arcuate (superior longitudinal) fasciculus
connects these language areas.
2-36. What gyrus
is important in language, especially in word retrieval?
Answer 2-36. Angular gyrus.
2-37. Do most
patients with dysphasia have Broca's, Wernicke's, or a combination of both?
Why is this so?
Answer 2-37. Combination because they are in same vascular distribution
on same side.
2-38. What language
abnormalities are manifested with a lesion to Broca's area? Wernicke's area?
Angular gyrus? Arcuate (superior longitudinal) fasciculus?
Answer 2-38. Broca's - expressive aphasia; Wernicke's - conductive
aphasia; Angular - dysnomic aphasia; Arcuate fasciculus - conductive
aphasia.
2-39. What part
of the corpus callosum transfers COMPLEX [i.e., verbal] visual info between
the two hemispheres?
Answer 2-39. The splenium.
2-40. What are
the predominant functions of the R cerebral hemisphere?
Answer 2-40. Visuospatial functions, attention to contralateral world,
musicality.
2-41. Which patient
will be more motivated to recover from a hemispheric lesion, one with damage
on the L or the R?
Answer 2-41. The left (the right hemisphere lesion can result in a lack
of appreciation for deficits and therefore problems in compensating).
2-42. Where is
the location of a lesion that causes visuospatial disorientation? How does
this manifest itself?
Answer 2-42. Right parietal lobe. Patients may get lost and have
trouble assembling things or figuring out how to make them work.
2-43. What type
of lesion will result in the loss of the ability to imprint new information?
Answer 2-43. Hippocampal lesions - medial temporal lobe (bilaterally).
2-44. Can well-learned
material be easily destroyed by a focal lesion? Why or why not?
Answer 2-44. No, there is diffuse representation.
2-45. What three
categories of questions need to be asked when testing a patient for problems
with learning and memory?
Answer 2-45. Immediate recall; short term recall (several minutes after
distraction); recall of remote events.
2-46. What evidence
would lead to the conclusions that a demented patient has disease localized
primarily in the frontal lobes (i.e., what are the manifestations of lesions
to the frontal lobes)?
Answer 2-46. Emotional lability, personality change
and/or loss of executive functions.
2-47. What is
the effect of lesions localized to the medial aspect of the frontal lobes
(parasagittal frontal cortex - supplementary motor area)?
Answer 2-47. Inability to initiate movements (abulia).
Chapter 3 - Olfaction and Vision
Questions
Define the following terms:
anosmia,
homonomous,
hemianopsia,
quadrantanopsia,
scotoma,
papilledema,
papillitis,
optic neuritis.
Anosmia is a loss of the sense of smell (this can be unilateral or
bilateral).
Homonomous is a term referring to overlapping areas of the visual field
of each eye.
Hemianopsia (or hemianopia) is a loss of visual perception of one-half of the visual
world.
Quadrantanopsia is a loss of visual perception of one-quarter of the
visual world.
Scotoma is a patch of vision loss.
Papilledema is swelling of the optic nerve head usually produced by
congestion of the central retinal veins. This usually happens due to
increased intracranial pressure.
Papillitis is swelling of the optic nerve head due to inflammation.
Optic neuritis is inflammation of the optic nerve.
3-1. How do you
test olfaction?
Answer 3-1. Olfactory nerve is tested with aromatic compounds presented
to each nostril.
3-2. What is the
most common cause of unilateral anosmia?
Answer 3-2. Most common cause of unilateral anosmia is blockage of
nasal passage.
3-3. In whom is
it particularly important to test olfaction?
Answer 3-3. Olfactory testing is most important in patients with head
injury, mental status change and seizure.
3-4. How can you
determine if visual acuity problems are due to refractive or to nerve problems?
Answer 3-4. Visual acuity problems that are refractive improve with
pinhole testing (retinal or optic nerve problems do not).
3-5. What is the
significance of finding a monocular visual loss?
Answer 3-5. Assuming that this is not due to refractive problems in the
eyeball (usually ruled out by a funduscopic examination) monocular
problems are anterior to the optic chiasm (retina or optic nerves).
3-6. What is the
significance of finding a homonomous visual field deficit?
Answer 3-6. Homonymous visual field problems are posterior to the optic
chiasm.
3-7. Where would
a lesion that produced bitemporal hemianopsia be located?
Answer 3-7. Bitemporal hemianposia is often due to problems at the
optic chiasm (such as with pituitary tumors).
3-8. How can lesions
of the parietal or temporal lobes produce vision loss? What kind of loss would
you expect to find?
Answer 3-8. Optic radiations that pass from the thalamus to the visual
cortex in the occipital lobe either pass through the parietal lobe
(lower visual field) or through the temporal lobe (Meyer's loop - upper visual
field) - may produce quadrananopsia of either the contralateral lower
visual world (parietal lobe) or upper visual world (temporal lobe).
3-9. Where on the
visual cortex is the representation of the center of vision?
Answer 3-9. The center of vision is represented near the occipital pole
(often supplied by middle cerebral artery).
3-10. What artery
supplies the visual cortex?
Answer 3-10. Most of the visual cortex is supplied by posterior
cerebral arteries.
3-11. How can
you distinguish papilledema from papillitis (i.e., optic neuritis affecting the optic nerve head at the optic disc)?
Answer 3-11. The appearance is quite similar during ophthalmoscopy.
However, with papilledema, there is little change in vision (there
might be expansion of the physiologic blind spot) while papillitis is
associated with severe vision problems. Also, papilledema is likely to
be bilateral (this is uncommon in papillitis).
Chapter 4 - Extraocular movement
Questions
Define the following terms:
strabismus,
abduction,
adduction,
elevation,
depression,
convergence,
accommodation,
diplopia,
miosis,
mydriasis,
myopia,
hyperopia,
conjugate,
consensual,
extraocular,
amblyopia,
ptosis,
anisocorea.
Strabismus is a position of the eyes where they are not directed at the
same target (in some parts of the country this is termed a "squint").
Abduction is bringing the pupil away from the nose.
Adduction is bringing the pupil toward the nose.
Elevation is moving the pupil above the horizon.
Depression is moving the pupil below the horizon.
Convergence is directing both eyes toward the nose.
Accommodation is a combination of convergence, pupil constriction and
change in lens shape to permit focus on a near object.
Diplopia is double vision. This can be horizontal, vertical or skew.
Miosis is constriction of the pupil.
Mydriasis is dilation of the pupil.
Myopia is an inability to see at distance ("nearsighted") with light
focusing in front of the retina.
Hyperopia is an inability to see close up ("farsighted") with light
behind the retina.
Conjugate - "together". That is, the eyes moving in parallel to keep
images focused on the same part of each retina (preventing diplopia).
Consensual means "happening on both sides at the same time". A
consensual reflex is one where the response is bilateral when the
stimulus is unilateral (such as the papillary light reflex).
Amblyopia literally means "dim eye". This is a drifting or "lazy" eye
that usually happens because one eye has bad vision. The brain often
"turns off" control of that eye and the eye drifts. The patient usually
does not have diplopia because input from that eye is turned off. In
one of the most remarkable illustrations of plasticity, the eye can
become permanently blind in children if this is not treated.
Ptosis is a drooping of the upper eyelid.
Anisocorea is an inequality of pupil size. This is usually not
clinically significant unless it reaches one millimeter in difference.
4-1. Which muscles
would be active in the right and left eye when looking up and to the right?
Answer 4-1. In the right eye the lateral rectus and the superior rectus would
be the prime movers, while in the left eye, the medial rectus and the
inferior oblique would be most active.
4-2. Which muscles
would be active in the right and left eye when looking down and to the left?
Answer 4-2. In the right eye the medial rectus and the superior oblique would
be the prime movers, while in the left eye, the lateral rectus and the
inferior rectus would be most active.
4-3. What position
will the patient's head assume (in order to prevent diplopia) if their right
trochlear nerve is damaged?
Answer 4-3. Head tilted to the left and chin turned slightly to the right
("cockeyed").
4-4. When a patient
has double vision, in which position will they have the furthest separation
of the images?
Answer 4-4. The images will be furthest apart when the eyes look in the
direction that the weak muscle is most active.
4-5. What is the
significance of horizontal diplopia (where the images are side-by-side) as
opposed to vertical diplopia?
Answer 4-5. Horizontal diplopia results from weakness of the lateral or medial
rectus muscles; vertical diplopia is due to weakness of one of the
other muscles.
4-6. Which eye
(the one that is moving normally or the weak one) will see the image that
is furthest displaced from the center of vision?
Answer 4-6. The "bad eye" sees the image that is furthest toward the periphery
of vision.
4-7. Where is the
cortical center that controls lateral gaze? Where is the lateral gaze center
in the brain stem?
Answer 4-7. Lateral gaze centers include the frontal eye fields in the frontal
lobes of the cerebral cortex and the paramedian pontine reticular
formation.
4-8. Is there a
vertical gaze center in the cerebral cortex? Is there a brain stem vertical
gaze center?
Answer 4-8. Vertical gaze is a diffuse cerebral cortical phenomenon, while
there is a vertical gaze center in the rostral midbrain (the rostral
interstitial nucleus).
4-9. What are the
potential causes of ptosis?
Answer 4-9. Ptosis may be due to weakness of the levator palpebrae muscle (or
CNIII damage) or due to damage to the sympathetics (due to weakness of
the small, superior tarsal muscle).
4-10. What are
the components of Horner's syndrome?
Answer 4-10. Horner's syndrome (ptosis, miosis, anhidrosis and possibly
flushing) is from damage to sympathetics anywhere along their course.
4-11. What are
the functions of sympathetic and parasympathetic nerves to the orbit?
Answer 4-11. Sympathetics dilate the pupil, parasympathetics (CN III)
constrict the pupil to light and accommodation; there is balance
between sympathetics and parasympathetics.
4-12.
Where is the brain stem center for the pupillary light reflex?
Answer 4-12. The pretectal area of the dorsolateral midbrain is the center for
the pupillary light reflex.
Chapter 5: Facial sensations & movements
Questions
Define the following terms:
hyperacusis,
ageusia.
Hyperacusis is the excessive perception of sound.
Ageusia is the loss of taste perception.
5-1. Which division
of the trigeminal nerve has motor fibers?
Answer 5-1. Only the mandibular division of the trigeminal nerve has
motor fibers (to the muscles of mastication).
5-2. What are some
good ways to distinguish hysterical sensory loss on the face?
Answer 5-2. The trigeminal nerve does not follow artificial lines on the
head (hairline, jawline), and there is no lesion that will abolish the ability
of the patient to detect a vibrating tuning fork placed on a bony prominence of
the skull. The corneal reflex may be useful as well.
5-3. Where is the
trigeminal ganglion located?
Answer 5-3. The trigeminal ganglion is lateral to the sella
turcica/pituitary and in wall of cavernous sinus.
5-4. Where does
the trigeminal nerve root enter the brain?
Answer 5-4. CN V enters the pons.
5-5. Which modalities
would test the integrity of the spinal tract of the trigeminal nerve?
Answer 5-5. Pain and temperature sense.
5-6. Where do pain
and temperature nerve fibers in the trigeminal nerve run after entering the
pons?
Answer 5-6. Pain and temperature fibers run caudally through the lateral
brain stem to reach the spinal nucleus of V in the medulla and upper spinal
cord; lateral brain stem lesions can block ipsilateral pain from face.
5-7. What is the
pathway of the corneal reflex?
Answer 5-7. The sensory limb of the corneal reflex is the ophthalmic
division of the trigeminal nerve and the motor limb is the facial nerve. The
response is consensual.
5-8.
What are the symptoms of Bell's palsy?
Answer 5-8. Bell's palsy damages the facial nerve in the facial canal
and weakens all muscles of facial expression on the side of lesion.
Depending on where the damage occurs, there may be hyperacusis or loss of taste
on that side of the tongue.
5-9. How can you
distinguish weakness of the face that is due to damage to the brain (such
as with a stroke) from weakness due to damage of the facial nerve?
Answer 5-9. Damage to corticobulbar fibers (from cortex to the pons)
will produce supranuclear weakness of the lower face (sparing of forehead) on
the contralateral side, while damage to the nerve should produce weakness of
all muscles of facial expression on that side.
5-10. Describe
the reflex arc of the jaw-jerk reflex.
Answer 5-10. Jaw jerk reflex - afferent is trigeminal, efferent is trigeminal. It is a muscle stretch reflex with the reflex center in the pons (sometimes called the pontine reflex).
Chapter 6 - Auditory & Vestibular Function
Questions
Define the following terms:
conductive
hearing loss,
sensorineural
hearing loss,
tinnitus,
vertigo,
nystagmus.
Conductive hearing loss is the loss of the ability to
transmit sound waves to the inner ear. Obstruction of the external ear,
problems with the tympanic membrane or problems with the middle ear (or the
ossicular chain) are the cause.
Sensorineural hearing loss is hearing loss due to damage to
the hair cells of the organ of Corti or to the auditory part of the
vestibulocochlear nerve.
Tinnitus is ringing or buzzing in the ears.
Vertigo is the illusion of movement.
Nystagmus is a to-and-fro movement of the eyes. It can be
pendular (even swings in both directions, often due to congenital vision
problems) or can be "jerk." In jerk nystagmus, there is a fast and a slow
component, typically due to vestibular problems (the direction is named by the fast
component).
6-1. What effect do lesions of the CNS have on hearing in one ear?
Answer 6-1. It is nearly impossible to cause loss of hearing in one
ear by damage to the brain beyond the point where the vestibulocochlear nerve
enters the brain stem. This is because the distribution of hearing is bilateral at
all levels of the central nervous system auditory pathway. Localization of
sound may be slightly affected by auditory cortex lesions. In fact it is nearly
impossible for central nervous system lesions to cause clinically detectable
hearing loss and if these is hearing loss you must look at the conductive
system, the inner ear and the vestibulocochlear nerve.
6-2. What kind of
hearing loss will be produced by damage to the inner ear?
Answer 6-2. Inner ear and CN VIII lesions will produce senorineural
deafness.
6-3. What do you
call problems in which the sound wave can not reach the inner ear?
Answer 6-3. Blockage of the outer ear or damage to the tympanic
membrane or middle ear is called conductive deafness.
6-4. What would
it mean if Weber's test lateralized to the left?
Answer 6-4. Weber's test lateralized toward the side of conductive
deafness and away from sensorineural.
6-5. What is the
most common symptom of damage to the vestibular system?
Answer 6-5. Vertigo is common with vestibular damage.
6-6. What does it
mean when someone says that nystagmus was in a particular direction?
Answer 6-6. Nystagmus is named according to the direction of fast
movement.
6-7. How can you
distinguish vertigo from inner ear damage from that caused by damage to the
central nervous system?
Answer 6-7. With peripheral causes of vertigo (the illusion of
movement), nystagmus is proportional to the amount of vertigo and nystagmus is always
in the same direction regardless of the direction that the patient looks. Also,
peripheral nystagmus is almost never in a vertical (up or down) direction. With
central vertigo (cerebellum, vestibular nuclei and brain stem) nystagmus is
usually greater than vertigo and may shift direction depending on gaze
direction.
6-8. What is the
only way to examine the integrity of the vestibular system on one side?
Answer 6-8. Caloric testing is the only way to check each inner ear
vestibular function independently.
6-9. What would you
anticipate finding during cold-water caloric testing in the intact patient
who is awake?
Answer 6-9. When the patient is awake, the eyes will drift slowly
toward the side of cold water with rapid correction to the opposite side (the
opposite for warm water). There is tonic balance in vestibular input from each
ear; cold water caloric testing decreases tonic input from the inner ear (warm
water increases it).
6-10. What would
you expect to find in the comatose patient whose brain stem was still working
if ice-water was infused into the right ear?
Answer 6-10. The eyes would drift toward the side of the ice-water
infusion and remain there for several minutes. There would be no nystagmus
(which is a response generated by the conscious cerebral cortex when the visual
image slips across the retina).
6-11. Damage to
the inner ear produces responses that look like (cold/warm) water caloric testing
(choose one)?
Answer 6-11. Damage to the inner ear or vestibular nerve decreases
vestibular input from that ear (acts like cold water caloric).
Chapter 7 - Lower cranial nerve function
Questions
Define the following terms:
dysarthria,
dysphonia,
dysphagia.
Dysarthria is the inability to speak clearly due to problems
with control of the motor apparatus of speech (generation and understanding of
language should be normal and reading/writing are unaffected).
Dysphonia is problems with speech due to disorders of the
vocal apparatus in the larynx (laryngitis is an example).
Dysphagia is difficulty with swallowing.
7-1. What are the
main functions of the glossopharyngeal nerve?
Answer 7-1. The glossopharyngeal nerve provides sensation to the
carotid baroreceptor and chemoreceptor, the pharynx and the middle ear.
7-2. What would be
the effect on soft palate movement of unilateral damage to the vagus nerve?
Answer 7-2. The vagus nerve activates the elevator of the soft
palate. The palate will elevate with deviation of base of uvula away from the
side of lesion (toward the intact side).
7-3. What would be
the effect of unilateral damage to the vagus nerve on larynx function?
Answer 7-3. The vagus (recurrent laryngeal) innervates larynx
muscle. Damage would produce painless hoarseness, with weakness or paralysis of the
vocal cord on that side.
7-4. Describe the
course of the spinal accessory nerve.
Answer 7-4. The spinal accessory nerve comes from cervical spinal
cord, enters the head through foramen magnum and exits through jugular foramen.
7-5. What does
the spinal accessory nerve innervate?
Answer 7-5. CN XI innervates the SCM and trapezius muscles.
7-6. What does
the hypoglossal nerve innervate?
Answer 7-6. The hypoglossal nerve innervates the tongue.
7-7. What would be
the findings in unilateral damage to the hypoglossal nerve?
Answer 7-7. The tongue deviates toward the side of weakness when protruded and
it will be weak when attempting to push against the cheek on the strong side of tongue. With time, there would be atrophy of the tongue on the side of the nerve damage.
7-8. What would be
the effect of a large stroke in the motor cortex on tongue movement?
Answer 7-8. Corticobulbar damage (like a stroke) will slightly
weaken the contralateral side of the tongue.
7-9. What is the
reflex pathway of the gag reflex?
Answer 7-9. Gag reflex - afferent is glossopharyngeal,
efferent is vagus. It is a consensual reflex.
7-10. What is the
reflex pathway of the cough reflex?
Answer 7-10. The cough reflex - afferent is vagus, efferent
is complex including respiration centers and vagus.
7-11. What is the
reflex pathway of the baroreceptor reflex?
Answer 7-11. The baroreceptor reflex - afferent is
glossopharyngeal, efferent is vagus.
Chapter 8 - Reflex evaluation
Questions
Define the following terms:
hyper-reflexia,
pathological spread of reflex,
clonus,
Babinski
sign,
Hoffmann's sign,
myotatic reflex,
upper
motor neurons,
lower motor neurons,
reinforcement.
Hyper-reflexia is excessively brisk reflexes
Pathological spread of reflex occurs when a reflex
contraction occurs in a muscle whose tendon was not stretched (i.e., finger
flexion when testing the brachioradialis reflex or thigh adduction when the
patellar reflex is tested). It is a suggestion of hyperactive reflexes.
Clonus is repeated contraction of muscles (usually the calf
muscles or the wrist flexor muscles) when the muscles are stretched manually
(such as by ankle dorsiflexion or wrist extension). Sustained clonus is when
this occurs repeatedly as long as the stretch is maintained.
Babinski sign is reflex dorsiflexion of the great toes and
fanning of the other toes by stroking the lateral side of the sole of the foot.
This stroke is often continued across the ball of the foot toward the base of
the great toe. This occurs in patients with upper motor neuron damage. The
normal plantar response is for the great toe to flex.
Hoffmann's sign is flexion of the thumb following a maneuver
that consists first of passive flexion of the patient's middle finger by
pressure over the nail bed, followed by sudden release of this pressure. It is
a sign of brisk reflexes but is not pathological unless it is accompanied by
other signs of upper motor neuron damage or is asymmetrical.
Myotatic reflex is the muscle stretch reflex (often termed
the deep tendon reflex).
Upper motor neurons are the principal descending motor
pathways for voluntary movement, including the corticospinal and corticobulbar
tracts (and some other associated tracts).
Lower motor neurons are the anterior horn motor neurons and
their axons that extend through the ventral nerve root and the peripheral
nerves to reach the neuromuscular junction.
Reinforcement involves the strong contraction of muscles outside of the area in which muscle stretch reflexes are being tested. This will serve to increase the reflexes. Specific examples include clenching the jaw, pressing the feet together or clasping the hands and attempting to pull them apart (the Jendrasik maneuver).
8-1. What is the
main effect of descending motor systems on reflexes?
Answer 8-1. Motor cortex and descending motor pathways are generally involved in suppressing
(inhibiting) reflexes.
8-2. What are the
7 Deep Tendon Reflex exams (DTRs)? What sensory/motor nerves are they testing?
Answer 8-2. Biceps - musculocutaneous nerve and mainly C6; Triceps - radial nerve and mainly C7; Brachioradialis (radial periosteal) - radial nerve and
mainly C6; Finger flexor - musculocutaneous nerve and mainly C7-8; Patellar - femoral nerve and mainly L3-L4; Achilles' reflex (ankle jerk) - tibial nerve and
mainly S1; Jaw jerk - trigeminal
8-3. What are the
superficial reflexes?
Answer 8-3. Superficial reflexes include: abdominal, cremaster,
plantar, anal wink.
8-4. What is the
effect of damage to corticospinal fibers on myotatic (deep tendon) reflexes?
What is the effect on superficial reflexes?
Answer 8-4. DTRs increase with damage to descending motor pathways;
superficial reflexes decrease with damage to descending motor pathways.
8-5. What primitive
reflexes emerge with diffuse bilateral hemispheric dysfunction?
Answer 8-5. Diffuse bilateral hemispheric dysfunction can
dysinhibit grasp, glabellar, suck, rooting, oculocephalic and nuchocephalic
reflexes.
8-6. What happens
to DTRs with lesions in the cerebellum & basal ganglia?
Answer 8-6. Usually no change, though may be sluggish with
cerebellar damage.
8-7. How are DTRs
graded?
Answer 8-7. 0-4+. To grade a reflex as "0", you must try reinforcement. 4+ means there is sustained
clonus. 1 is sluggish, 2 is "normal" and 3 is "brisk".
8-8. What is the
most important consideration in testing reflexes?
Answer 8-8. Symmetry.
8-9. What reflex
changes would occur in lesions of muscles?
Answer 8-9. No change
unless end stage.
8-10. What reflex
changes would occur in lesions of the neuromuscular junction?
Answer 8-10. Normal to decreased depending on severity of weakness.
8-11. What reflex
changes would occur in lesions of the peripheral nerves?
Answer 8-11. Decreased in clinically affected areas.
8-12. What reflex
changes would occur in lesions of the nerve root?
Answer 8-12. Decreased in clinically affected areas.
8-13. What reflex
changes would occur in lesions of the spinal cord and brain stem?
Answer 8-13. Usually reflexes will be increased unless the gray
matter (anterior horn cells, lower motor neurons) is damaged right at the
reflex level. Acute spinal cord injury can result in spinal cord shock
(flaccid, decreased reflex).
8-14. How can damage
to sensory nerve fibers affect reflexes?
Answer 8-14. Damage to sensory nerve fibers may also decrease
reflexes by damaging the afferent limb of the reflex arc.
8-15. What is the
effect of neuropathy on muscle stretch reflexes?
Answer 8-15. Neuropathy often produces decreased reflexes out of
proportion to weakness.
8-16. What are some
visceral reflexes that can be tested?
Answer 8-16. Visceral reflexes include: pupillary light reflex,
oculocardiac, carotid sinus, bulbocavernosus, rectal (internal sphincter) and
orthostatic blood pressure regulation.
Chapter 9 - Sensory system evaluation
Questions
Define the following terms:
conscious
proprioception,
agnosia
(sterioagnosia),
graphesthesia,
dermatome,
sclerotome,
myotome,
radiculopathy,
myelopathy,
anesthesia/hypoesthesia,
hyperpathia,
allodynia,
hyperesthesia,
dysesthesia,
paresthesia,
polyneuropathy,
subjective.
Conscious proprioception is the ability to tell where a body
part is in space. It is largely based on joint position sense.
Agnosia (sterioagnosia) ia the inability to recognize what a
sensation is despite relatively normal perception of the sensation. When it is
tactile it is termed sterioagnosia (or asteriognosis). It would be the
inability to determine the denomination of a coin despite normal ability to
perceive it, for example.
Graphesthesia is the ability to identify letters or figures traced
on the skin (without looking).
Dermatome is the area of skin supplied by a nerve root.
Sclerotome is the area of bone and joints supplied by a
single nerve root.
Myotome is the muscles supplied by a single nerve root.
Radiculopathy this is damage to a nerve root (radiculitis is
irritation).
Myelopathy is damage to the spinal cord from any cause.
Anesthesia/hypoesthesia is loss (or decrease) in sensation.
Hyperpathia is the exaggerated perception of normally painful
stimuli.
Allodynia is the perception of normally innocuous stimuli as
being painful.
Hyperesthesia is excessive sensitivity to any modality.
Dysesthesia is the perception of the pain when no stimulus
is present.
Paresthesia is the detection of a sensation in the absence
of any stimulus.
Polyneuropathy is generalized damage to peripheral nerves. This
is usually due to a systemic cause.
The sensory exam is by definition subjective, that is,
relies on the patients report.
9-1. What are the
steps involved in the sensory exam?
Answer
9-1. First, the exam needs to determine if the patient can detect
modality; next, you need to know if it is the same on both sides; then you need to know
if the patient can interpret the sensation.
9-2. How is it possible
to lose some types of sensations and not others?
Answer
9-2. Different sensory modalities follow different types of
nerve fibers and different pathways (tracts) through the nervous system.
9-3. What sensations
are conveyed by the small-diameter sensory nerve fibers in a peripheral nerve?
Answer
9-3. Small, unmyelinated or lightly-myelinated (slow) nerve
fibers convey pain and temperature sense.
9-4. What sensations
are conveyed by large-diameter sensory nerve fibers in a peripheral nerve?
Answer
9-4. Large, heavily myelinated (fast) nerve fibers convey
proprioception and well-localized touch sensation. They are also the sensory
limb of the muscle stretch reflex.
9-5. What sensations
are conveyed by the dorsal columns?
Answer
9-5. Dorsal columns convey vibration, 2-point discrimination
and joint position sense.
9-6. What sensations
are conveyed by the spinothalmic tract?
Answer
9-6. The spinothalamic tract conveys pain, temperature and
very light (poorly localized) touch.
9-7. What is tested
by double simultaneous stimulation?
Answer
9-7. Double simultaneous stimulation tests attention/neglect
(parietal lobe).
9-8. Where would
the lesion be if the patient was able to detect all modalities of sensation
but could not recognize an object placed in the right hand?
Answer
9-8. The left parietal lobe (somatosensory association
area).
9-9. What is the
common sensory loss from damage to the spinal cord?
Answer
9-9. Spinal cord lesions often result in sensory level (loss
of sensations below lesion) due to damage to ascending sensory tracts. .This
loss (especially of pin sensation) usually begins at least several segments
below the level of the lesion of the tract.
9-10. What would
be the expected sensory loss from damage restricted to the left side of the
spinal cord?
Answer
9-10. There would be ipsilateral loss of vibration and joint
position sense and contralateral loss of pain and temperature sense below the
level of the lesion. The pain and temperature sense loss would start at least
several dermatomes below the injury.
9-11. What is the
characteristic of sensory loss due to damage of peripheral nerves in a limb?
Answer
9-11. Peripheral nerve injury (mononeuropathy) usually
results in well-localized sensory loss (often with appropriate motor loss).
9-12. What is the
pattern of sensory loss seen in diffuse damage to peripheral nerves (polyneuropathy)?
Answer
9-12. Diffuse peripheral nerve injury (polyneuropathy)
results in stocking (and, later, glove) sensory loss.
Chapter 10 - Motor system examination
Questions
Define the following terms:
spasticity,
rigidity,
hemiparesis/plegia,
bradykinesia,
paraparesis/plegia,
upper motor neurons,
lower
motor neurons,
internal
capsule,
chorea,
athetosis,
dystonia,
hemiballism,
tic,
fasciculation.
Spasticity is a resistance to passive movements that is
greatest at the initiation of motion (particularly of a rapid movement). It is
often a sign of overactive muscle stretch reflexes.
Hemiparesis/plegia paralysis or paresis (weakness) of one
side of the body.
Rigidity is a smooth resistance to passive movement that
occurs throughout the range of motion and usually results from extrapyramidal
disorders such as Parkinson's disease.
Bradykinesia is a pathological slowing of motor performance often seen with Parkinson's disease and parkinsonism.
Paraparesis/plegia paralysis or paresis of both lower
extremities.
Upper motor neurons are the principal descending motor
pathways for voluntary movement, including the corticospinal and corticobulbar
tracts (and some other associated tracts).
Lower motor neurons are the anterior horn motor neurons and
their axons that extend through the ventral nerve root and the peripheral
nerves to reach the neuromuscular junction.
The internal capsule is the primary locus through which the
upper motor neuron (corticospinal and corticobulbar) pathways descend.
Chorea is a purposeless, involuntary, random twitching
movement.
Athetosis is a purposeless, involuntary writhing movement.
Dystonia is an involuntary, sustained twisting position of the
body or a body part (torticollis, for example, when it involves the head).
Hemiballism a repeated, involuntary, flinging or flipping
movement of a part of the body on one side, usually due to damage to the
subthalamic nucleus.
Tic is a rapid movement, tending to be repeated in the same
pattern over and over.
Fasciculation is an involuntary twitching of individual motor
units, usually visible as a rippling of the skin but not resulting in
any actual movement of the body part.
10-1. Describe
the course of "upper motor neurons".
Answer 10-1. Upper motor neurons (coticospinal and corticobulbar
tracts) arise in the motor cortex, traverse the internal capsule, cerebral
peduncle and pyramids of the brain stem.
10-2. Over what
functions do the upper motor neurons exert the greatest control (what movements
are most affected by damage)?
Answer 10-2. They are mostly involved in control of distal movements
(such as hand and fingers). Proximal functions (such as shoulder shrug) have bilateral
control.
10-3. Where are
sites of potential lesions producing lower motor neuron signs and symptoms?
Answer 10-3. Lower motor neuron damage can be anywhere along the
pathway from the anterior horn motor neuron, ventral root, plexus or peripheral
nerve.
10-4. What are
the features of lower motor neuron damage?
Answer 10-4. Lower motor neuron damage results in decreased reflex
and usually atrophy. It may also produce fasciculations.
10-5. What is
the significance of fasciculations?
Answer 10-5. Diffuse, persistent and extensive fasciculations
suggests motor neuron disease or damage (transient fasciculations are common
and benign if unaccompanied by weakness or reflex change).
10-6. What are
the characteristics of peripheral nerve damage?
Answer 10-6. Effects of nerve damage are most often seen distally,
reflexes are affected early and atrophy is often present.
10-7. What are
the characteristics of muscle disease?
Answer 10-7. Symptoms are usually most evident proximally, there is
no sensory loss, reflexes only affected late and atrophy is not severe.
10-8. What are
the characteristics of basal ganglia disease?
Answer 10-8. Muscle tone, postures, and patterned movements are most
affected. Parkinsonism is common, with bradykinesia, difficulty initiating
movements, delayed postural reflex responses and rigidity. Abnormal movements
at rest are common: resting tremor, chorea, athetosis, dystonia and hemiballism.
10-9. What are
the characteristics of cerebellar disease?
Answer 10-9. There are usually a variety of problems with
coordination of voluntary actions, there may be trunkal ataxia (drunken gait)
and muscle tone may be variably affected. Reflexes may be decreased or pendular.
Chapter 11 - Neurologic Tests
Questions
Define the following terms:
electroencephalogram;
alpha/beta/theta/delta waves;
electromyogram;
motor unit;
fasciculation;
fibrillation;
nerve conduction study;
compound muscle action potential (CMAP);
sensory nerve action potential (SNAP);
lumbar puncture (spinal tap);
oligoclonal bands;
IgG synthesis;
pleocytosis;
opening pressure.
An electroencephalogram is the electrical recording of brain waves in crebral cortical neurons.
Brain waves fall in differnt frequencies. Delta waves are the slowest (<3 Hz); theta waves (4-7.5Hz); alpha waves (8-12Hz); beta waves (<12Hz).
Electromyography is the electrical recording made from muscle. The overall activity from the muscle can be recorded from the surface of the body (surface EMG), but a needle placed in the muscle is necessary if responses from individual muscle fibers are to be recorded or if the morphology of motor units is to be evaluated.
A motor unit is a motor neuron and all of the muscle figers to which it is connected.
A fasciculation is the spontaneous activation of a motor nerve axon and all of the muscle fibers attached to it. There is usually an involuntary twitch of the muscle seen on the skin surface. Persistant fasciculations in a weak muscle are usually idicative of motor neuron disease though transient fasciculations can be seen in overworked or fatigued muscles. A fasciculation potential is the electrical activity recorded during a fasciculation.
A fibrillation is the involuntary contraction of an individual muscle fiber. Normal muscle fibers never contract without a nerve stimulus and, therefore, the entire motor unit response is see. Denervated muscle fibers become spontaneously active and fibrillation potentials and positive sharp waves (the electrical signals from a single muscle fiber ) can be seen.
A nerve conduction study tests the speed and amplitude of conduction along a peripheral nerve. The speed of conduction is a reflection of the health of the fiber (particular the large, myelinated fibers) while the amplitude is reflective of the signal that is transmitted. Motor conduction studies and seonsory conduction studies test motor and sensory fibers, respectively.
Compound muscle action potential is the electical signal recorded from the skin surface following electrical stimulation of the nerve to the muscle.
Sensory nerve action potential is the electical signal recorded from the skin surface directly over a sensory nerve following electrical stimulation of the nerve elsewhere along its course.
A lumbar puncture (spinal tap) is the insertion of a needle between the lamina of the vertebrae and into the thecal sac with the purpose of obtaining cerebrospinal fluid. This is done below the L2 level (usually between L3-4 or L4-5) in order not to injure the spinal cord.
Oligoclonal bands (of protein) are specific bands of IgG in spinal fluid seen with electrophoresis of the CSF.
IgG synthesis rate is the measure of how much immunoglobulin is being synthesized in and around the brain. This can also be expressed as the IgG synthesis ratio. It is elevated in infectous or inflammatory disease of the brain.
Pleocytosis is the presence of white blood cells in the cerebrospinal fluid.
Opening pressure is the pressure measured in the CSF (expressed in millimeters or centimeters of water) right after entering the thecal sac with the needle.
11-1. What is recorded in the electroencephalogram?
11-1. The electroencephalogram records brain waves, electrical rhythms arising from activity of neurons in the cerebral cortex
11-2. What are the normal brain waves when awake?
11-2. The normal waves when awake and relaxed, with the eyes closed are: alpha waves posteriorly and beta waves elsewhere else.
11-3. What is seen during sleep?
11-3. The specific findings in sleep stages include: delta waves in slow-wave sleep (stage 3 and 4 sleep); and vertex sharp waves and sleep spindles in stage 2 sleep.
11-4. What kinds of waves are seen over damaged brain tissue?
11-4. Slowing of waves. This is a nonspecific finding of brain dysfunction from any cause.
11-5. What does diffuse slowing of brain waves indicate?
11-5. If the slowing is diffuse, it usually indicates diffuse encephalopathy (often due to toxic, metabolic or drug-related effects on the brain).
11-6. What findings are seen in epileptic patients?
11-6. In between seizures, epileptiform discharges are often seen in areas that generate seizures. These are not necessarily associated with actual seizures although they are almost always seen during seizures. There are usually very fast frequencies seen during the actual seizure.
11-7. How often are EEGs abnormal in patients with epilepsy?
11-7. About 60% of patients with epilepsy have epileptiform discharges in the interictal period (between seizures) on a single EEG. If you do 3 EEGs, about 85% will show abnormalities,
11-8. What does electromyography refer to?
11-8. Electromyography is the electrical record of muscle activity. It can be recorded from the surface of the body if overall muscle function is to be examined. Needles placed in the muscle can record from individual muscle fibers.
11-9. What does the electromyogram show in a muscle at rest?
11-9. Normal muscle is electrically silent at rest. When muscles are severely damaged or when muscle fibers are disconnected from their nerve, they may become spontaneously active.
11-10. What is seen in a muscle that is denervated?
11-10. Muscle fibers that are separated from their motor nerve fiber show fibrillation potentials and positive sharp waves beginning about a week or so after damage of the nerve.
11-11. What is recorded in the muscle when the muscle is voluntarily contracted?
11-11. When muscles are contracted, motor units can be recorded. These are the electrical discharges of the motor nerve fiber and all of the muscles to which it is attached (the motor unit). As more force is exerted, the individual motor units fire faster and more motor units are recruited.
11-12. What happens to motor units with time after partial denervation of a muscle?
11-12. When nerves to a muscle have been damaged, they attempt to regenerate. Also, surviving nerve fibers in the muscle sprout in order to reinnerve denervated muscle fibers. The size of the motor unit increases (i.e., the number of muscle fibers attached to a given nerve fiber). This results in a giant motor unit potential, indicating a chronic process that has had time to attempt to recover (usually over months).
11-13. What are motor and sensory nerve conduction studies?
11-13. A motor nerve conduction study includes stimulating a motor nerve at several places along its course and recording from a muscle that is attached to the nerve. Sensory nerve conduction requires recording the electrical response directly in the nerve to stimulation of a sensory nerve. The distance between the various stimulation sites and the location of recording, along with the time until the response is seen (the latency) can be use to compute the speed of conduction.
11-14. How fast do nerves conduct in the limbs?
11-14. Conduction velocities are compared to normal and to those in the unaffected limb. Generally, sensory conduction is about 5 m/sec slower than motor conduction and upper limb conduction is about 5 m/sec faster than lower limb. In the upper limb, the lowest normal motor conduction is about 45 m/sec and lowest normal sensory conduction is about 40 m/sec.
11-15. What are the advantages of CT scans?
11-15. They are fairly quick to perform and relatively widely available. The create excellent images of bone lesions and are good for recent hemorrhage into tissues (such as in or around the brain). Therefore, they are very useful in trauma.
11-16. What are the limitations of CT scans?
11-16. There are several. CT scans use x-rays, with potential harmful effects of ionizing radiation. They can only be done in the axial (horizontal) plane (although they can be computer “reformatted” in other planes). They have trouble creating images of soft tissue, especially near thick bone. Therefore, lesions of brain parenchyma are not well seen (unless large).
11-17. What are the advantages of MRI scans?
11-17. MRI creates the best image of brain paraenchyma (infection, inflammation, stroke). Bone does not interfere with the image at all. MRI creates the most sensitive image for detecting early stroke (perfusion and diffusion-weighted images). Images can be made in any plane of interest. You can also make images of the blood vessels (MRAngiogram or MRVenogram).
11-18. What are the limitations of MRI scans?
11-18. Patients may be too claustrophobic or unable to stay still (and motion artifact is a major problem). It also takes quite a while to create an image and it is difficult to continue treatment and monitoring during the procedure. You cannot do MRI with certain implanted devices (defibrillator, pacemaker, certain aneurysm clips, cochlear implant, etc). Metal objects create a lot of artifact.
11-19. What is the role of IV contrast in MR and CT scans?
11-19. Contrast given IV during CT or MRI scan does not get into normal brain. Therefore, contrast entering a lesion (“enhancement” of a lesion) shows conditions that break down the blood-brain barrier. This highlights such lesions as: tumors, infections, severe inflammation, etc. Some patients may be allergic to CT dye (iodine) and a heavy dye load can impair renal function.
11-20. What are angiograms?
11-20. Conventional angiography involves taking x-ray images while introducing contrast into blood vessels. This creates the best image of blood vessels (arteries or veins, depending on how long you wait. It does involve heavy dye loads (which can be decreased somewhat by digital subtraction angiography. Recently, CT angiograms may be done by 2-D and 3-D reconstructions after intravenous contrast administration and MRA can also show blood vessels (although artifacts are more problematic with this technology).
11-21. What is tested with a lumbar puncture?
11-21. Lumbar puncture/spinal tap is performed below the L2 level (to avoid the spinal cord). Cerebrospinal fluid pressure is measured and collected fluid is tested for protein, glucose, cells, microorganisms and other specialized tests depending on the suspected clinical problem.
11-22. What is indicated by and elevated protein level in the CSF?
11-22. Protein in the spinal fluid is normally less than 45mg/dl. Elevation of protein level is nonspecific but indicates some problem with the blood-brain barrier (it is mostly seen in neoplasm, infection, inflammatory lesions and slight elevations are seen in diabetics).
11-23. What are oligoclonal bands and what do they signify?
11-23. Oligoclonal bands (of protein) are specific bands of IgG in spinal fluid seen with electrophoresis of the CSF. This finding indicates that there are very specific antibodies present in the CSF and indicates the presence of some inflammatory or infectious condition (multiple sclerosis or Lyme disease, for example).
11-24. What is a normal CSF glucose level and what do abnormalities indicate?
11-24. Glucose level should be more than 1/2 of the blood glucose level. It may be decreased in certain infections, severe inflammations and some neoplasms (especially carcinomatous meningitis).
11-25. What is the significance of finding white blood cells in the spinal fluid?
11-25. There are normally only a few WBCs in spinal fluid, and these are overwhelmingly lymphocytes. Increase suggests certain inflammations or infections (increased lymphocytes may suggest viral infection; polys are usually due to bacterial infections, for example).
11-26. What is the significance of finding red blood cells in the spinal fluid?
11-26. There should be no red cells in spinal fluid. A “traumatic tap” is suggested by many red cells in the first tube collected with quite a bit of clearing in subsequent tubes. However, hemorrhage should be considered if there are more than a few RBCs.
11-27. How are infections of the nervous system evaluated?
11-27. There are many types of cultures that can be done (depending on the organism) and there are some tests for bacterial or fungal antigens or PCR for certain viral agents (particular Herpes simplex).
11-28. What conditions elevate CSF pressure?
11-28. Pressure is elevated by anything that takes up space, inhibits resorption of CSF or blocks CSF flow (spinal taps should not be done if increased pressure is suspected until an images shows that the CSF pathways are all open).