Medrano Neuro Notes 2.0

DEMYER’S
TECHNIQUE OF THE NEUROLOGIC EXAMINATION 1
MENTAL STATUS EXAM and HIGHER COGNITIVE FUNCTIONS B. Cover-Uncover Test

I. MENTAL STATUS IV. CN V TRIGEMINAL NERVE (Motor Function)
A. General Behavior and Appearance A. Inspection - Atrophy/Hypertrophy
B. Stream of Talk B. Jaw Opening/Closure
C. Mood and Affective Response V. CN VII FACIAL NERVE
D. Content of Thought A. Inspection
E. Intellectual Capacity B. Muscle Strength Testing
F. Sensorium C. Taste Testing
1. Consciousness VI. CN VIII VESTIBULOCOCHLEAR NERVE
2. Attention Span A. Rinne’s Test
3. Orientation to time, place and person B. Weber’s Test
4. Memory (Immediate, Recent and Remote) C. Schwabach’s Test
5. Calculation VII. CN IX,X: GLOSSOPHARYNGEAL and VAGUS NERVE
6. Fund of Information A. Voice and Speech
7. Insight, Judgment and Planning B. Swallowing
II. LANGUAGE C. Inspect Palatal Arch
A. Handedness D. Gag Reflex
B. Spontaneous Speech VIII. CN XI SPINAL ACCESSORY NERVE
C. Comprehension A. SCM Test
D. Repetition of simple and complex statements B. Shrug Test
E. Naming and Word Finding IX. CN XII HYPOGLOSSAL NERVE
F. Reading A. Inspection - Atrophy, Tremors, Fasciculations, Deviation of
G. Writing Tongue
B. Tongue against Tongue Depressor
SOMATOSENSORY SYSTEM
I. TRIGEMINAL NERVE (CN V) MENINGEALS
A. Touch AUTONOMICS
B. Temperature
2
C. Pain NEUROLOGIC SYMPTOMS AND SIGNS: Mental, Motor, and Sensory
D. Corneal Reflex
II. THE BODY and EXTREMITIES MENTAL
A. Touch
D e M yer ’s The Neurologic Examination
• Alterations of level of consciousness

B. Temperature Lethargy/stupor/delirium/coma
Seizures/syncope/sleep disorders
C. Pain Attention deficit
D. Position Sense by Digital Movement • Cognitive dysfunctions
Retardation/dementia
E. Romberg’s Test Amnesia, disorientation to time, person, and place
F. Vibration Sense IlIusions/hallucinations/delusions
Impaired insight, judgment and planning
DyscaIcuIia
Dysphasia/dyslexia/agnosia
MOTOR EXAMINATION
• Affective dysfunction
I. Inspection (Head to Toe, Left and Right) Anxiety
A. Atrophy/Hypertrophy, Symmetry, Joint Malalignments, Flat/emotional lability
Mania/depression
Fasciculations, Tremors, Involuntary Movements Phobias/obsessions
Episodic dyscontrol: rage and aggression
B. Gait, Station, Steadiness, Verticality of Standing Position
II. Palpation
A. Muscle Tone MOTOR
B. Spasticity/Rigidity • Somatomotor
Fatigability/weakness/paralysis
III. Muscle Strength Testing Atrophy/hypertrophy of muscle/fasciculations/cramps/exercise intolerance
Hyperactivity
IV. Muscle Stretch Reflexes Hypo-/hyperkinesias: tremor, rigidity, dystonia, athetosis, chorea, tics
Spasticity/hypotonia
Dystaxia/dyspraxia
BASAL GANGLIA and CEREBELLUM Dysphonia/dysarthria/dysphagia/dysprosody
I. Stand with Feet Together Respiratory dysrhythmias: dyspnea/apnea/hyperventilation/cough/
hiccoughing/sneezing
II. Inspection • Visceromotor/homeostatic
A. Hypotonia Cardiovascular: dysrhythmias/hypertension/hypotension
Vasomotor instability/flushing/Raynaud’s phenomenon
B. Nystagmus Trophic skin/nail changes
Dyshidrosis: hyperhidrosis/anhidrosis
C. Decomposition of Movement Bladder: dysuria/polyuria/oliguria/anuria/discoloration of urine
D. Dysarthria Bowel: anorexia/hyperphagia/vomiting/constipation/diarrhea
Sexual dysfunction: impotence/dyspareunia
III. Tandem Walking
IV. Finger-To-Nose Test SENSORY
V. Rapid Alternating Movements Test • Deficits of sensation
A. Rapid Pronation-Supination Test Anesthesia/hypesthesia/numbness
Blindness/amaurosis/diplopia/scotomata/blurring
B. Thigh Slapping Test Deafness/hyperacusis
Anosmia/ageusia
VI. Heel-To-Shin Test
• Excessive sensation
VII. Heel-Tapping Test Pain: head, chest, abdomen, extremity, back, muscles, or joints
Neuralgia
VIII. Overshooting Test Hyperesthias/tingling/tickling/itching
IX. Arm-Pulling Test Nausea/cramping/bloating
Dizziness/vertigo
Tinnitus
CRANIAL NERVE EXAMINATION
I. CN I OLFACTORY NERVE - Sniff Test FIGURE 1-1. Dendrogram summarizing neurologic symptoms and signs.
II. CN II OPTIC NERVE MENTAL STATUS EXAMINATION

A. Visual Acuity A. General Behavior and Appearance (Normal, hyperactive, agitated,
B. Color Vision quiet, or immobile? Dresses according to age, sex and
C. Central Vision background?) Note: never say just normal.
D. Peripheral Visual Fields by Confrontation B. Stream of Talk (Converse normally? Able to reach conversation
E. Pupillary Light Reflex goal? Speech rapid, slurred, under pressure, or slow?)
1. Pupil Size C. Mood and Affective Responses (Appropriate under the
2. Direct Pupillary Light Reflex circumstances, euphoric, agitated, angry, weeping?)
3. Consensual Pupillary Light Reflex D. Content of Thought (illusions, delusions, hallucinations,
4. Swinging Flashlight Test misinterpretations, obsessions? Preoccupied with fear, bodily
F. Fundoscopy complaints or other phobias?)
III. CN III, IV, VI: OCULOMOTOR, TROCHLEAR and ABDUCENS Illusion: false sensory perception based on natural stimulation of a
A. Range of Eye Movement sensory receptor e.g. water on a highway on a summer day
MEDRANO NEURO NOTES 1

2 DEMYER’S TECHNIQUE OF THE NEUROLOGIC EXAMINATION
Hallucination : false sensory perception not based on a natural

stimulation of a sensory receptor e.g hearing voices of dead
people
Delusion : false belief that reason cannot dispel e.g.
E. Intellectual Capacity (Bright, average, dull? Consider educational
background)
F. Sensorium
1. Consciousness (Where is the ARAS? Neurons of the reticular
formation in the pontomesencephalic tegmentum and
diencephalon)
2. Attention Span (repeat a random number sequence)
3. Orientation to Time, Place and Person
4. Memory
Immediate : repeat a random number sequence
Recent : ask what they had for breakfast
Remote : ask their birthday
5. Calculation: Sequentially subtract 7 from 100. Consider
educational background
6. Fund of Information : Enumerate Filipino presidents. Ask
about current events
7. Insight, Judgment, and Planning : Kapag may napulot ka na
wallet ano ang gagawin mo? Ano kaya ang ginagawa mo 10
taon mula ngaun.

Language
A. Handedness (contralateral side controls handedness)
B. Spontaneous Speech (Does the patient talk straight? Fluent?)
1. Dysphonia – difficulty in producing voice sounds; pitch, volume
2. Dysarthria – difficulty in articulating words
3. Dysprosody – difficulty with melody and rhythm of speech,
intonation that give shades of meaning
4. Dysphasia – difficulty in expressing or understanding; premise Higher Cerebral Functions
that the patient has intact consciousness, expressive, receptive
or global The (very) specific effects of brain injury to specific regions in the
C. Comprehension (can the patient understand instructions? The best brain (Nice-to-Knows/for higher learning)…
way to test comprehension is to test patient’s response to yes-no FRONTAL LOBE SYNDROME
questions) I. Effects of unilateral frontal disease, either left or right
D. Repetition of simple and complex statements (for testing A. Contralateral spastic hemiplegia
dementia; if the patient cannot repeat – transcortical aphasia) B. Slight elevation of mood, increased talkativeness, tendency to
Examples: bola, ospital, karimarimarin, Umuwi na ang bata, joke inappropriately (Witzelsucht), lack of tact, difficulty in
Kami ay namasyal sa Enchanted Kingdom adaptation, loss of initiative
E. Naming and Word Finding (Ask the patient to name at least 3 C. If entirely prefrontal, no hemiplegia; grasp and suck reflexes
colors, 3 body parts, and at least 3 objects in the room) or instinctive grasping may be released
F. Reading D. Anosmia with involvement of orbital parts
G. Writing (Have the patient write his/her full name and address. II. Effects of right frontal disease
Describe the level of adequacy and note types of error) A. Left hemiplegia
B. Changes as in I.B, C, and D
Constructional Ability III. Effects of left frontal disease
Have the patient draw a triangle, a 2-dimensional cross, and a 3- A. Right hemiplegia
dimentional cube. If patient cannot draw on command, draw and B. Motor speech disorder with agraphia, with or without apraxia
have the patient copy. Describe the quality of the drawing particularly of the lips and tongue
in terms of asymmetry and spatial neglect. You may also use barbecue C. Sympathetic apraxia of left hand
sticks for forming figures instead of drawing. D. Loss of verbal associative fluency; perseveration
E. Changes as in I.B, C, and D
The Mini-Mental Status Examination is a useful bedside method of IV. Effects of bifrontal disease
scoring cognitive impairment and following its progress. A score of 24 A. Bilateral hemiplegia
on the widely used “mini-mental” is considered normal and scores B. Spastic bulbar (pseudobulbar) palsy
below 21 generally indicate cognitive impairments C. If prefrontal, abulia or akinetic mutism, lack of ability to
sustain attention and solve complex problems, rigidity of
thinking, bland affect, social ineptitude, behavioral
disinhibition, inability to anticipate, labile mood, and varying
combinations of grasping, sucking, obligate imitative
movements, utilization behavior.
D. Decomposition of gait and sphincter incontinence
TEMPORAL LOBE SYNDROME
I. Effects of unilateral disease of the dominant temporal lobe
A. Homonymous upper quadrantanopia
B. Wernicke’s aphasia
C. Amusia
D. Impairment in tests of verbal material presented through the
auditory sense
E. Dysnomia or amnesic aphasia
F. Visual agnosia
G. Occasionally amnesic (Korsakoff) syndrome
II. Effects of unilateral disease of the nondominant temporal lobe
A. Homonymous upper quadrantanopia
B. Inability to judge spatial relationships in some cases
C. Impairment in tests of visually presented nonverbal material
D. Agnosia for sounds and some qualities of music
III. Effects of disease of either temporal lobe
2 MEDRANO NEURO NOTES

4 DEMYER’S TECHNIQUE OF THE NEUROLOGIC EXAMINATION 3
socially in liking or disliking the Pt. You are not subject to the Pt’s sorrows, seductions,
and transgressions nor captive to your own reactions to the Pt’s personality and life
A. Auditory, visual, olfactory, and gustatory hallucinations style.• Free from fears ofaphasia
Wernicke’s censure or– entrapment,
fluent, Pts can revealto
inability theirunderstand
full sentiency
and needs. Although you should achieve empathy, you must remain emotionally calm
B. Dreamy states with uncinate seizures (Localization: Temporal Infrasylvian)
because you cannot think rationally when weeping over a Pt’s illnesses, fuming about

C. Emotional and behavioral changes a Pt’s• behavior
Global oraphasia
faults, or- feeling
scant, too
non-fluent
attracted tospeech in addition
the Pt. Perhaps to a
this approach
D. Delirium (usually nondominant) throughseverely impaired
elemental biology will workcomprehension
for you; if not, it may(Localization:
encourage you to findLarge
your
E. Disturbances of time perception own way to foster the professional humility and grace that enables Pts to fully reveal
Perisylvian/Frontal and Temporal)
their personhood.
IV. Effects of bilateral disease ü Why do you have to check for the presence of primitive reflexes?
A. Korsakoff amnesic defect (hippocampal formations) • Residual primitive reflexes such as sucking, grasp, palmomental,
B. Apathy and placidity II. LOOKING
glabellar AT EYESand others suggest diffuse cortical brain
blink,
C. Hypermetamorphopsia (compulsion to attend to all visual
You candysfunction
see an awful lot just by looking.
stimuli), hyperorality, hypersexuality, blunted emotional ü What are the components of the Gerstmann’s Syndrome?
reactivity (Klu¨ver-Bucy syndrome) —Attributed to Yogi Berra
• Gerstmann’s Syndrome – dysgraphia, dyscalculia, finger agnosia,
right-left disorientation, lesion on left angular gyrus
PARIETAL LOBE SYNDROME If restricted to one part of the examination, choose inspection, the most efficient

method of physical diagnosis. Inspection begins the moment you approach your Pt.
I. Effects of unilateral disease of the parietal lobe Glasgow Coma Scale
Immediately you might notice pinpoint pupils and numerous needle scars over the
A. Corticosensory syndrome and sensory extinction (or total Eye Response
antecubital veins. In two glancesVerbal Response Motor Response
you suspect a drug addict. This is the diagnostic
hemianesthesia with large acute lesions of white matter) power of inspection. But wait a minute. Eye drops to treat glaucoma may have con-
6 Obeys command
B. Mild hemiparesis (variable), unilateral muscular atrophy in stricted the pupils, and repeated blood transfusions may have scarred the antecubital
5 The diagnostic value ofOriented
veins. signs emerges only afterLocalizes to pain
integration with a complete
children, hypotonia, poverty of movement, hemiataxia (all
4 Spontaneous
history Confused
and physical examination. No single diagnosticWithdraws from pain
technique is sufficient.
seen only occasionally)
3 After a lifetime of looking,Inappropriate
To verbal you may consider yourself a keen observer. To test how
Decorticates to pain
C. Homonymous hemianopia or inferior quadrantanopia well you have observed something, try to draw it. What you have seen well, you can
command
(incongruent or congruent) or visual inattention draw well. Complete the requested drawings faithfully. They are tremendous tools.
2 Before
To pain Incomprehensible
starting this section, please get a hand mirrorDecerebrates to pain
and a transparent millimeter
D. Abolition of optokinetic nystagmus with target moving
1 Come
ruler. No response No response
on now; be fair. Give the tactics a chance.No response to pain
toward side of the lesion

E. Neglect of the opposite side of external space A. Relation of the eyelid margins to the iris
II. Effects of unilateral disease of the dominant (left) parietal lobe
1. An opening, the palpebral fissure, separates the upper and lower eyelid margins.
(in right-handed and most left-handed patients) EXAMINATION OF THE FACE AND HEAD
See the vertical arrow in Fig. 1-2A.
A. Disorders of language (especially alexia)
B. Gerstmann syndrome (dysgraphia, dyscalculia, finger Examination of the Eyes
agnosia, right-left confusion) Palpebral fissure
C. Tactile agnosia (bimanual astereognosis) Apex of lateral canthus
Lacrimal papilla
D. Bilateral ideomotor and ideational apraxia Caruncle
III. Effects of unilateral disease of the nondominant (right) parietal Apex of medial canthus A B
lobe
Limbus
A. Visuospatial disorders Pupil
B. Topographic memory loss Iris C D

C. Anosognosia, dressing and constructional apraxias • 1-2.
FIGURE Normal intercanthal distance: 1.9 cm
(A–D) Nomenclature of the external eye.
D. Confusion • Intercanthal distance in canthus dystopia: 2.5 cm
E. Tendency to keep the eyes closed, resist lid opening, and Definitions
blepharospasm 2. Observe your eyes in a hand mirror; in the space on the left side of this page,
• drawLid thelag – upper
exact eyelid
contours does
of the not of
margins drop
yourduring downward
upper and rotation
lower eyelids. Espe-
IV. Effects of bilateral disease of the parietal lobes of the eye.
cially notice the configuration at the apices of the medial and lateral canthi
A. Visual spatial imperception, spatial disorientation, and • (medial and lateral angles) of the palpebral fissure.
Exophthalmos – protrusion of the eye, widens palpebral fissure
complete or partial Balint 3.• Compare your drawing with the one shown in Fig. 1-2A. Then look again into the
Reptilian stare – absence of blinking due to parkinsonism
mirror and identify the parts of your eye, as listed in Fig. 1-2A.
OCCIPITAL LOBE SYNDROME 4.Examination of the Face, Hair
In Fig. 1-2A and in your mirror notice the caruncle, the tiny mound of meaty
I. Effects of unilateral disease, either right or left tissue that occupies the apex of the medial canthus.
• Inspect the nose, mouth, chin, and ears.
II. Contralateral (congruent) homonymous hemianopia 5. In the mirror study the iris, the colored disc, surrounded by the white sclera
• (Fig.Cornelia
1-2C). Is de lange in
it uniform syndrome
color? – Midline union of the eyebrows
III. Elementary (unformed) hallucinations
(synophrys) may indicate malformation syndromes
IV. II. Effects of left occipital disease
• Hypothyroidism – Absence of the lateral eyebrow
A. Right homonymous hemianopia
• Frontonasal dysplasia = Widow’s peak + hypertelorism + canthus
B. Alexia and color-naming defect
dystopia
C. Visual object agnosia
• Holoprosencephaly = Microcephaly, hypertelorism, median cleft
V. Effects of right occipital disease
of the upper lip
A. Left homonymous hemianopia
• Café-au lait spots = suggestive of Neurofibromatosis, not specific
B. With more extensive lesions, visual illusions
(metamorphopsias) and hallucinations (more frequent with • Tuberous sclerosis = Nevus anemicus (Ashleaf spots) & Facial
right-sided lesions) angiofibromas
C. Loss of topographic memory and visual orientation • Sturge-Weber syndrome: portwine stain, Facial hemangiomas:
VI. Bilateral occipital disease • Myotonic dystrophy = ptosis, temporal and masseter atrophy,
A. Cortical blindness (pupils reactive) expressionless face, sagging jaw
B. Anton syndrome (visual anosognosia, denial of cortical • Waardenburg syndrome = white forelock, slight synophrys,
blindness) heterochromia
C. Loss of perception of color (achromatopsia)
D. Prosopagnosia (temporo-occipital), simultanagnosia (parieto- Neurovascular Examination
occipital) • Strong localized bruit indicates stenosis
E. Balint syndrome (parieto-occipital) • 90% occlusion: most ominous – soft, high pitched sound
• 95% occlusion: bruit disappears
FREQUENTLY ASKED QUESTIONS • Carotid artery bruits – anterior to SCM
ü Definitions • Vertebral artery bruits – posterior edge of SCM
• Agnosia – not knowing or understanding despite intact sensory • Blood pressure difference of 10-20mmHg between each arm
system and sensorium e.g. visual word agnosia or dyslexia indicative of subclavian occlusion
• Apraxia – inability to do willed acts despite intact motor system
and mentals tatis e.g. gait apraxia, dressing, constructional and Neonatal Head
ideomotor • Transillumination: to distinguish between scalp edema, subdural
• Aphasia – inability to understand and express words to fluid, porencephaly and hydrocephaly.
communicate despite intact sensorimotor pathways and mental • Increased ICP = bulging fontanel
status • Brachycephaly: sagittal > coronal growth
ü Differentiate Broca’s aphasia, Wernicke’s aphasia and global • Dolichocephaly: coronal > sagittal growth
aphasia
• Broca’s aphasia – nonfluent, inability to express (Localization:
Frontal Suprasylvian)

4. Bonethedeposition along thetissue
parieto-occipital
at the sutures(lambdoidal) suture would
pli- increase
HAPTER 1
5. In fetuses, fibrous connective is broad and somewhat
ER 1
the ____________________
ant. Where the fibrous connectivediameter of the
tissue forms calvarium.
large, nonossified membranes
between
5. As athe margins
general of some
rule, we canskull bones,
state thatthe sites are
growth called
along fontanels.
a suture Learnincreases
margin the the
4 head DEMYER’S TECHNIQUE OF THE NEUROLOGIC EXAMINATION
Examination of the Face and Head

sutures, fontanels, and that
diameter bonesisin____________________
Fig. 1-18. to the plane of the suture.
6. Study the head shapes of your classmates. Some will have unusually short and

wide heads, others will have long and thin heads. Both groups will have heads
Fontanels: Bones: the same circumference. Therefore,
with approximately Sutures: a head that is relatively
small in oneFrontal
diameter will, in compensation, enlarge
Frontalin the opposite diameter.
Anthropologists designate short-headedness as brachycephaly
(Metopic) (brachy = short)
Somesthetic cortex (Postcentral gyrus, parietal lobe)
and long-headedness as dolichocephaly (dolicho = long). Which head type would
Anterior
Coronal Tertiary neuron (in thalamus)
have the greatest lateral diameter? ____________________
(Frontoparietal)
Thalamocortical relay axon
7. In brachycephaly, growth from the ____________________ suture proceeds rap-
idly relative Parietal
to that from the ____________________ suture.
Sagittal
Thalamus (diencephalon)
8. In dolichocephaly, growth from the ____________________ suture proceeds rap-
idly relative to that from the ____________________ suture.
Lambdoidal
Posterior
(Parieto-occipital)
Occipital
F. Closure of the sutures and fontanels Medial lemniscus Secondary neuron (in spinal cord)
1. With maturation, the cranium becomes increasingly rigid because the synchon-
droses, sutures, and fontanels progressively uniteCoronal
Frontal and finally ossify completely. Primary neuron (in dorsal root ganglion)
Before the synarthroses ossify, we say they are “open.” Afterward, they are Medullocervical junction Vibration
“closed.” TheParietal
time of closure of the various sutures by ossification varies consid- Deep Position sense
erably (TableOccipital
1-2). sensation Two-point
Spinal lemniscus discrimination
Sphenoid Touch
Temporal Pain
Superficial
sensation
TABLE 1-2 • Time of Ossification of Some Cranial Synarthroses Temperature

Synarthrosis Time ossification completed
FIGURE 1-18. Fontanels, bones, and sutures of the infant cranium. Top: superior view of cranium.
Bottom:Frontal
lateral (metopic) suture
view of cranium. 2y
Coronal suture 30 y FIGURE 2-28. Decussation of the somatosensory pathways. The pathway for deep sensation
decussates at one level, the cervicomedullary junction. The pathway for pain and temperature
Basilar synchondroses 2–20 y
synapses at or near the level of entry of the primary axon up and down the cord. The impulses
Anterior fontanel 1.5 y (range, 3–27 mo) that mediate light touch travel in both pathways.
6. ThePosterior
bones that border the largest fontanel, the anterior,
fontanel are2 mo
Birth to the ______________

bones.

Misshaped Heads turn rostrally in the contralateral ventrolateral quadrant of the spinal cord
C. Pliancy
• of the synarthroses in the infant’s cranium
Cephalohematoma white matter. This pathway of second-order neurons is called the spinal lem-
1. A 2.
• The anterior
is a sheetfontanel
Meningocele
fontanel usually
of fibrous closestissue
connective by 18that
months (normal
bridges range,
the gaps 4 to
at the 27 months).
inter- niscus to designate that it ends in the thalamus (Figs. 2-28 and 10-6).
If
sections
• increased intracranial pressure occurs before closure, the anterior
of the sutures in the neonatal skull. Later the fontanels ossify. The sheet
Scalp edema/caput succedaneum fontanel c. The superficial modality of touch is mediated by dorsal and ventral column path-
reflects
of •connective it first
tissue by
at bulging.
the Suppose
fontanels increased
allows an up intracranial
and down, pressure began
diaphragm-like after that ways. The ventral column component comprises part of the spinal lemniscus
Subgaleal hemorrhage (Fig. 2-28).
action, whereas
time.
Which thesynarthrosis
narrower connective tissue
would yield strip
next toatthe
thepressure,
sutures permits only
the ❒ synchondroses
a limited, hinging
of the cranialaction. Thus
base or ❒ thethesutures
infant skull
of theis cranial
most pliant
vault?at the ❑ sutures/
Causes of Megalocephaly
❑ fontanels. 35
3. Palpation will disclose wide separation, or “splitting,” of the sutures. Otherwise,The law of the level of decussation of the somatosensory pathways: The gen-
2. The cartilage Megalocephaly
uniting the
skull radiographs or synchondroses
CT are essential. of the cranial
If the base split,
sutures is lesswhat
pliant than to theeral somatosensory pathways decussate at the level of the nucleus for the
happens
fibrous connective
head tissue. Rank the three skull synarthroses, the synchondroses,
size? ________________________________. perikarya of the second-order neurons. The law holds for the spinothalamic,
fontanels, and sutures, in order from
Obstructive most to least pliant: __________________,
hydrocephalus spinocerebellar, touch, pain and temperature, and dorsal column pathways.
4. Although suture
_________________, closure
and by ossification continues into adulthood, functional clo-
_______________.
CHAPTER 1
sure by dense connectiveedema tissue occurs much earlier. By 10 to 12 years of age, the
3. During morphogenesis andBrain birth, the cranium serves the contradictory functions
sutures have adhered so firmly, although not ossified, that they no longer yield to3. The third-order neuron of the somatosensory pathways resides in a sensory relay
of plasticity and rigidity. The plasticity of the cranium permits expansion and
increased intracranialSubdural
pressure. If a 16-year-old girl has a big head and split sutures, nucleus of the thalamus. The thalamic neurons relay to the ipsilateral
hematoma/
deformation, whereas the rigidity of the bones protects the brain during passage somatosensory cortex in the postcentral gyrus of the parietal lobe (Fig. 2-28).
as shown by a skull hygroma
radiograph, what is the minimum time she could have had
Association fibers then connect the visual and somatosensory areas with other
increased intracranial pressure? _______________.

Thickened cranium
association cortices.
sutures 5. List three physical signs of pathologically increased intracranial pressure in a young
4. The pathways of two special senses, smell and hearing, are partial exceptions to
diogra- infant.________________________________________________________________ the contralaterality law. Their stimuli, odors and sounds as distinct from light, go
__________. Megalencephaly
around corners and over obstructions. Contrary to other sensory pathways, the
ascending pathways for hearing contain about an equal number of decussated
Benign familial anatomic and undecussated axons (Fig. 9-7). Thus, a unilateral CNS lesion does not ordi-
variation in brain size
narily cause a strongly lateralized hearing loss.
Pathologic megalencephaly,
anatomic or metabolic

FIGURE 1-26. The five most common causes for megalocephaly.
MRI is almost always superior to CT in diagnosing intracranial lesions, except in

a few acute emergencies when intracranial bleeding is suspected. Use CT to show
the cranial bones, the sutures, and calcified intracranial lesions (Alper et al., 1999;
Barkovich, 2000).
BIBLIOGRAPHY . Abnormalities of Head Size and Brain Size

Alper G, Ekinci G, Yilmaz Y, et al. Magnetic resonance imaging characteristics of benign macro-
cephaly in children. J Child Neurol 1999;14:678–682.
Barkovich AJ. Pediatric Neuroimaging, 3rd ed. Philadelphia, Lippincott Williams & Wilkins,
2000.
DeMyer W. Microcephaly, micrencephaly, megalocephaly and megalencephaly. In Swaiman K,
Ashwal S, eds. Pediatric Neurology, 3rd ed. St. Louis, Mosby, 1999, Chap. 18, pp. 301–311.
DeMyer W. Small, large or abnormally shaped heads. In Maria BL, ed. Current Management in
Child Neurology, 2nd ed. Hamilton, BC Decker, 2002, Chap. 49, pp. 299–304.
Tisserand DJ, Bosma H, Van Boxtel MPJ, et al. Head size and cognitive ability in non-demented
older adults are related. Neurology 2002;56:969–971.
IX. THE GENERAL RULES FOR THE NEUROLOGIC

EXAMINATION
Having learned some of the steps of the NE, you can now appreciate the general,
operational, analytic, and attitudinal rules that determine success or failure.
A. Operational rules for the neurologic examination

1. Follow the prescribed technique for each step of the NE.
2. Systematize the NE: The actual order is less important than the fact that you follow
an order:
a. Anatomic order: Work from top to bottom (rostrocaudal order).
b. Functional order: Test for mental, motor, and sensory dysfunctions in packages;
the Standard NE (see Introduction) follows this rule.
DEMYER’S TECHNIQUE OF THE NEUROLOGIC EXAMINATION 5
SENSORY EXAMINATION (Tertiary Neuron) parietal lobe

Definitions ↓
• Esthesia – touch or feeling SOMESTHETIC CORTEX
• Hypesthesia – partial loss of touch Postcentral gyrus, parietal lobe
• Anesthesia – total loss of touch

• Hyperesthesia – oversensitivity to touch
TRIGEMINAL NERVE: TEST FOR TOUCH AND PAIN
• Thermhypesthesia – partial loss of temperature sensation
Before doing the examination, always explain to the patient what you
• Thermanesthesia – total loss of temperature sensation
are going to do.

Adding the prefix hyp- means partial loss, while adding the prefix an-
TESTING TOUCH
means total loss, and adding the prefix hyper- means oversensitivity
to a stimulus • Ask the patient to respond to each touch by wisp of cotton
• Hyperpathia (anesthesia dolorosa) – extreme oversensitivity to (Sabihin nyo po kung may nararamdaman kayo ha?)
pain but often with a raised threshold • With the patient’s eye closed, lightly brush each area of the 3
• Neuralgia – multiple, very severe, electric, shock-like pain that sensory divisions of CN V.
radiate into a specific root or nerve distribution e.g. trigeminal • Touch alternate areas and side of face randomly. (Always
neuralgia compare the right with the left. You can make use of the “Piso
• Causalgia – a constant, intense, unbearable, burning relentless Technique”. Kung dito po sa kaliwa ay 100 pesos, magkano
hyperesthesia-hyperalgesia that may follow injury to the fibers naman po dito sa kanan?)
of a peripheral nerve • To test the reliability of the patient, vary time between touches
• Paresthesia – uncomfortable sensations of numbness, tingling, to keep the patient from getting into a rhythm of answering
or pins and needles, or burning pain short of neuralgia or without actually attending to the stimulus, and occasionally, you
causalgia, accompanying a normal external stimulus to the skin can withhold the stimulus and ask whether the patient felt
• Dysesthesia – when the sensation described in paresthesia occur something.
spontaneously without any obvious external stimulus
GENERAL PRINCIPLE OF SENSORY PATHWAYS TESTING TEMPERATURE
• Ask the patient to close his eye.
• Tuning Fork vs Finger Test- Apply the metal shaft (cold) to the
SOMATOSENSORY FUNCTION OF THE FACE
side of the patient’s cheek for a few seconds and then remove it.
Apply the side of your little finger (warm) to the same spot. Ask
Trigeminal Nerve (CN V) the patient whether each is warm or cold.
• Mediates all general sensory modalities (touch, pain, • Randomly alternate finger and tuning fork.
temperature, position, and vibration) for the face, teeth, mucous
membranes of the nose, cheeks, tongue, and sinuses REMEMBER:
• Mediates proprioception from the ocular, facial and chewing • Pain and temperature share the same peripheral receptors and
muscles pathways in the spinal tract of V and in the spinothalamic tract.
• Conveys NO special fibers (sight, smell, taste etc.) • Testing one tests both modalities
• Always test temperature discrimination first before testing pain
3 major sensory divisions of CN V (If the patient discriminates temperature, normally there is no
• Opthalmic (CN V1) – sensation from cornea, akin of forehead, need to test for pain)
scalp, eyelids, nose, mucosa of nasal cavity, and paranasal • If the history suggests a sensory disorder, test pain sensation
sinuses over the face after testing the temperature discrimination.
• Maxillary (CN V2) – skin of face over maxilla, upper lip, maxillary
teeth, mucous membranes of the nose, maxillary sinus, and TESTING PAIN
palate
• Use the sharp and blunt end of a pin
• Mandibular (CN V3) – skin over mandible including lower lip,
• Alternatively, you can split your tongue depressor in half
side of head, mandibular teeth, temporomandibular joint,
creating a sharp edge.
mucosa of mouth and anterior 2/3 of tongue

CORNEAL REFLEX
Note. The angle of the mandible is NOT innervated by CN V. It id
innervated by C2 • Consists of the closure of both eyelids in response to touching
one cornea
SOMATOSENSORY PATHWAY FOR THE FACE • The afferent arc of the corneal reflex travels through the
ophthalmic division of CN V.
IPSILATERAL side CONTRALATERAL side • The efferent arc travels through CN VIII with the orbicularis oculi
of the face stimulated of the face stimulated muscle closing the eyelids.

Stimulus REMEMBER:
↓ CN VIII closes the eyelids (7- imagine a hook), while CN III opens your
Nerve endings eyes (III – imagine columns that keep your eyes open)
↓
Mandibular/Maxillary/Ophthalmic Nerve CORNEAL REFLEX TESTING
↓ • Tell the patient, “I’m going to just touch your eyeballs very
Trigeminal/Semilunar/Gasserian ganglion lightly”
(Primary Neuron) • Instruct the patient to look at one side and a little up
↓ • With the use of cotton rolled to a fine point, touch the lateral
PONS – Trigeminal Nuclei side of the cornea of the adducted eye.
(Secondary Neuron) • Bring the cotton directly from the side to avoid entering the field
↓ of vision. That would cause a visually mediated flinch reflex, not
Mesencephalic nucleus a corneal blink reflex.
(proprioception)
↓ Clinical Interpretation
Main sensory nucleus of V in pontine and • Most normal individuals display a corneal reflex
medullary portion (touch) Trigeminal lemniscus • Exceptions are some aged and post-cataract surgery patients
↓ ↓ • If no response occurs, do not conclude that the V-VII arc is
Spinal nucleus (pain and temperature) THALAMUS nucleus interrupted until you have CHECKED FOR A CONTACT LENS
↓ ventralis posterior • Acute hemispheric lesions may abolish the corneal reflex on the
Trigeminal lemniscus ↓ contralateral side for hours or days as a deficit of the “shock”
↓ SOMESTHETIC CORTEX phenomenon.
THALAMUS – nucleus ventralis posterior postcentral gyrus,

54
REMEMBER: ↓
• The highly sensitive skin of the face and armpits contrasts with Decussate and turn rostrally in contralateral ventrolateral quadrant of

C2 C2
the horny skins of the palms and soles 3 spinal cord 3
• Hairy skin perceives tickling and touch better than glabrous skin 4 (decussates at the SPINAL CORD) 4
5 5
• The forehead is the most sensitive area for temperature 6 ↓ 6
discrimination Ascend in the ventral and lateral funiculi to form the lateral
7
8
7
8
• Cold skin loses sensitivity so you should ensure a warm skin spinothalamic (also called spinal lemniscus)
T1 T1
2 2
before testing the patient ↓ 3
rd 3
• Corneomandibular reflex – consist of a twitch of a lower jaw to 3 order neuron at the sensory nucleus of the thalamus
4 4
5 5
the opposite side, along with the eyelid closure, after stimulation (VPLN-ventroposterolateral nucleus)
A B
of the cornea. It appears contralaterally after a hemispheric ↓
lesion and bilaterally in coma General thalamus radiations through the internal capsule and the
• Glabellar blink reflex – consists of a bilateral contraction of the corona radiata
orbicularis oculi muscles in response to percussion of the ↓
glabella with the fingertip or percussion hammer, or to electrical Ipsilateral somatosensory cortex in the POSTCENTRAL GYRUS of the
C2
PARIETAL LOBE
stimulation of the supraorbital branch of CN V. Various lesions of 3
the efferent and afferent arc reduce the blink response. It 4
5 6
disappears on the side of an acute hemiplegia and disappears REMEMBER: 7
8
bilaterally in coma • Decussation takes place, so the pain perceived by the right side of
3
2 T1
the body will be interpreted by the left brain and vice versa.
4
5
Hysterical Sensory Loss vs Organic Sensory Loss • Lamination occurs in the tract. That is, the first fibers entering the
Hysterical Sensory Loss Organic Sensory Loss tract (representing sacral levels) Care the most lateral and dorsal.
Loss of facial sensation Loss of facial sensation from FIGURE 2-9.Fibers entering dislocations
Dermatomal at successively higher
caused by levels ofare
development the more medial
limbs. Notice thatand
C2 is the
trigeminal nerve lesions ventral in position.
first of the cervical dermatomes. Cranial nerve V innervates facial sensation. See Fig. 2-10.
INCLUDES the angle of the SPARES the angle of the

mandible mandible
C2
Lose sensation according to the Lose sensation according to the
patient’s mental image of body wiring diagram of the nervous C3
parts system C7 C6 C5
T2
C4
C5 C6 C7
C8 T1 C8
T1 3
4
5
SOMATOSENSORY FUNCTION OF THE BODY AND EXTREMITIES 6
7
8
2 General Rules: 9
10
1. For screening purposes, you may test only the dorsum of the 11
12
hands and feet L2
L1
L3 L2
L5 L5
2. To explore suspected sensory loss test each area as carefully as L5 S1 S2 S3 S2 S1 L5
L4 L3 L3 L4
required by the history S4 S5 Coc.

Important dermatomal levels (MEMORIZE)
C2
• Trigeminal nerve to interaural line where it abuts on C2 (Note:
There’s no C1) C3
C4 C4
• C3-C4: over the “cape area” of shoulders C7
C8
C6
T1
C5
T2 T2
C5
T2
C6
T1
C7
C8
• C5, C6, C7, C8 and T1: arms 3

4
5
• T4: nipple 6
7
• T10: umbilical area 8
9
10
• L5: medial side of the foot (big toe) 11
12
• S1: lateral side of the foot (small toe) S1 L2 L1 L2 S1
L3 L3
L5 L4 S3 S3 L4 L5
TESTING TOUCH
FIGURE 2-10. Sensory innervation areas by dermatomes.The numbers correspond to the spinal cord
• Same as CN V exam, wisp of cotton would do level of the dermatomes. C = cervical; L = lumbar; S = sacral; T = thoracic. (Reproduced with permis-
Light touch is a combination of the PAIN-TEMPERATURE and the
• Always compare right and left sides sion from Haymaker W,Woodhall B. Peripheral Nerve Injuries, 2nd ed.Philadelphia,W.B.Saunders,1962.)
PROPRIOCEPTIVE PATHWAYS. Therefore, hemisection of the spinal
cord would not result in loss of light touch sensation.
TESTING TEMPERATURE AND PAIN
• Same principles as CN V examination TESTING POSITION SENSE BY DIGITAL MOVEMENT
• When testing position sense, use digits three and four because
TYPES OF PAIN AXONS: they have the smallest cortical representation. Thus, even if the
1. Small myelinated A fibers (IA gamma fibers) – mediate sharp, brain sustains just a minor injury/damage, any neurologic deficit
bright localized, “fast pain” and also cold sensations; ascend can be detected at once (the 3rd and 4th digits are easily
through the lateral spinothalamic pain and temperature affected).In contrast, the 1st, 2nd and 5th digits of the hands and
pathways. feet have the richest innervations and the largest cortical
2. Unmyelinated C fibers – mediate an afterglow of dull, diffuse, representation. Thus, any neurologic deficit involving these digits
stinging and burning pain, and also warm sensation; ascend may only be detected when the brain sustains a major
through diffuse polysynaptic pathway, have strong connections injury/damage.
with reticular formation and ultimately the limbic system • Use your non-dominant hand to support the part to be tested
(just proximal to the joint that you are testing)
NOTE: Touch impulses ascend to the somesthetic content by 2 spinal
• Use your dominant hand to grasp the digit by its side and wiggle
pathways: the dorsal column and the ventral column. So if you want
it up and down, stopping in one direction or the other
to eliminate only the pain and temperature sensation without
RANDOMLY.
eliminating touch, you can transect the VENTROLATERAL column.
• Demonstrate the “up” and “down” position.
Neurosurgeons make such cut in the ventrolateral column of the
• Have the patient close his eyes.
spinal cord to relieve patient of intractable pain, a procedure known
• Instruct the patient to report whether the finger is up or down.
as cordotomy.
Test several digits, several times on both hands and feet. Do not

alter your tone of voice.
PAIN AND TEMPERATURE PATHWAY
• The patient must make NO errors and answer PROMPTLY to be
Pain/temperature receptor considered normal
↓ • If you are not sure, add a NEUTRAL (straight) position to
Primary neuron on dorsal root ganglion decrease the probability of chance.
↓
Synapse with secondary neuron at or near level of entrance TESTING POSITION/PROPRIOCEPTION THROUGH THE ROMBERG
TEST
• Proprioception is the sense of movement of position of • NOTE: Aging increases the threshold to vibration and reduces
musculoskeletal tension provided by the deep mechanical the sensitivity, particularly in the feet.
receptors located in muscles, joints, connective tissues, or
vestibular system. VIBRATIONS, POSITION AND PRESSURE PATHWAY
• Compare the degree of swaying when the patient is standing
with heels together, eyes open versus eyes closed. Receptor
• If the patient is hysterical, ask him to stand up, eyes open and do ↓
the finger-nose test for cerebellar function. While performing Primary neuron in dorsal root ganglion
the test, ask him to close his eyes. The finger-to-nose test will ↓
serve as a distraction (to divert the patient’s attention and Enters spinal cord and ascends in the IPSILATERAL dorsal column
reduce the swaying especially among malingerers). ↓
Synapse in nuclei gracilis (leg) and nuclei cuneatus (arm) and
Sensory Cerebellar decussates at that level (Decussation at the CERVICO-MEDULLARY
Clinical Testing junction)
Dystaxia dystaxia
Loss of vibration and position sense + ↓
Areflexia + Axon turns rostrally in CONTRALATERAL half of brainstem tegmentum
Nystagmus + ↓
Hypotonia + + Ascend as medial lemniscus
Dystaxia (much worse with eyes + ↓
rd
closed) 3 order neuron at sensory nucleus of thalamus (VPLN)
↓
Overshooting +
Ipsilateral somatosensory cortex in the POSTCENTRAL CYRUS of the

PARIETAL LOBE

NOTES:
PROPRIOCEPTION PATHWAY
• Gnosia – knowing

Receptors: encapsulated organs • Association area – parietal lobe behind the postcentral gyrus
such as Meissner’s, Pacinian, etc • Posterior Parasylvian Area – confluence of somatosensory,
↓ occipital, and auditory association area
Peripheral nerve • Statognosia – awareness of posture
↓ • Stereognosia – sense of form
Medial division of the dorsal root to the spinal cord o To test: place various objects (keys, paper clip) and ask the
↓ patient to identify.
Dorsal funiculus where they bifurcate into ascending and descending o If the lesion is within the Association Area, add the prefix “a-”
limbs (e.g.astatognosia, astereognosia). If the lesion is between the
receptor to the primary sensory cortex, add suffix “–
Reflex pathway anesthesia” instead of “–gnosia” (e.g. stanesthesia – loss of
position sense due to spinal cord lesion)
Lamination occurs in the dorsal funiculus (the • Topognosia – localization of skin stimulus
fibers entering at the lowest level assume a position • Graphognosia – sense of numbers or letters drawn on skin
adjacent to the dorsomedial septum). As more and • Nosognosia – awareness of disease
more fibers enter, they take up a more lateral • Anosognosia –described by Babinski as left hemiplegia and left-
position sided sensory loss yet the patient is unaware of his neurologic
↓ deficit; usually on the left side after right parietal lobe lesions
At the midthoracic region, a septum begins to appear in the dorsal o If you ask whether the patient can move his left arm, the
funiculus: DORSAL INTERMEDIATE SEPTUM, which seperates the patient will say “yes” even though it is completely hemiplegic.
dorsal funiculus into: o Lay your own left arm across the patient’s waist. Ask the
patient to reach over and pick up his own left hand. He will
feel across his abdomen, grasp your hand and hold it
Fasciculus gracilis Fasiculus cuneatus triumphantly aloft, never realizing the error.
(medial group of fibers; (lateral group of fibers) • Auditory Agnosia – inability to understand meaning of sounds
“G for Gitna”) • Autopagnosia – inability to locate, recognize, and orient one’s
↓ ↓ body parts
Nucleus gracilis in medulla Nucleus cuneatus in medulla o To test: elevate the patient’s arm and ask him to do the same
↓ on the other
Fibers arising from the nuclei decussate across the midline in a • Finger agnosia
sweeping arc: INTERNAL ARCUATE FIBERS o To test: Number fingers 1 to 5 (thumb=1). Then, with the
↓ patient’s eyes closed, randomly touch digits on the right or left
Ascend in a tract called MEDIAL LEMNISCUS hand and ask the patient to identify the finger.
↓ • Right-to-left disorientation
VPLN thalamus o To test: “Touch your right hand to your left ear”
Fibers ascend via the internal capsule and corona, radiate to the o Both finger agnosia and right-to-left disorientation are
cortex of the POSTCENTRAL GYRUS common in LEFT PARIETAL LOBE LESIONS.
↓ o GERSTMANN’S SYNDROME – lesion of the posterior
Association areas parasylvian area; clinically presents with bilateral finger
agnosia and right-to-left disorientation
• Tactile Inattention
TESTING VIBRATION SENSE (PALLANESTHESIA) o To test: touch both cheeks, face, dorsum of hand and feet and
• Hold the shaft of the tuning fork and strike it against the ulnar ask whether the patient felt the stimuli
side of your palm o RIGHT PARIETAL LOBE LESIONS cause inability to attend to
• Apply the free end of the vibration shaft to the patient’s stimuli on the left
fingernail or toenail while pressing your finger against the pad of • Inattention to one entire half of space
the patient’s digit (so you can both feel the vibration) o To test: ask the patient to draw a figure bisecting (intersecting
“Naramdaman niyo po ba? Sabihin niyo po kung tumigil na, at two points) a horizontal line
ha.” o Both Inattention and Anosognosia are common in RIGHT
• If the patient cannot feel the vibration as long as you can, apply PARIETAL LOBE LESIONS.
it to the bony prominences (wrist, malleoli, elbow, knee) • Prosopagnosia – inability to recognize faces, either in person or
• Reliability testing: Occasionally apply the tuning fork when it is by photos (inferomedial temporooccipital region defect
not vibrating OR strike the fork but squeeze the tines after
striking to stop it vibrating and then apply the fork to the
patient.

EXAMINATION OF THE SOMATIC MOTOR SYSTEM MOTOR STRENGTH TESTING

• General Principle: Ask the patient to resist while you counteract
Inspection the primary action of the muscle being tested
• Check for atrophy, hypertrophy of muscles, asymmetries, joint • Follow a rostro-caudal system:
malalignments, fasciculations, tremors, and involuntary • Neck Extensors: (extensors stronger than ex’s arm strength)
movements. Do this from head to toe, left and right • Shoulder Girdle Muscles
• Observe the patient’s station, the steadiness, and verticality of • Upper Arm: Elbow extension and flexion
the standing posture and the patient’s somatotype (body build) • Forearm: Wrist flexion and extension
• Test gait by having the patient walk freely across the room, look • Finger muscles: abduction-adduction, extension, flexion (grip –
for unsteadiness, a broad-based gait, and lack of arm swinging. strongest grip in partial dorsiflexion)
Ask patient to walk on their toes, heels, and in tandem (heel-to- • Abdomen: umbilical migration test
toe along a straight line) • Back muscles
• Hip Girdle: hip flexion, thigh abduction and adduction, hip
Fasciculations vs Fibrillation extension
• Fasciculations – contraction of muscle fascicles, may indicate a • Thigh Muscles: knee extensors, flexors (hamstrings)
hyperexcitable state of the cell membrane of the lower motor • Ankle and Toe: plantar flexion > ex’s arm strength
neurons
• Fibrillation – spontaneous contraction of individual denervated Muscles Action tested Roots
muscle fibers, indicate hyperexcitability of the muscle fibers Deltoid Abduction and elevation of arm C5, C6
following denervation up to 90°
Pectoralis Major Adduction of extended arm C5, C6
Palpation
Biceps brachii Flexion of supinated forearm C5, C6
• Check muscle tone, spasticity, rigidity
Triceps Extension of forearm C6, C7, C8
Spasticity – initial catch or resistance and then yielding when the
Brachioradialis Flexion of semi-pronated forearm C6
examiner quickly manipulates the patient’s resting extremity
(clasp-knife spasticity) Extensor carpi Wrist extension C7, C8
Rigidity – increased muscular resistance felt THROUGHOUT the ulnaris
entire range of movement when the examiner slowly manipulates Flexor carpi Wrist flexion C6, C7
a patient’s resting joint (lead-pipe rigidity) radialis
Opponens pollicis Opposition of the thumb against C8, T1
Percussion th
5 finger
• Percussion irritability of the muscle Interossei Abduction and adduction of C8, T1
• Myoedema: hump at percussion site, seen in myxedema and fingers
uremia Iliopsoas Hip flexion L1, L2
• Myotonia: sign of myopathy, “sustained after contraction”/ Gluteus maximus Hip extension L5, S1
delayed relaxation Adductor longus, Adduction of thigh L2, L3
magnus, brevis
DEFINITION OF TERMS Gluteus medius Abduction of thigh L4, L5
• Myokymia: Abnormal discharge of muscle groups for prolonged Quadriceps Knee extension L3, L4
periods producing a rippling worm like action of the muscle femoris
• Cramps: Sustained muscle contractions lasting seconds to Biceps femoris, Knee flexion L5, S1, S2
minutes; EMG shows 200-300 impulses/sec. semitendinosus,
• Wallerian Degeneration: Dissolution of the axon and myelin semimembranosus (Hamstring Muscles)
sheath upon the death of the neuronal perikaryon. Tibialis anterior Dorsiflexion of foot L4, L5
• Fibrillation: random, spontaneous contraction of DENERVATED Gastrocnemius, Plantar flexion of foot S1, S2
muscle (Cannon’s law of hypersensitivity of denervated soleus
structures); Seen on oscilloscope only.

• Fasciculation: Contractions of muscle fascicles detected by Muscle Grading
clinical inspection or EMG waves indicating hyperexcitable state 0 – no muslce twitch, denervated
of the cell membranes of the LMN. 1 – with muscle twitch
• Clonus: To-and-fro rhythmic oscillation (5-8 cycles/sec) elicited 2 – with movement, but not against gravity (side-to-side only)
by a quick stretch after interruption of UMNs. 3 – with movement, against gravity but no resistance
• Abortive Clonus: 4 – can move against gravity, moderate resistance
5 – can move against gravity, maximum resistance
Voluntary contraction
Muscle at rest
Slight contraction Strong contraction MOTOR PATHWAYS

Calibration 100
microvolts Corticospinal Tract
10 milliseconds
• Also called Pyramidal tract
Normal
• Concerned primarily with skilled movements of distal muscles of
limbs
No electrical activity Normal single
motor unit
All motor units of the muscle
discharge, filling the
• Transmitters: glutamate and GABA
oscilloscope screen.
Fibrillations
Neuropathic
(LMN)
disease
Fasciculation Giant polyphasic The total number of the units is

motor unit decreased, but the amplitude
The muscle at rest shows is normal or greater than
spontaneous electrical activity; normal because of the giant
fibrillations and fasciculations. polyphasic units.
(1) (2)
Myopathic
disease No electrical activity The individual motor Low amplitude motor units with
units are of brief duration increased number of motor unit
and low amplitude. (1) discharges per streng th of
Some are miniature poly- contraction, and less crowding
phasic units. (2) of units. (less “interference”).

FIGURE 7-21. Electromyographic (oscilloscopic) tracings of the electrical activity recorded from
muscle. (Courtesy Dr. Mark Dyken.)

axon of the motoneuron contract, resulting in spontaneous fasciculations
(Fig. 7-21B). Some normal individuals who do not have neuronal disease
show benign fasciculations, particularly after exercise.
6. Wallerian degeneration and the EMG of denervation
Motor Cortex Fibers from the same areas that give rise to corticospinal
1/3 from 1˚ motor cortex (Area 4) tract form CORTICORUBRAL TRACT
1/3 from premotor regions (Area 6)
1/3 from parietal lobe (Area 3, 1,2) IPSILATERAL RED NUCLEUS in tegmemtum of
midbrain
Posterior limb of internal capsule
Middle crus of cerebri Gives rise to RUBROSPINAL TRACT fibers that

cross the midline in the ventral tegmental
Breaks up into bundles forming the
decussation
MEDULLARY PYRAMID

10% Don’t cross 90% Decussate Descend through lateral tegmentum of pons
the medulla in the lower levels of the and medulla
250 medulla
LATERAL CORTICOSPINAL TRACT Dyken P. Extraocular myotonia in families with dystrophia myotonica. Neurolo
Fibers synapse at all cord levels in the lateral
VENTRAL / ANT. 1966;16:738–740.
aspect of Laminae V- VII (and thus overlap part
CORTICOSPINAL Synapse on interneurons of Harper PS. Myotonic Dystrophy, of the corticospinal tract’s termination)
3rd ed. Philadelphia, W.B. Saunders, 2001.
TRACT laminae IV - VIII Jones HR, DeVivo DC, Darras BT. Neuromuscular Disorders of Infancy, Childhood, and Adol

cence. A Clinicians
Approach. Philadelphia: Butterworth-Heinemann, 2002.
Interneurons synapse with α & γ Corticobulbar Tract
Karpati G, Hilton-Jones D, Griggs RC. Disorders of Voluntary Muscle. New York, Cambrid
At their levels of motor neurons in lamina IX University Press, 2001.
termination, fibers
Katirji B, Kaminski HJ, Preston DC, et al, eds. Neuromuscular Disorders in Clinical Pract
Area 4 & 6 of Cortex
decussate via Boston, Butterworth-Heinemann, 2002.
VENTRAL WHITE Motor neurons innervate muscles
Koppel HP, Thompson WAL, Peripheral Entrapment Neuropathies. Baltimore, Williams
Axons accompany corticospinal tract

COMMISSURE in distal parts of extremities Wilkins, 1987.

Sunderland S, Nerves and NerveTakes a divergent route at MIDBRAIN
Injuries. 2nd ed. London, Churchill Livingston, 1978.

Corticoreticular and Reticulospinal Tracts
Fibers terminate in the BRAINSTEM, where they influence
MOTOR CORTEX
V. EXAMINATION OF MUSCLE STRETCH REFLEXES
MOTOR NUCLEI of CN III – XII (except VII) and SENSORY RELAY
NEURONS
Synapse on reticular formation (BILATERALLY)
A. Physiology Muscle Stretch Reflex
of the muscle stretch reflexes
PONTINE (Medial) MEDULLARY (Lateral) • The muscle spindles are receptors that are sensitive to stretch.
1. Evolution has perfected
They consist of muscle
small fibers
bags of asmuscle
contractile
fibers engines. Whatever
interspersed along the stim
Reticulospinal Tract Reticulospinal Tract
ulus—a nerve the impulse,
muscles, chemical agent,
but are also electricity,
connected to the or mechanical
tendons. deformatio
However,
such as by percussion—the
muscle fibers have fiber responds
this intrinsic by contracting.
property called percussion
In the brainstem: passes Passes to all cord levels 2. Stretch of the irritability wherein causes
entire muscle the muscles also contract ofupon
reflex contraction direct muscle,
the entire
ventral to medial percussion of the muscle. That is why in order to test for reflex
in the lateral funiculus contrasted to percussion irritability of individual muscle fibers.The stretch-sensiti
longitudinal fasciculus irritability, which involves the muscle spindles, we hit the
just anterior to the receptors for the muscle stretch reflexes (MSRs) are the muscle spindles, whi
tendon and NOT the muscle itself
rubrospinal tract consist of small bags of small muscle fibers (Lance and McLeod, 1981).
• When a muscle is denervated, the deep tendon reflexes (DTRs)
In the spinal cord: passes
are abolished because DTRs involve the nerves, while percussion
ventral fasciculus
Synapse in laminae VII & Mnemonic: Remember irritability is retained and sometimes even enhanced because as
muscle spindles as “muscles within a muscle” (Fig. 7-4).
IX we said earlier, this property is intrinsic to the muscle
Synapse in laminae VII
&VIII Dorsal root
Ventral root

Corticotectal Tract Muscle spindle A B
• Has a greater influence on reflexive rather than voluntary eye Perimysium C
movement
Muscle fiber

Cortex of Occipital and Parietal lobes

FIGURE 7-4. Muscle spindle innervation.The muscle spindles are tiny bags of specialized mus
Fibers project to upper parts of brainstem to influence MUSCLE STRETCH REFLEX PATHWAY
fibers, located in the equatorial plane of the muscle.They have afferent (A) and efferent (B) axo
The regular
muscle fibers receive only efferent axons (C).
EOM activity
REMEMBER: We tap the tendon and not the muscle itself because of
percussion irritability. Percussion irritability is the intrinsic property
These nuclei project through the PONTINE 3. Effects of of stretch on the
the muscle muscle spindles
to contract when percussed. This action does not
RETICULAR FORMATION and MEDIAL involve the nerves, unlike the deep tendon reflexes.
a. The muscle fibers of the spindle originate and insert into the perimysial co
LONGITUDINAL FASCICULUS nective tissue, which ultimately is continuous with the tendons. If the jo
shownUsing the neurohammer
in Fig. 7-4 extends, the tendon pulls on the perimysium and stretches t
• Swing, don’t peck
muscle spindles. Flexion of the joint causes relaxation of the muscle spindle
Synapse on Nuclei of II, IV, and VI • Wrist action – loose, double pivot action at the wrist and fingers
b. To reset themselves to remain sensitive to stretch throughout the entire ran

of muscle length, the muscle spindles must readjust their length whenever t
The Reflexes
Corticorubral and Rubrospinal tracts muscle length changes.
• Represent an indirect route from cerebral cortex to spinal cord c. Flexion of a part momentarily relaxes the spindle tension. The muscle fibers
the spindles respond by contracting slightly to maintain their original tensio
d. During extension of the part, the spindles adjust to maintain their origin
tension by lengthening slightly.
4. Innervation of the muscle spindles
a. Each muscle spindle has its own afferent and efferent axons that maintain
constant tension; see afferent axon A and efferent axon B in Fig. 7-4. T

Tap on muslce tendon o Ask the patient to very slightly tense the muscle being
tested in order to counterbalance the slight pressure that
Stretching of extrafusal fibers the examiner applies against the action of the muscle
• Absent MSR? Consider these first:
Stretching of intrafusal fibers o Neural shock / Spinal shock
o Difficult to reach tendon
o LMN problem: poliomyelitis (ant. Horn of afferent fibers)
Stretching stimulates group IA fibers
(primarily afferents)
o Efferent axon: motor neuropathy
o Neuromyal junction: Myasthenia gravis, botulism,
Lambert-Eaton Syndrome
Impulse travels via dorsal root fibers
o Effector (Muscle): Myopathy

Fibers enter posterolateral fasciculus
(Lissauer’s tract)
Scoring
0 – areflexia 0 Areflexia
± - hyporeflexia 1 Hyporeflexia
Synapse with interneurons 1 to 3 – average 2 Normal
3+ to 4+ - hyperreflexia 3 Hypereflexia (4 Clonus)
Synapse with γ-motor neurons
in lamina IV
Superficial Reflexes
• Altered by upper motor neuron lesions
Efferent fibers exit spinal cord as • Corneal reflex, gag reflex, abdominal skin-muscle reflex, anal
ventral root fibers
wink and bulbocavernosus reflexes, and the plantar reflex

Efferent impulses stimulate muscle Plantar Reflex
spindles
• Place the patient supine with limbs relaxed and symmetrically
arranged
Muscle contraction • Have the knees straight or slightly flexed
• Hold the patient’s ankle with a hand and keep the foot in place
Jaw • With the pointed end of your neurohammer, stroke the lateral
• With the patient’s jaw sagging open, examiner rests a finger side of the sole, starting from the heel, and then turning medially
across the jaw and strikes it towards the base of the great toe
• The jaw closes in response • Normal response: if the large toe flexes
Biceps • UMN lesion: if the large toe extends and there is fanning of the
• Ask patient to sit, have the arm partially bent across her thigh toes (Babinski sign)
• Examiner applies slight tension with his thumb on the patient’s • 3 variables involved: length (the plantar stroke stops short of
biceps tendon. Strike the thumbnail the base of the toes), pressure, and velocity
Triceps Reflex arc of the Babinski Sign
• Dangle the patient’s forearm over your hand • Reflexogenous zone – the arc from which a reflex can be elicited
• Strike the patient’s elbow a few inches above the olecranon is restricted to the S1 dermatome
process • Since the skin contains the receptor (nerve endings), the plantar
Almost any stimulus of any part of the skin caudal to the level of the lesion results
Brachioradialis in toe extension, with a strong flexor synergy or flexor spasms.
reflex is a superficial reflex
3. Additional maneuvers for eliciting superficial toe reflexes
• Cradle the patient’s forearm in one hand • The afferent nerve
a. Many is
otherthe tibial maneuvers
eponymic nerve, besides
a branch of elicit
Babinski’s the toesciatic
movement from
• With the examiner’s thumb on the lower end of the radius, strike nerve, if the tibial nerve
superficial was
stimuli (Ghoshcut,
andboth
Pradhan,the
1998;afferent and These
van Gijn, 1996b). the maneu-
vers, in particular those outside the S1 dermatome, generally are less effective
the thumbnail efferent parts of the arc would be interrupted
than stimuli within the S1 dermatome. In normal persons, these stimuli usu-
• Watch for elbow and finger flexion • Mediating the reflex are the L4-S2 levels of the spinal cord
ally fail to elicit toe flexion, but after UMN lesions, they may elicit toe exten-
sion, just as with Babinski’s maneuver (Fig. 7-33). Ghosh and Pradhan (1998)
Finger Flexion • Terminal summation found thatis involved
the maneuver because the 7-34G)
of Gonda (Fig. movement
elicits toeof the more
extensions
Tromner’s Method object from the readily
heel than to planter
the instep requires
stimulation in childrena with
finite amount
spastic of
cerebral palsy.
• Examiner supports the patient’s relaxed finger by holding on time
b. The multitude of eponyms implies that the maneuvers represent different phe-
nomena, but physiologically, as stimuli, the maneuvers betray a unifying sim-
to the sides and briskly flips the patient’s distal phalanx • Spatial summation is Do
plicity. also involved
the maneuvers because
shown the
in Fig. 7-34 on moving
yourself andobject
a partner, paying
upward, as if “trying to flip a handful of water high into the attention to the stimulus properties of each maneuver.
stimulated successively more receptors
air”
• Patient’s fingers and thumbs flex in response Other ways to elicit an Extensor Toe Reflex
Hoffman’s Method Descriptive Name Eponym Maneuver
• With a thumb, the examiner flexes the distal phalanx of the A. Plantar toe Babinski Move an object along
reflex the lateral aspect of
patient’s finger while pressing up with the index finger the sole.
• The examiner then releases the phalanx suddenly, allowing it

to flip up sharply B. None Chaddock Move an object along
• The fingers and thumb flex in response the lateral side of the
foot.
Quadriceps Femoris
• patient sits, the examiner strikes the patellar tendon
• To “enhance” the reflex, the patient may lock his hands and pull C. Achilles-toe
reflex
Schaeffer Squeeze hard on the
Achilles tendon.
them apart hard while the examiner strikes the tendon
(Jendrassik maneuver)
Triceps Surae D. Shin-toe Oppenheim Press your knuckles
reflex on the patient’s shin
• patient relaxes the leg, examiner dorsiflexes the foot and then and move them down.
strikes the Achilles’ tendon

• Watch for calf muscle contraction and plantarflexion E. Calf-toe Gordon Squeeze the calf
reflex muscles momentarily.
Toe flexion (Rossolimo’s Sign)
• Similar to Tromner’s but of the toe

F. Pinprick- Bing Make multiple light
WHAT TO DO when there’s no reflex is elicited toe reflex pinpricks on the
dorsolateral surface of
• Strike a crisper blow the foot.
• Change the mechanical tension on the muscle

o Flex or extend the joint slightly to alter tendon tension G. Toe-pull Gonda, Pull the fourth toe
o Compress the tendon slightly more (or less) with your reflex Stransky outward and
downward for a brief
thumb time and release
suddenly.

• Reinforcement
o Jendrassik maneuver – the voluntary upper motor The Abdominal and Cremastric Reflexes
FIGURE 7-34. Methods for eliciting the extensor toe sign.
neuron of the arm muscles “overflows” to “increase the • The patient may sit or recline
excitability of the LMN pool of the lower extremities”

• Use a broken tongue blade, key, or butt of a reflex hammer

• The umbilicus twitches toward the quadrant stimulated in
response to stimulus on the abdomen
• The ipsilateral testicle elevates in response to the stimulation of
the inner thigh
• These two reflexes cannot be elicited after UMN lesions

Clinical Variations in the Pyramidal (UMN) Syndrome

1) Standard hemiplegic distribution
a) Unilateral interruption of the pyramidal tract at any level from
the cortex to the caudal level of the pons
b) Weakness in the contralateral side, from the lower facial
muscles down
2) Double hemiplegia

a) Lesion interrupts both pyramidal tracts rostral to the medulla
Basal Ganglia
b) Lower part of the face affected bilaterally & the 4 extremities
Extrapyramidal System
3) Pseudobulbar palsy
1. caudate nucleus
a) Bilateral interruption of the corticobulbar component of the
2. putamen
pyramidal tract, at the cerebral or brainstem levels
3. globus pallidus interna
b) Causes weakness of the oropharyngeal muscles leading to
4. globus pallidus externa
dysphagia, dysarthria, spastic dysphonia
5. subthalamic nucleus
c) Patient is emotionally labile – exaggerated smiling and crying
6. substantia nigra
responses

4) Spastic diplegia
Remember:
a) Bilateral pre- or perinatal cerebral lesions – bilateral
1 + 2 = striatum
pyramidal syndrome
1 + 2 + 3 + 4 = corpus striatum
b) patients often display involuntary movements such as
2 + 3 + 4 = lentiform nucleus
athetosis

5) Locked-in syndrome
a) Bilateral interruption of the pyramidal tracts in the basis
pontis or cerebral peduncles – UMN paralysis of all volitional
movements except vertical eye movements
6) Quadriplegia (tetraplegia)
a) Bilateral interruption of the pyramidal tracts in the caudal
medulla or cervical region
b) Causes paralysis of the volitional movements of the trunk and
all four extemities, with loss of volitional bladder and bowel
control, and volitional control of breathing
7) Paraplegia
a) Bilateral interruption of the pyramidal tracts caudal to the
cervical region
b) Spares the arms, but causes UMN paralysis of the legs, with
loss of bladder and bowel control • The basal ganglia is involved in the selection, triggering, and
8) Monoplegia generation of basic motor programs assembled within the CNS.
a) Small lesion of the motor cortex or internal capsule, where • Involved in the accuracy of movement by inhibiting
the pyramidal fibers have a discrete somatotropic arrangment inappropriate behavior and reinforcing relevant behavior
b) May cause contralateral weakness of one arm or leg
88 • Has NO connection with the brainstem
c) Interruption on one side of the thoracic spinal cord causes
monoplegia of the ipsilateral leg Basal Ganglia Pathway

Paralysis and Sensory Deficits right after Spinal Cord Transection Motor cortex

Midline
If lesion is at the medullocervical junction or at segments C1-C3
• Results in complete apnea, complete quadriplegia, complete
anesthesia caudal to the lesion Pyramidal tract
• paient dies of hypoxia unless given artificial respiration
Striatum
During the stage of spinal shock Thalamus
Pallidum
• patient loses all somatomotor and most visceromotor responses
caudal to the level of the lesion
• Flaccid paralysis of somatic muscles and sphincters, and flaccid
(atonic) bladder and bowel paralysis, with incontinence Subthalamic nucleus
• All superficial and deep tendon reflexes and most autonomic Substantia nigra Cerebellum
reflexes are abolished

UMN signs gradually appear
• Increased MSR’s
• Spasticity
• Extensor toe signs Corticobulbar tract

“The spinal cord, when separated from the brain, can reflexly twitch Corticospinal tract

some muscles, sweat, and ejaculate, and reflexly eliminate urine MOVEMENT DISORDERS
FIGURE 2-32. Diagram for conceptualizing the maze of basal motor circuits that feedback through
and feces, but the isolated spinal cord cannot breath or move into the ipsilateral cerebral motor cortex. The decussation of the pyramidal tract then
the thalamus
muscles voluntarity.” projects theExtrapyramidal Diseases
influence of the basal motor nuclei modulation of the motor cortex to the contralat-
eral side. • Effects can be regarded as negative (primary functional deficit)
or positive (secondary effect due to release or disinhibition in
undamaged regions)
• Most of these appear while testing for other motor signs
may be superimposed on muscles at rest or superimposed on voluntary actions.
Almost all abnormal involuntaryMEDRANO NEURO NOTES
movements caused by lesions in the11 basal motor
nuclei disappear during sleep.
5. Review the summary of the clinical syndromes of motor systems lesions in
Table 2-14.
3 CEREBELLAR PEDUNCLES
Negative Features 1. Superior Cerebellar Peduncle (connects to midbrain)
1. Bradykinesia o Brachium conjunctivum (major efferent cerebellar pathway,
• Loss or slowness of voluntary movements projects towards the red nucleus and thalamus)
• Major feature of Parkinsonism o Ventral Spinocerebellar Tract (projects towards anterior
o Reduced facial expression (mask-like) lobe)
o Reduced blinking 2. Middle Cerebellar Peduncle (connects to pons)
o Reduced adjustments of posture when seated o Brachium pontis
• kinesia paradoxica - when agitated, the patient will move o Largest, simplest, most lateral bulk of pons; last to develop
swiftly o Corticopontocerebellar fibers (projects towards the
2. Postural Disturbance posterior lobe)
• Most commonly seen in Parkinson’s Disease 3. Inferior Cerebellar Peduncle (connects to medulla)
• Fixation of limbs and trunk associated with failure to make o Medullocerebellar, Olivocerebellar, Cerebellovestibular
quick postural or “righting” adjustments to correct imbalance Pathways
o Restiform and juxtarestiform Bodies
Positive Features
I. Involuntary Movements CEREBELLAR PATHWAY
A. Movements that the standard normal person can start or stop
at the person’s will and/or the examiner’s command Cerebellar Circuit: Cortico-ponto*-cerebello-dentato*-rubro-
B. Tremors thalamo-cortico-bulbo-spinal circuit
1. Rhythmic; more or less regular oscillation of a body part * - points of decussation
2. 4 Basic Types:
i. Resting – tremors while body part (e.g. hand) is at rest Cerebellar hemispheres coordinate volitional movements on the
ii. Ataxic/Intentional – while the body part is making ipsilateral side of the body because of double decussation (pons to
voluntary movements cerebellum and dentate nucleus to red nucleus)
iii. Postural – while the body part is sustaining volitional
posture Motor Cortex
iv. Terminal/Endpoint – tremor increases as the body part (precentral gyrus, frontal lobe)
reaches a certain endpoint (e.g. finger-to-nose) ↓
C. Chorea Thalamus: nucleus ventralis lateralis
1. Irregular, repetitive, jerking movements ↓
2. Resembles the “fidgets” Decussates at the red nucleus of mesencephalon
D. Athetosis ↓
1. Irregular, repetitive, writhing movements Rostral cerebellar peduncle (pons)
2. Slow movements ↓
E. Dystonia Middle cerebellar peduncle (pons)
1. Slow, sustained abnormal movements ↓
2. Alternating contraction and relaxation of agonists and Dentate nucleus at the posterior part of the cerebellum
antagonists ↓
F. Ballismus Purkinje cell of cerebellum
1. Explosive, violent movement ↓
2. Hemiballismus – ballismus of ½ of the body Middle cerebellar peduncle where it decussates at the basis pontis
↓
II. Rigidity Ascend to thalamus: nucleus ventralis lateralis
A. Lead Pipe Rigidity – same degree of “resistance” is present ↓
throughout full range of movement Motor cortex: frontal lobe
B. Cogwheel Rigidity – tremor is superimposed upon rigidity (click- ↓
click) Pyramidal tract (motor pathways)

PARKINSON’S DISEASE
CEREBELLAR EXAMINATION
I. Stand with feet together
• Progressive disorder associated with loss of dopaminergic
A. Tests stance dystaxia
neurons in the substantia nigra
II. Tandem walking
• Presents a quatrain of basic motor signs:
A. Tests gait dystaxia
o Resting tremor
B. Ask the patient to walk along a straight line, placing the heel
o Cogwheel rigidity
of one foot directly in front of the toe of the other
o Overall bradycardia
III. Finger-to-nose Test
o Akathisia (abrupt, restless shifts of position)
A. Tests arm dystaxia

B. Ask the patient to place his index finger on the tip of us
nose, then ask hum to move it alternately from your finger
to nose
CEREBELLUM
C. Distinguishing postural tremor from intentional tremor
1. Postural Tremor – ask the patient to extend arms in
• Coordinates willful muscular contractions (volitional front, incoordination in maintaining this posture is
movement) called postural tremor
• Comatose or paralyzed patients cannot be tested for 2. Intentional Tremor – if the patient maintains the
cerebellar dysfunction because they cannot make willed posture but has tremor during the finger-to-nose
movements or maintain willed postures movement
D. Dysmetria – if the patientunder/overshoots target
IV. Rapid Alternating Movements (RAM) Tests
3 CEREBELLAR LOBES A. Test for arm dysdiadochokinesia (dystaxia-dysmetria)
• Flocculonodular Lobe (Archicerebellum) 1. Rapid Pronation-Supination Test -ask the patient to
o Vestibular system rapidly pronate and supinate his hands
o For posture, balance and eye movements 2. Thigh Slapping Test - ask the patient to rapidly slap his
• Anterior Lobe (Palleocerebellum) thigh with his palm and the back of his hand
o Spinocerebellar tracts (trunks and extremities) B. Observe differences in speed and listen to differences in
o For regulation of movement sound of slapping
• Posterior Lobe (Neocerebellum) V. Heel-to-Shin Test
o Corticopontocerebellar and olivocerebellar tracts A. Tests leg dystaxia


B. Ask the patient to place one heel on the opposite knee and
run the heel in a straight line down the shin
VI. Heel-tapping Test
A. Tests leg dystaxia
B. Ask the patient to tap the shin with the heel of the other
foot as rapidly as possible on one spot
C. Missing the target (dysmetria)
D. Tapping dysrthythmically (dysdiadochokinesia)
VII. Inspect patient for a hypotonia (floppy posture), nystagmus,
decomposition of movement (robot-like) and dysarthria
VIII. Overshooting Test
A. Ask the patient to stand, eyes closed, and extend arms in
front
B. Tell the patient that you are going to move their arms, and
that they should hold their arms still
C. Strike the back of the patient’s wrist to displace the arms
downward, and inspect for overshooting as the patient
attempts to return his arms to the original position
IX. Arm-pulling Test
A. The patient flexes his arm and you try to pull it
B. When you suddenly release your hold, observe if the
patient falls to check his arms flight
C. Use your left hand to pull the patient’s right arm, and vice
versa
D. Your other hand should be placed on the patient’s shoulder
(to prevent the patient’s arm from hitting his face)

4 major clinical signs of Cerebellar Syndrome
• Dystaxia – incoordination of volitional movements or
posture
• Dysarthria – slurred speech
• Nystagmus – oscillating eye movements
• Hypotonia – floppiness of extremities

CEREBELLAR SYNDROMES
• Cerebellar Hemisphere Lesion
§ Posterior lobe is affected
§ Dystaxial hypotonia of ipsilateral extremities
• Rostral Vermis Lesion
§ Anterior lobe is affected
§ Leg and trunk dystaxia, difficulty standing up
• Caudal Vermis Lesion
§ Flocculonodular and posterior lobes affected
§ Truncal dystaxia
• Pancerebellar Lesion
§ All lobes affected
§ All cerebellar signs affected
§ Usually observed in severely alcoholic patients


CRANIAL NERVE EXAMINATION • Use E printed on a card (rotate and have the patient point
in the direction of the bars) if patient is mentally retarded
CN I: OLFACTORY NERVE or is a small child
• Use coffee in an opaque container to avoid visual cues • Test the acuity of partially blind patients by having them
• Don’t use irritating substances (e.g. ammonia) because it count the number of fingers held up at various distances
irritates the mucus membrane and thus, you are testing CN • If visual loss is so severe that the patient cannot see the
98 fingers, find out if light perception remains
V and not CN I. 1. One set of axons comes from the ipsilateral, temporal half of the retina (Fig. 3-4).
• With the patient’s eyes closed, ask the patient to compare
one of the nostrils and hold the vial of coffee in front of the VISUAL PATHWAY
other nostril. Ask patient to identify the odor.
• For the second trial, compress opposite nostril but this
time, do not present the stimulus (done as safeguard for

the patient’s suggestibility and attentiveness)
• For the third time, present the stimulus to the untested
nostril.
A
A. Complete blindness, L eye

101
2. Do this experiment to demonstrate
B. Complete color vision in the central field:
bitemporal B
Olfactory mucosa A
a. Fixate on the same book in the middle of the row. Be sure to position yourself
hemianopia Optic nerve
↓
so that the row of books extends to the peripheral limit of your field.
B
C. at
i. While staring the book Ganglion cells
Complete nasal hemianopia,
directly in front of you, try to determine the color of C
CHAPTER 3
the most distant book that you can↓
L eye see in the periphery. Do not shift your vision. C Optic chiasm
Formation of Olfactory Nerve Filaments
ii. After trying to determine the
D. Complete R homonymous color, shift your gaze to look straight at the
D
drab, nearly book. How does the color of the ↓ book differ when seen by your central D Optic tract
field of visionhemianopia
on it imme-
as contrasted to its color when seen in the peripheral field?
d vivid. Perforate Cribriform Palate and attached dura
____________________________________________________________ Lateral geniculate body
E. Complete R superior E
Examination of Vision
↓
3. Now do this experiment concerningquadrantanopia
homonymous color vision: Geniculocalcarine tract
Primary/Olfactory Axon crosses Subarachnoid Space F
a. Hold out, at the periphery of your temporal field, a colored pen, preferably red,
or any other F. Complete
small, colored item. ↓
R inferior F E
b. Stare fixedly straight Synapse on Olfactory Bulb
homonymous
ahead and move the colored item until it is in line with
quadrantanopia
your central vision. How does the color ↓ differ as the item moves from periph- Calcarine fissure of
item, the G
eral to centralG.vision? occipital lobe
Complete Secondary Pathways
R homonymous G
_______________________________________________________________
hemianopia ↓
4. Self-demonstration of the perimeter of the peripheral fields.
Basal Forebrain/Basal Frontotemporal Junction TESTING PERIPHERAL VISUAL FIELDS BY CONFRONTATION
a. Close or cover one eye and fixate straight ahead with the other. Extend the arm
FIGURE 3-4. The visual pathway from the retinal images to the calcarine cortex of the occipital
↓
that is ipsilateral to the fixating eye straight out to the side and
• Station yourself directly (about 50cm) in front of the patient
Tertiary Pathways lobe, aspoint
seenyour from above.• TheHold
lettersup onyour
the left
left indicate lesion
index finger sites
just and the
outside visual
your own field defects
peripheral
index finger up. Now, keeping the elbow extended, rotate the arm forward
they would cause.
from the shoulder. The point at which ↓ you first see the finger defines the tem- field, in the inferior temporal quadrant
poral perimeter of your visual field.
Olfactory Cortex • Hold the finger about equidistant between your eye and the
b. Repeat the experiment, fixating with the same eye and closing the other. This patient’s
time extend the arm that is contralateral to the fixating eye and rotate the arm
CN II: OPTIC NERVE • Request the the
patient to look directly into of
your
forward until your finger just becomes visible. Did you have2. to move it farther
A second set of axons comes from contralateral, nasal half theeye and These
retina. to say
•forward than the
Visual ipsilateral
Acuity arm? yourself in front of a long row of
– position “now” as soon as the wiggling finger is seen.
two groups of axons unite the right and left visual half fields from each eye.
_______________________________________________________________.
books. If you stare fixed at 1 book title without moving your • Wiggle the finger and move it very slowly toward the central
c. Ostensibly the nose would seem to limit the nasal part of
eyes at will, you cannot read more than 1 book title. the visual field. Phy-
The field.
F.
logenetically this may be true, but the extent of the retina itself limits the
very small central area of sharpest vision is the central field.
extent of the nasal field.
Dual pathways branch
• from the optic tract
Compare the patient’s visual field against your own.
d. •To locate
Color theVision
vertical – in front
perimeter of of
the the
visualsame row of
field, fixate The books,
straight optic
ahead if tract
you conveys
with • visual
Test and
the midpoint
nonvisualof each posteriorly
axons quadrant of each the
from eye separately,
chiasm.
if it is ptotic. one eyestare at a book directly in front of you, a distant book that
and bring your index finger down from above and then up from below. starting at the limit of your own vision.
he lid while
Whatyou structure
see limits the height
in the of the visual
periphery would field?
look drab 1. The and nonvisual
nearly axons of the optic tract go to the pretectum of the midbrain and to
_______________________________________________________________.
colorless. the hypothalamus. PUPILLARY LIGHT REFLEX
5. The importance of testing central and peripheral vision: Diseases,a.such Theas retini-
retinopretectal• tract synapses in the pretectum and midbrain for pupillocon-
In a room with normal illumination, ask the patient to gaze at a
tis pigmentosa and glaucoma, and some drugs, such as vigabatrin, affect the rods
DUALITY OF THE VISUAL FIELD
first and cause constriction of the peripheral fields. Other disorders, such striction
as the to light (Fig. 4-30). point to avoid pupilloconstriction from the
distant
•
macular Cone Neurons
degeneration – occupy
of aging, impair the the macula,
cones and cause which
loss offorms Thea vision,
b.central disc
retinohypothalamic accommodation reflex.
tract synapses on the paraventricular nucleus and medi-
and yet centered on the fovea centralis
other diseases affect both rods and cones and cause loss of central and • Compare the size of the 2 points and record papillary size in mm.
peripheral vision. Hence, the examiner (Ex) must test for these two types of ates the diurnal cycle of sleep and wakefulness.
• loss.
visual Rod Neurons – occupy the remaining retina, concentrically Check for anisocoria (unequal pupils). Look for faint rapid
surrounding the macular disc 2. The visual axons in theoscillations of the papillary margins, called hippos, which may be
optic tract, the retinogeniculate tract, synapse on the lateral
• Cones mediate the central field of vision and its 2 functions: geniculate body of thebenign or reflect metabolic encephalopathy
thalamus (Fig. 3-4).
D. Nomenclature for the visual fields and visual field defects
1. Learn the visual acuity (20/20) and color vision (mnemonic 4 C: Cones,
nomenclature of the visual fields in Fig. 3-7.
a. The geniculocalcarine • tract then synapses on the primary visual (calcarine) cor-
Check the direct and consensual papillary light reflexes
Central field, Color and aCuity). tex (Figs. 3-4 to 3-6). o Direct Pupillary Light Reflex – constriction of the
b. The association cortex illuminated pupil
surrounding the calcarine cortex then interprets the
Superior temporal
Superior nasal
quadrant significance
Superior temporal and o
meaning Consensual
of the visualPupillary
image.Light Reflex – constriction of the
quadrant
Central field
quadrant opposite pupil when light stimulates one eye
• Do not shine the light abruptly into the patient’s eyes from
Inferior temporal Inferior nasal G. Inferior
Dualtemporal
banks of the calcarine cortex
directly in front. Approach the eye separately. Observe whether
quadrant quadrant quadrant
Right eye 1. The primary
both pupils constrict promptly and equally to unilateral
Left eye visual cortex forms dual, upper and lower, banks along the calcarine fis-
FIGURE 3-7. Nomenclature of the normal visual fields. sure on the medial surface illumination. After prompt
of the occipital lobe (area initial
17 ofconstriction,
Brodmann;the Figs.pupils
2-2,
Nomenclature of Visual Field Defects 3-4, and 3-5A). normally dilate slightly.
• Quadrantanopia – blindness in ¼ of a field 2. The macula is represented • Swinging Flashlight Test – alternately swing the light from one
eye to toward the occipital
the other pole of area
at 3- to 5-second 17. The
interval. remaining
Normally, there
• Hemianopia – blindness in ½ of a field retina is topographically represented forward (Fig. 3-5B).
• Homonymous – when corresponding quadrants or halves of should be a sustained pupilloconstriction as you swing the light
the field are affected. from one eye to another.
• Heteronymous - when non-corresponding quadrants or • Marcus Gunn Pupil – pupils will dilate as the light swings form
halves of the field are affected. However, they are easier to the normal to the affected eye, rather than maintaining the
describe directly (e.g. superior bitemporal quadrantanopia) same degree of constriction; AFFERENT (optic nerve) defect.
• Complete – whole quadrant is affected
• Incomplete – only part of the quadrant is affected PUPILLARY LIGHT REFLEX PATHWAY

• Scotoma – an irregular field defect; may be central,
Usual visual Pathway up to Optic Tract
paracentral, or peripheral
↓

Lateral Geniculate Body
TESTING CENTRAL VISION
↓
• Use a Snellen/Jaeger or Rosenbaum Chart for numerical
Pretectal Nucleus (where bilateral synapses occur)
evaluation of acuity
↓
Nucleus of CN III (Edinger-Wesphal nucleus) o Optomotor mechanism must foveate when eyes hold still and
↓ during all movements, including head tilts, and vergences
CN III (convergence-divergence).
↓
Ciliary Ganglion Primary Position of the Eye
↓ o Patient looking straight ahead
Ciliary Muscle o Point of fixation at infinity
↓ o Visual axis essentially parallel.
Pupilloconstrictor muscle (sphincter pupillae muscle) o Visual Axis – a line drawn from the fovea centralis of one
eye to the center of the visual field of that eye.
FREQUENTLY ASKED QUESTIONS
o Will lesions in the lateral geniculate body affect the reflex? Muscle 1° Action 2° Action 3° Action
Why? Ans. No. The fibers of the optic tract concerned with the Medial Rectus Adducts
reflex do not reach the lateral geniculate body but instead go Lateral Rectus Abducts
directly to the pretectal area in the midbrain. Therefore, lesions Superior Elevates Adducts Intorts
in the optic radiation or the calcarine cortex will not affect the Rectus
reflex. Inferior Rectus Depresses Adducts Exorts
o Where is the CN III nucleus found? Ans. MIDBRAIN Superior Depresses Abducts Intorts
o Will anti-cholinergic drugs cause dilatation? Why? Ans. Anti- Oblique
cholinergic drugs cause dilatation of the pupils. The Inferior Elevates Abducts Extorts
PARASYMPATHETIC portion of the CN III is the one that Oblique
subserves pupil constriction. Acetylcholine is the
neurotransmitter for the parasympathetic system. Thus, anti- CN III – innervates MR, SR, IR, IO
cholinergics inhibit pupillary constriction and cause dilatation. CN IV – innervates SO
CN VI – innervates LR
Pathways from the Optic Tract Mnemonic: LR6SO4; AO (all others) 3
• Retinopretectal – pupillary constriction
• Retinohypothalamic – PVN – diurnal rhythm Yoking of strongest actions of the EOMs in moving the eyes in the
• Geniculocalcarine – vision cardinal directions of gaze:
you don’t. Should you try again? While wrestling with your conscience, listen to
FUNDOSCOPIC EXAMINATION
Walt Whitman:
S IO S
o To examine the Failingright eye,
to fetch hold
me at the encouraged,
first keep ophthalmoscope with your R R
right hand and look with your right eye.
Missing me one place, search another,
o Ask patient to look straight ahead at a distant object. Check for
I stop somewhere waiting for you. LR M LR
R
ROR (Red Orange Reflex).
o Follow the vessels to optic disc. The normal cup-disc (comparing
13. Table 3-1 summarizes common vascular lesions visible by funduscopy.
diameters of the optic cup and the optic disc) ratio is 1:3 while S
IR IR
the normal A-V ratio (comparing the diameter of the optic O
TABLE 3-1 . Vascular Lesions Disclosed by Funduscopy
arteries and veins and not the number!) is 2:3.
Emboli: talc/corn starch emboli in IV drug users; Hollenhorst plaques: yellow cholesterol emboli in retinal
Evaluating the Range of Eye Movement
arterioles; fibrin–platelet emboli: white emboli in arterioles; septic emboli: small retinal hemorrhages
with a central white spot (Roth’s spots) o Judge the range of volitional eye movements during the history
Trauma/subarachnoid hemorrhage: subhyaloid hemorrhages between the retina and the vitreous, char- o With the patient sitting, gently press on the top of the patient’s
acteristic of battered infants
Central retinal artery occlusion: pale retina, attenuated arterioles, and red macula (cherry-red spot)
head with one hand, fitting the head in position by a
Central retinal vein occlusion: widespread intraretinal hemorrhages and dilated retinal veins “proprioceptive link” between you and the patient permitting
Hypertensive retinopathy: “copper or silver wire” arteries, A-V nicking, flame hemorrhages,“cotton-wool” only the eyes to move. (NOTE: Mentally retarded or demented
exudates, and papilledema
patients have difficulty separating eye and head movements.)

Diabetic retinopathy: microaneurysms,“hard” exudates, retinal hemorrhages; vitreous hemorrhage
o Ask the patient to fixate on your finger, which you hold up in the
ABBREVIATIONS: A-V = arterial to venous diameter ratio; IV = intravenous.
PAPILLEDEMA midline, about 50 cm away, at station 1. Request the patient to

C.• Papilledema
Blurred or elevated optic papilla from edema in the nerve fiber. follow your finger horizontally with the eyes to station 2, the
• Definition:
Types: Early, fully developed chronic, chronic atrophic extreme end of the lateral gaze. (In testing the horizontal eye
1. Papilledema means a blurred or elevated optic papilla (optic nerve
• headOther causes: retrobulbar lesions
or optic disc) resulting from edema fluid in the nerve fibers as they cross the
movements, hold the finger vertically and in testing the vertical
eye movements, hold the finger horizontally so that the patient
• discOphthalmoscopic
to perforate the lamina cribrosa and
features: (+) enter the optic cup
hyperemia, nerve. obliteration,
Papilledema is
classed as early, fully developed, chronic, and chronic atrophic. can better appreciate any minimal separation of diplopic images
rugae/folds
2. Pathophysiology: Most often, papilledema results from transmission of increased that might occur.)
Examiner pressure intoPatient
intracranial the eye via142the subarachnoid Disease
space, which extends out o Hold the finger at station 2 and inspect the corneal light
Swollen disc
along the optic nerveGood vision
(Fig. 3-19). Other causes include Papilledema
direct pressure on the 10. Figure 4-21 shows the normal range of eye movements in m
reflections and the relation of the limbus to the lid margins,
optic nerve from retrobulbar
Swollen disc lesions.
Poor vision Papillitis that upward gaze has the least range. Diffuse brain disease im
canthi, and caruncles. Look for nystagmus.
Normal Poor vision ACUTE retrobulbar neuritis restricted upward movements more thanthe
other movements, bu
o Move your finger back to station 1 and instruct patient to
look can selectively
at your impair
finger as upward
you move it to or downward
touch movements
the bridge of the or b

Retinal patient’s nose. Observe for convergence and the accompanying

CORTICAL BLINDNESS veins
pupilloconstriction (accommodation reflex).
• Complete blindness, no light perception and no response to a
menacing gesture.
6 3 7 mm
• Loss of smooth pursuit of the Ex’s moving finger but preservation
of volitional movements.
• No optokinetic nystagmus.
5 1 2 10 mm 10 mm
• Normal pupillary reactions, funduscopic examination, and no
nystagmus.
• Sometimes the Pt will deny the blindness and will claim that
FIGURE 3-19. Section of optic papilla and optic nerve. The arrows show how the subarachnoid
vision is present (Anton’s syndrome).
space extends around the optic nerve. 7 4
10 mm
CN III, IV, VI: OCULOMOTOR, TROCHLEAR AND ABDUCENS NERVE
a. The retinal veins converge on the optic papilla to form the ophthalmic vein,
which enters the retinal end of the optic nerve. If the pressure around it Cover-Uncover Test for Ocular Malalignment
increases, the ophthalmic vein, being thin walled, collapses, obstructing the
Foveation Place your thumb between the patient’s eyes
o FIGURE
retinal veins (Fig. 3-19). 4-21. Range of ocular rotations, in millimeters.
o The act of aligning each eye so that the central ray falls on the o Instruct the patient to stare at a distant point and to
b. The retinal veins and papillary capillaries distend and leak fluid into the nerve
fovea on the optic papilla and into the surrounding retina. The veins may rup-
fibers
maintain fixation
The causing
o ture, entire visible
retinal image onof
hemorrhages the two
or around eyes fall on the
the papilla. o Move the thumb in front of one eye, then back to the
corresponding retinal points, promoting visual acuity and a single bridge of the nose, and then over the other eye. (You do
11. Because the Pt may have experienced diplopia while observi
not have to occlude all vision with your thumb; just the
(fused) mental image.
the
central vision) it. Select the best-phrased question:
Pt about
a. ❒ You are seeing two fingers instead of one, aren’t you?
MEDRANO NEURO NOTES
b. ❒ Do you have diplopia? 15
✓c
❒ c. ❒ Do you see one or two fingers?
Avoid questions that imply the answer 12. Students frequently make type a and b errors. The first ques
or that use technical terms. Ask ques- erroneous answer, because the Pt expects the doctor to know
157
Miller NR, Newman NJ, Biousse V, Kerrison JB, eds. Walsh and Hoyt’s Clinical Neuro-ophthal-
mology, 6th ed. Philadelphia: Lippincott Williams & Wilkins, 2005.
Shingleton BJ, O’Donoghue MW. Blurred vision. N Engl J Med 2000;343:566–562.
o Interpretation: o Produces all volitional movements and the fast phase of
o No ocular malalignment (normal) – when both eyes are reflex eye movements (frontal lobe)
CHAPTER 4
V. INNERVATION locked together in fixation; neither eye moves
OF THE OCULAR MUSCLES o Fronto-tegmental pathways
Malalignment – if the eye moves upon occlusion of the central vision 3. Smooth Pursuit system
A. Classification of ocular muscles into intraocular and extraocular o Keeps the eyes on moving targets (occipital lobe)
HeteroTROPIA
1. Each eye has 11 ocular muscles: four smooth muscles and seven striated mus- o Retino-occipito-tegmental pathways
Examination of the Peripheral Ocular Motor System

Any they
o Because
cles. ocular deviation
derive from somites, the detected by observing
striated muscles receive somitenon-CrNs 4. Vergence system
III, IV, and VI. Learn Fig. 4-29.
correspondence of the corneal light reflections when the o Converges or diverges the eyes to ensure fusion of the 2
eyes are in any position retinal images and appropriate refraction when the person
Eleven Manifest strabismus
o Ocular Muscles Four smooth (involuntary) muscles
looks at near or distant objects (occipital lobe)
Exotropia – lateral deviation 5. Eye Counter-rolling system
Pupilloconstrictor Parasympathetic
Esotropia – medial deviation
Three intraocular Ciliary muscle via CrN III o Vestibular and neck proprioceptive system; produces
Hypertropia – upward deviation
muscles Pupillodilator muscle
Sympathetic via carotid
postural information to align eyes, head, neck, and trunk
Hypotropia – downward deviation
Superior tarsal muscle sympathetic nerve o In the alert patient – there are 2 systems collaborating to
HeteroPHORIA Eight extraocular Seven striated counterroll the eyes when the head moves: (1) the ocular
muscles (voluntary) muscles
o In contrast to heterotropia, the ocular deviation is apparent
One lid elevator fixation system and (2) the proprioceptive motion receptors
only when central vision is blocked (as when you do cover-
Levator palpebrae in the vestibular system and the neck
Six rotator muscles
uncover test) Superior rectus CrN III
o The proprioceptors mediate counterrolling via pathways
Inferior rectus through the brainstem to the optomotor nuclei (III, IV, VI)
Medial rectus
Suppression amblyopia is a Inferior preventable
oblique cause of monocular o In the comatose patient, do Doll’s Eye Maneuver to test the
blindness, treated by the simple Superior expedient
oblique of CrN
placing
IV a patch integrity of the vestibuloproprioceptive counterrolling
Lateral rectus CrN VI
intermittently over the sound eye to require the Pt to use the errant reflex
186
eye. 4-29. Classification of the 11 ocular muscles according to type and innervation. Note that
FIGURE 2. Pathologic nystagmus arises most commonly from lesions located in:
superior tarsal muscle is both a smooth and an extraocular muscle, the only one so classified.
the UNILATERAL MLF LESION
a. The media, retina or optic nerve or optic chiasm that interfere with vision.
LAWS OF DIPLOPIA • b. Heterotropia and monocular nystagmus.
Vestibular end organ or nerve.
• One
2. The aberrant or “false” image is always hazier than the “true”
ocular-related muscle, the orbicularis oculi, a sphincter that closes the eye- • c. They appear tegmentum
The brainstem only when andthe Pt attempts
cerebellum (Leighto
andlook
Zee, away
2006). from the
lids,image.
derives from a brachial arch and belongs to the facial muscles, innervated by side of the interruption of the MLF.
3. Diencephalic or cerebral lesions infrequently cause nystagmus.Thalamic lesions or in
• CrN VII.
The false image appears peripheral to the true image • infants retinal
Other or hypothalamic
eye movements, lesions, such as optic
including nerve hypoplasia
conjugate vertical or gliomas, can
gaze and
cause mixed forms of nystagmus. Cerebral lesions may cause a type of gaze paretic
• The false image projects in the opposite direction as the pupillary responses remain normal.
nystagmus.Although the clinical findings usually suffice to diagnose the cause of nys-
B. Peripheral innervation of the extraocular muscles
direction of eye deviation. tagmus, magnetic resonance imaging examination of the brain often is necessary.
Six
• nerves innervate the eye, four motor and two sensory (Table 4-4).
The false image projects toward from the normal direction of PARINAUD’S SYNDROME
pull of the paretic muscle. B.
• Symptoms of nystagmus of the midbrain, as from a pineal tumor,
Dorsal compression 183
TABLE 4-4 . Afferent and Efferent Innervation of the Eye by Its Six Nerves J.1. Symptoms
Themesencephalic hemorrhage or obstructive hydrocephalus
rostralmay
midbrain syndrome
accompany (Sylvian aqueduct syndrome;
nystagmus:
Number (name) of nerve Innervation Clinical effects of interruption of nerve • a. pretectal syndrome)
Selectively impair upward vertical movements first.
Oscillopsia: apparent oscillation of objects viewed.
Efferent
•1. b.Many
Convergence
Vertigo:
nuclei palsy
a sensation
and pathways and
thatlight-near
of movement, thedissociation
generally
control a feeling
actions theof
of of the and
rotation
eyes pupils
or pupilsare
spinning
sur-
CrN III (oculomotor nerve) Striated muscle: superior, medial,
Diplopia, eye abducted and turned of self
round theorrostral
the environment
part of the(Chapter 8).
Sylvian aqueduct, in the midbrain tectum, pretec-
CHAPTER 5
and inferior recti; inferior oblique
down commonly present also.
tum, tegmentum,
with orand periaqueductal
vomiting gray matter. The actions controlled include
Levator palpebrae Ptosis (paralysis of volitional lid c.upward
Nausea:
and
without
downward gaze, vertical ocular alignment, pupillary size, palpebral
elevation) d. Blurred vision
Smooth muscle: pupilloconstrictor; Pupil dilated and fixed to light;
Motor Impersistence – inability to sustain gaze deviation for even 30
fissure height, vergences, and the movements mediated by CrN III (Table 5-2).
2. The presence of symptoms depends on the rapidity of onset and the duration and
ciliary muscle loss of lens thickening seconds.
site of the lesion. Just as heterotropia of congenital or early origin usually does not
CrN IV (trochlear nerve) Striated muscle: superior oblique Diplopia, most severe on looking cause diplopia, nystagmus of congenital or early origin may not cause symptoms.
Examination of the Central Ocular Motor Systems

down and in; eye extorted;
head tilted to side opposite TABLE 5-2 . Rostral Midbrain Syndrome (Sylvian Aqueduct Syndrome; Pretectal Syndrome)
paralyzed eye C.Pupillary
The signs of nystagmus
changes: anisocoria, corectasia, corectopia, absence of constriction to light or dissociated reac-
CrN VI (abducens nerve) Striated muscle: lateral rectus Diplopia, most severe on looking
TABLE 4-4 . Afferent and Efferent Innervation of the Eye by Its Six Nerves (Continued)
to side of paralysis; eye turned in
tions
If you canto light and accommodation
describe the Pt’s nystagmus well, you need not memorize its endless kinds
Eyelid abnormalities: eyelid retraction (Collier’s sign), lid lag, reptilian stare or conversely ptosis.
and causes. Dendrograms (Figs. 5-6 and 5-7) based on the clinical features listed in
Number (name) of nerve Innervation Clinical effects of interruption of nerve
(adducted)
Supranuclear upward or downward gaze palsy, or combined palsy of upward and downward gaze
Table 5-3 will lead to the probable diagnosis. Begin by describing the plane, the type
G.Carotid
Thesympathetic
syndromenerve
of sympathetic paralysis of the eyeHorner
Smooth muscle: superior tarsal
and pupillodilator
and face:
syndrome (ptosis, miosis,
hemifacial anhidrosis,(Continued )
Convergence/accommodation paralysis
(jerk or pendular), and the direction, if a jerk nystagmus.
Nystagmus: convergence nystagmus or convergence-retraction nystagmus, vertical nystagmus on
Bernard-Horner or Horner syndrome vasodilation) 1.attempted
Note the planegaze,
upward of eye nystagmus (Table 5-3)
movements
see-saw
Afferent CrN a. Horizontal: eyeball oscillates around the vertical axis.
III palsy
1. The sympathetic pathway to the eye: This pathway displays the typical features
CrN II (optic nerve) Visual afferents Blindness Strabismus: III nerve or pseudoabducens palsy, thalamic esotropia, skew deviation
of all sympathetic innervation. b. Vertical: eyeball oscillates around the lateral axis.
CrN V (trigeminal nerve) Corneal/conjunctival afferents Corneal anesthesia of cornea; loss Head tilt
a. The upper motoneuron pathwayafferents
Proprioceptive begins in hypothalamic neurons
of corneal and
reflex No descends
known c. Rotatory
Oculogyric (torsional):
crises: forceful eye
deviation oscillates
of the around
eyes, common the anteroposterior (A-P) axis.
in parkinsonism
through the brainstem tegmentum to the spinal cord. Learn
clinical effectFig. 4-31. d. Mixed.
ABBREVIATION: CrN = cranial nerve.
ABBREVIATION: CrN = cranial nerve.
NYSTAGMUS
Nasociliary branch of
nerve V TABLE 5-3 . Steps in the Clinical Analysis of Nystagmus
To superior tarsal muscle 2.1. Pure paralysis of upward gaze is known as Parinaud’s syndrome
1.Trigeminal
Of the four essentially motor nerves, three convey somatic
(in efferent
eyelid) fibers: CrNs
Note the plane of eye movements (horizontal, vertical, torsional or mixed), type (jerk or pendular), and
ganglion
III, IV, and VI. 3. Midbrain signs in addition
direction (unidirectional to the
or bidirectional), if itSylvian aqueduct syndrome per se include:
is a jerk nystagmus.
Hypothalamus Pupillodilator muscle
2. a.
Note the type of nystagmus,
Oculogyric crises pendular or jerk.
a. Two of the three somatomotor nerves serve only oneInternal EOM:carotid
CrNartery
VI inner- 3. Note the direction of the fast movement of the nystagmus, if the Pt has jerk nystagmus.
Midbrain
vates the lateral rectus, and CrN IV innervates the superior oblique. CrN III
Sweat gland 4. b.NoteMinimal to severe
the amplitude and rate.impairment of consciousness
Cerebellum
serves the remaining EOMs and two of the three intraocular Vasoconstrictor
muscles.axon
5. c.NoteHemiparesis or quadriparesis
whether the nystagmus is binocular and symmetrical, monocular, or dissociated (different ampli-
External carotid artery
b. Only CrN III of the somite group also conveys parasympathetic
Medulla (GVE)
Common carotid artery fibers. d.
tude in the two eyes or different directions).
Decerebrate rigidity
6. Note whether the nystagmus occurs in the primary position or the eccentric positions and the effect of
These fibers innervate two of the three intraocular smooth muscles,
cervicalthe pupil-
Spinal cord, T1
Superior ganglion e.eyeCentral
movements neurogenic
in the cardinalhyperventilation
directions of gaze (Figs. 5-6 and 5-7).
loconstrictor and ciliary muscles. Paravertebral sympathetic 7. f.Look for a null
Tremor orpoint where bidirectional nystagmus is minimal or absent.
ataxia
2. The fourth motor nerve of the eye, the carotid sympathetic ganglion
nerve,chain
innervates the 8. Test for the effects of changes in head position or posture on nystagmus.
third intraocular muscle, the pupillodilator muscle and one clinically important 4.9. The top
Test for of the
latent basilar
nystagmus syndrome
by covering eachis
eyecaused
separatelybyandinfarction
inspectinginthethe terminal
other branches
eye with magnifi-
FIGURE
EOM, 4-31.
theDiagram
superioroftarsal.
the sympathetic pathway
The carotid from the nerve
sympathetic hypothalamus (part of
travels from thethe dien-
carotid of theprovided
cation basilar byartery, the posterior cerebral arteries. These arteries irrigate the mid-
the ophthalmoscope.
HORNER’S SYNDROME
cephalon) 10. brain-diencephalic junction and the
of theinferomedial aspect of the temporo-occipital
artery to at the
thepupillodilator
level of the and superior tarsal muscles, sweat glands of the face, and the
cavernous sinus into the superior orbital fissure and to Look for associated rhythmic movements lids, face, jaw, tongue, palate, pharynx, neck, or limbs
• theIpsilateral ptosis, pupilloconstriction (cormiosis), anhidrosis, and
smooth muscle of the carotid arteries.
eyeball by hitchhiking along other orbital nerves (Fig. 4-31). region. Infarction
(palatal and may cause any combination of midbrain, posterior thalamic, or
ocular myoclonus).
11. temporo-occipital region signs, including loss offall,consciousness,
and past-pointing depending
and do caloric on the
3. Test your knowledge of Table 4-4 by completing frames 4-12.
In selected Pts, test for optokinetic nystagmus, the Romberg
flushing (vasodilation) irrigation. of the occlusion, the extent of the thrombus, and the collateral flow.
location
• CrN
4. b. A diagnostic feature of unilateral Horner syndrome is an increase
TheIII upper motoneuron pathway synapses on the GVE lower motoneurons of 12. Consider electronystagmography and radiographic imaging.
the intermediolateral cell column of the spinal cord gray matter.
in the degree of the anisocoria just after dimming the room light.
a. CrN III is called the ________________________ nerve. Types of Nystagmus (REFER TO DEMYER Addendum)
ABBREVIATION: Pt = patient.
rior recti, i. The sympathetic visceral efferent column extends in the spinal cord from
levator
b. TheT1 EOMs innervated
to L2 and L3. by III are ____________________________________ 1.
BIBLIOGRAPHY . Central Systems for the Control of Eye Movements
Jerk nystagmus - fast and slow component
____________________________________________________________. 2. Pendular nystagmus – to and fro metronomic oscillation
Bender MB. Brain control of conjugate horizontal and vertical eye movements. A survey of the
oblique
Examination of the Central Optomotor System
c. CrN III innervates two intraocular muscles and all EOMs, except for structural and functional correlates. Brain 1980;103:23–69.
_______________________________________________________________.
Mnemonic: T1-L2-3. Bender MB, Rudolph SH, Stacy CB. The neurology of the visual and oculomotor systems. In
d. In addition, CrN III innervates a muscle that elevates the eyelid, the
5 major eye movement systems: CN V: TRIGEMINAL NERVE (Motor Function)
Joynt RJ, Griggs RC, eds. Clinical Neurology. Philadelphia, Lippincott Williams & Wilkins,
________________________ muscle. 1998, Vol. 1, Chap. 12, 1–132.
1. Fixation (position maintenance) system o Inspect the temples and cheeks for atrophy of the temporalis
5. CrNii.IV Bhihdayasiri R, Plat GJ, Leigh J. A hypothetical scheme for the brainstem control of vertical
o Axons to the eye derive from T1 and T2 (also called the ciliospinal center of
Fixates and maintains eyes on the target and locks them in and masseter muscles
gaze. Neurology 2000;54:1985–1993.
a. CrNBudge).
IV is named the ________________________ nerve.
unison to fuse the 2 retinal images into visual image oBrazis Palpate both masseters for atrophy – 1
st
muscle to atrophy
PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 5th ed. Philadelphia: Lippin-
b.c. CrN
As isIV
also typical, the only
innervates sympathetic
EOM to GVE
have aaxons, thethe
trochlea, second-order neurons in
___________________
(occipital lobe)
the sympathetic
muscle. pathway, exit with a spinal nerve to synapse in a paravertebral cott Williams and Wilkins, 2007.
o Test for jaw closure by having the patient clench the teeth
c. Theo Retino-occipito-tegmental
ganglion.
superior and retino-occipito-fronto-
oblique has three actions: ________________________________,
Frohman EM, Zhang H, Kramer PD, et al. MRI characteristics of the MLF in MS patients with
strongly
orsion chronic internuclear ophthalmoparesis. Neurology 2001;57:762–768.
d. Fromtegmental pathways
the paravertebral ganglion,
________________________, the superior cervical for the carotid sympa-
and ________________________. o Test the lateral pterygoids by having the patient forcefully open
Gaymard B, Siegler I, Rivaud-Pechoux S, et al. A common mechanism for the control of eye
6. CrNthetics,
VI the third-order axons, then hitchhike as a plexus along blood vessels
2. Saccadic system and the jaw
head movements in humans. Ann Neurol 2000;46:829–822.
oor nerves
a. CrN VI
to their effectors.
Eye movements by means of rapid, incremental jerks
is named the ________________________ nerve. It innervates the
e. ________________________
The carotid sympathetic nerve innervates the smooth muscles of the vessels of
muscle.
the entire internal and external carotid systems.
b. The only action of the lateral rectus is to ________________________ the eye.
i. The external carotid artery carries sympathetic axons to the sweat glands
of the face.
ii. The internal carotid artery carries the sympathetic axons to the ocular
VI. EXAMINATION OF THE PUPILS
smooth muscles and the sweat glands of the forehead.
f. The sympathetic axons innervate two ocular muscles, __________________
ator
A. Technique of pupillary
(extraocular) examination (intraocular).
and __________________
Motor Part of CN V Conductive Hearing Loss – impedance in the conduction of sound

Ipsilateral to Cortex that Acts Contralateral vibrations through the external auditory canal or ossicles of the
Motor Cortex middle ear.
Neurosensory Hearing Loss – lesion in the Organ of Corti or the
Corticobulbar tract auditory nerve. A unilateral CNS lesion does not ordinarily cause a
strongly lateralized hearing loss.
CN V motor nucleus CN V Motor nucleus
Sound Lateralizing Test of Weber
CN V CN V o Place a vibrating tuning fork in the middle of the forehead
or the vertex of the patient’s skull. Normally the sound

Chewing muscles
Chewing muscles should seem to come from the center and should be equally
One HEMISPHERE OF THE CORTEX innervates both sides. Thus loud in both ears.
unilateral motor cortex lesions will cause bilateral weakness of o If there is a mechanical impediment (e.g. impacted
chewing muscles (but perhaps greater paresis of contralateral side). cerumen), sound will lateralize to the obstructed ear
Unilateral lesions of CN V will cause paralysis of only the IPSILATERAL (conduction hearing loss)
side. o If there is neurosensory hearing loss, sound will lateralize to
the normal ear.
CN VII: FACIAL NERVE (Motor Function)
o SENSORY: Assess taste one side at a time (anterior 2/3 of Schwabach Test
tongue). Put sugar / salt on the right / left half tongue and o Hearing of the patient compared with that of the examiner
massage with well – moistured cotton tip of applicator stick. Do o A vibrating tuning fork is placed beside the patient’s ear and
not allow tongue to return into the mouth until the patient has the patient is asked to tell you when the sound
responded. After patient rinses his mouth, test the opposite side disappeared. Immediately transfer the fork beside your
of the tongue. ear. Normally, you shouldn’t hear any sound.
o MOTOR: Inspect nasolabial folds, wrinkle forehead (frontalis),
close eyes tightly (orbicularis oculi), purse lips tightly as in kissing CN IX and X: GLOSSOPHARYNGEAL AND VAGUS NERVE
(opticularis oris), smile (buccinator), pull down corners of mouth o Check patient’s voice. Vocal cord paralysis = CN X Palsy
(platysma): o Observe speech: if not normal, test competency of
o CENTRAL versus PERIPHERAL FACIAL PALSY articulation by soft tissues, the soft palate, tongue, and lips
CENTRAL: Eyelid closure is usually paretic (incomplete paralysis), (Ask the patient to produce the sounds K, L, and M. K tests
and there is paralysis of lip retraction. The frontalis is usually CN IX, L tests CN XII, while M tests CN VII)
normal. o Kuh – Soft palate function
PERIPHERAL: One side of the face is completely paralyzed. o La – Tongue
o Mi - Lips
Sensory component of CN VII: o Check for swallowing – dysphagia defined as swallowing
<10ml/s.
Receptor: taste buds o Inspect palatal arch. Ask patient to say “Ah” and check for
↓ deviation of the uvula. Palatal asymmetry = CN X palsy.
Nerve fibers forming chorda tympani Uvula swings to the side opposite palatal weakness.
↓ o Elicit the gag reflex: afferent – CN IX; efferent – CN X
Joins facial nerve o CN IX is responsible for the sense of taste in the posterior
↓ 1/3 of the tongue (no need to test this)
Internal auditory canal where it synapses with geniculate ganglion
(primary neurons) Examples of Hoarseness
↓ • Cerebral palsy: slow, ratchet like onest
Pons: CN VII nucleus • Cri du chat: chromosome 5p deletion syndrome
↓ • Paralysis agitans (parkinsonism): “plateau speech”
Ascends homolaterally without decussation to thalamus • Cerebellar disease: “scanning speech”, overaccentuates and
↓ underaccentuates random sounds.
Insular cortex (Island of Reil)
Parietal operculum (BA 43) CN XI: SPINAL ACCESSORY NERVE
o Innervates the SCM and trapezius muscles
Motor component of CN VII: o Spinal part: SCM and trapezius
o Accessory: Accessory to Vagus, from the nucleus ambiguus
Motor cortex – distributes to the pharynx and larynx.
(precentral gyrus, frontal lobe) o To test CN XI, instruct the patient to: “Turn your head to the
↓ left, hold it there, don’t let me push back.”
Corticobulbar tract o The left SCM turns the head to the right, and vice versa.
↓ Thus, if the right spinal accessory nerve is damaged, the
Decussates at the level of the brainstem, pons in particular, patient will not be able to turn his head to the left.
where it synapses at the nucleus of CN VII (Mnemonic: face your problem)
↓ o “Push your head forward as hard as possible”
efferent nerve o Let the patient shrug his shoulders. Ask the patient to resist
↓ while you try to push the shoulders down (testing the
effectors: major facial muscles trapezius)
frontalis, orbicularis oculi, buccinators, orbicularis oris, platysma, and
stapedius CN XII: HYPOGLOSSAL NERVE

o Check for atrophy, tremors, fasciculations, deviation of the
CN VIII: VESTIBULOCOCHLEAR NERVE
tongue
Air – Borne Conduction Test of Rinne o Moves the genioglossus muscle.
o Compares the efficacy of the conduction of sound vibrations by o Tongue deviates to the side of wounds (Mnemonic: Lick
bone and by air your wound. Similar to facing your problem) – deviated to
o Normally, air conduction > bone conduction left, left sided lesion.
o Hold a vibrating tuning fork beside the patient’s mastoid process. o Ask the patient to move tongue side to side against a
Transfer the fork beside the patient’s ear when the patient tells tongue depressor
you that the sound disappeared.
o Normally, the patient should hear the sound again. MULTIPLE CRANIAL NERVE PALSIES
o NOTE: A mechanical impediment in the auditory canal causes an
• Example: Myasthenia Gravis: (+) pathologic fatigability of
apparent decrease in air conduction but in reality it causes an
multiple muscles innervated by cranial nerves.
apparent increase in bone conduction

nation of the Motor Cranial Nerves V, VII, IX, X, XI, and XII
for survival, the reticulospinal pathway. It activates the LMNs of the muscles
of respiration, essentially the diaphragm and intercostal muscles. The reticu-
lospinal tracts decussate at the medullocervical junction, just ventral to the
18 DEMYER’S TECHNIQUE OF THE NEUROLOGIC EXAMINATION obex, and descend in the ventrolateral quadrants of the spinal cord to activate
the phrenic and intercostal motoneurons (Fig. 6-17).
o Diagnosis of MG: Antibodies against AchR or IgG

antibodies against MuSK.
• Syndrome of Pseudobulbar Palsy:
o Slow speaking initiation; dysarthria or near mutism Cerebrum
Corticospinal
o Voice has a strained pitch and quality tract
o Chew, yawn, swallow reflexively but cannot do these

volitionally. Midbrain
o Extreme emotional lability; fourire prodominique
o Most common causes in adults are bilateral strokes
Pons PTC
and amyotrophic lateral sclerosis.
Trigeminal ganglion
o Gelastic seizures are another cause, and most APC
commonly result from hypothalamic hamartomas
Carotid
o Most common cause (pedia): bilateral perisylvian DRG
CN IX body
opercular and insular lesions from congenital Medulla
Aortic
body
malformations, hypoxia, or encephalitis. VRG CN X

Phrenic nerve
Lungs
THE NEUROLOGY OF BREATHING (C3-C5)
Corticospinal
• Origin of the drive to breathe: forebrain and brainstem tract
reticular formation (ISOLATED SPINE CREATES NO DRIVE) Intercostal Reticulospinal
tract
• Forebrain mediates volitional and emotional control nerves
(T2-T12)
• Reticular formation controls automatic breathing
o Caudal half (midbrain to the medullocervical junction):
rhythmic drive to breathe; also controls swallowing,
chewing, rooting, coughing, sucking)
o Medullary reticular formation: single most important • 6-17.
FIGURE Ondine’s Curse:
Neuroanatomy intact Bypyramidal
of breathing. tracts but
stimulating motoneurons in theinterrupted
spinal cord from C3
pathway for survival: RETICULOSPINAL Pathway to T12, the reticulospinal pathway
corticospinal tracts control volitional breathing, and the reticulospinal tracts control
automatic breathing. APC = apneustic center; CN = cranial nerve; DRG = dorsal respiratory group
232 • Coughing is an important function that protects the lungs of neurons, mainlySleep removes px’s respiratory drive.
o inspiratory, associated with the dorsal motor nucleus of the vagus nerve; PTC =
BIBLIOGRAPHY Breathing
from irritants and pathogens, quantitative measurement of . EXAMINATION OF AN UNCONSCIOUS PATIENT
pneumotaxic center;VRG = ventral respiratory group of mixed inspiratory and expiratory neurons
associated with the nuclei ambiguus and retroambigualis. (Reproduced with permission from
air flow is the most reliable way to assess sufficiency of Considerations:
DeMyer W. Neuroanatomy, 2nd ed. Baltimore, Williams & Wilkins, 1998.)
coughing. Markand O, Kincaid JC, Pourmand R, et al. Electrophysiologic evaluation of diaphragm by
1. Trauma
transcutaneous phrenic nerve
2. stimulation.
d. nerves are 1984;34:604–614.
The phrenicNeurology
Seizure the most important nerves in the body. With intact
Polkey MI, Lyall RA, Moxhan J,3.et al.
Insulin/diabetes mellitus, alcohol.
phrenic nervesaspects
Respiratory and the drive to breathe descending
of neurological disease. through
J Neurol theNeu-
reticulospinal
4. tracts, the Pt can maintain life by diaphragmatic action alone, even after spinal
Depressant medications or street drugs.
rosurg Psychiatry 1999;66:5–15.
5. Allergies, insect bites, anaphylactic shock.
Smith Hammond CA, Goldstein LB, Zajac DJ, et al. Assessment of aspiration risk in stroke with
6. Heart, liver, lung, or kidney disease.
quantification of voluntary cough. Neurology 2001;56:502–506.
7. Past hospitalizations for serious health problems

Initial Management:
X. LOCALIZING DIAGNOSTICON FOR BRAINSTEM
1. A and B = Airway and Breathing.
SYMPTOMS AND SIGNS
2. C = Circulation.
3. D=Dextrose – also give thiamine if patient is a suspected
alcoholic
Figure 6-19 summarizes the clinical effects of brainstem lesions. One important, clas-
4. EE = Examine the Eyes.
sic localizing combination is paralysis of a CrN in the midbrain, pons, and medulla
• pupillary size and reactions – if pinpoint, consider naloxone
ipsilateral to the lesion and motor or sensory signs contralateral to it due to interrup-
• optic fundi
tion of a decussating tract, i.e.,•right VI nerve palsy and left-sided pyramidal signs
position and movement of the eyes spontaneously and in
caused by a lesion of the basis pontis. response to the vestibulo-ocular reflex
• faciociliary and spinociliary reflex
Motor cortex Thalamocortical Clinical findings after destructive lesions

pyramidal tract radiations
Diencephalon
Unilateral lesions: Contralateral hemisensory loss, including face (ML and its terminal
nucleus {posterior ventral nucleus}); contralateral involuntary movements,
especially hemiballism (subthalamic nucleus and rubrosubthalamic connections)
Third
Diencephalon ventricle Bilateral lesions: Akinesia, unconsciousness; Cheyne-Stokes respiration, especially if
lesion extends bilaterally into cerebrum
Midbrain
Unilateral lesions: Ispilateral cranial nerve (III) palsy, corectasia; intention or postural
tremor (CDRTCT) or contralateral hemiballism, hemiplegial (PT), and hemisensory
Midbrain CN III
loss, including face (ML)
CN IV
Bilateral lesions:
In basis: Quadriplegia, pseudobulbar palsy
CDRTCT In tegmentum: Unconsciousness, hyperventilation, decerebrate rigidity;
Pons ML parkinsonism (SN)
CN V PT Pons
Unilateral lesions: Ipsilateral cranial nerve (V, VI, or VII) palsy, no corneal reflex;
Trigeminal ganglion
Loss of pain and temperature sensation (descending root of CN V); contralateral
and descending
hemiplegia (PT) and hemisensory loss (ML) in face and body, depending on
root of CN V ML involvement of descending root of CN V or trigeminal lemniscus; nystagmus,
CN vertigo and nausea (VP and RF)
CN VI
VII
CN Bilateral lesions:
VIII In basis: Quadriplegia (locked-in syndrome)
In tegmentum: Unconsciousness if in rostral half of pons; apneustic or cluster
breathing if in caudal half; nystagmus, vertigo, nausea and vomiting (VP and RF)
Cerebellum
CN TL Medulla
Medulla IX Unilateral lesions: Ipsilateral cranial nerve palsy: of pharynx (IX, X), palate (X), or
CN
CN XII
tongue (XII); Horner’s syndrome; dysphagia; hiccups; loss of corneal reflex
X (sometimes); loss of pain and temperature sensation on face (descending root of
TL CN V); contralateral hemiplegia (PT), hemisensory loss on body (ML); nystagmus,
vertigo, nausea and vomiting (VP and RF)

Spinal cord
CN Bilateral lesions: Quadriplegia; ataxic breathing or apnea; hypotension
XI
PT
At the very least, assign the Pt to one of the five basic etiologic types of coma:
intracranial lesion, toxic-metabolic disorder, anoxia, ischemia, or mental illness. See
Preparation fo r the Tex t

Fig. NE-2.
WOF: Hypoxia, Hypotension, Hypoglycemia, Hyperthermia, and

Herniation

Physical Exam
• Head: signs of basilar skull fracture (Battle’s sign, raccoon eyes,
CSF rhinorrhea/otorrhea)
• Nuchal rigidity
• Movement spontaneity
• Posturing:
o Persistent deviation of eyes, head, limbs
o Opisthotonus – ant. Reticulospinal tract, cerebral palsy,
tetanus, strychnine poisoning, extrapyramidal side effect
o Decerebrate (extensor) – rubrospinal, lateral corticospinal
o Decorticate (flexor) – below the red nucleus (pontine
stroke)
o Clenched jaws, extremities
• Extremity paralysis
o Muscles in acute hemiplegia are usually flaccid
o Eyelid release test
o Check for paratonia – hypertonia with an involuntary
variable resistance during passive movement
o Flexibilitas cerea (waxy flexibility) – catatonic schizophrenia
and encephalopathies
• Muscle stretch reflexes
• Chvostek’s sign
• Primitive reflexes

NE-2. Categories for the differential diagnosis of the unconscious patient.
FIGURE
VI. SELECT THE SAFEST AND MOST CRITICAL TESTS TO

CONFIRM OR REJECT YOUR PROVISIONAL DIAGNOSIS
Additional neurologic tests to consider are magnetic resonance imaging (MRI), lum-
bar puncture (LP), and angiography. In general, CT or MRI should precede the LP
because the scan may disclose the diagnosis or impending brain herniation, making
the tap unnecessary or dangerous. Obtain radiographs of the cervical spine, if trauma
is suspected.
BIBLIOGRAPHY
Fleck JD, Biller J. Tips on the neurologic examination. Basic neurologic life support, James J.
Corbett, Ed., BC Decker, Inc. 2004 236–257.

CONTRALATERALITY
Learn Table 2-15.
CHAPTER 2
TABLE 2-15 . Summary of the Clinically Important Sensorimotor Decussations of the Central
ADDENDUM Nervous System
Pathway Site of decussation
A Brief Review of Clinical Neuroanatomy

Optic decussation Optic chiasm (Fig. 2-26)
Somatic sensory decussations
Pain and temperature Near or at levels of entry of the dorsal root axon (Fig. 2-28)
Light touch Two routes: near or at levels of entry and the cervi
comedullary junction (Fig. 2-28)
Vibration and position sense (deep Cervicomedullary junction (Fig. 2-28)
modalities)
Descending reticulospinal tract for breathing Cervicomedullary junction at the obex, dorsal to other
decussations (Fig. 6-17)
Pyramidal tract
Corticobulbar component Various sites along the brainstem (Fig. 2-29)
Corticospinal component Cervicomedullary junction (Fig. 2-29)
Horizontal eye movement pathway
Corticobulbar component Decussates broadly from the midbrain level to the ros-
tral pons (Fig. 5-1)
Medial longitudinal fasciculus component Decussates near the VI nerve level to make the medial
rectus act equal to the lateral rectus, thus fulfilling
Hering’s law (Fig. 5-1)
Cerebro-ponto-cerebello-thalamo-cerebral Decussates at the pons on the way down from the
pathway motor cortex and the midbrain on the way back
up to the thalamus and motor cortex (Fig. 2-30)

TABLE 4-5 . Differential Diagnosis of Argyll Robertson and Adie Pupils
XIV. REVIEW OF THE
Characteristic LAW pupil
Argyll Robertson OF CONTRALATERAL
Adie tonic pupil/syndrome
Size HEMISPHERIC SENSORY AND MOTOR CONNECTIONS

Laterality Usually bilateral Usually unilateral (anisocorial)
Cormiosis Mild corectasia
Pupillary outline Irregular Regular (normal circle)
1.IrisThe contralaterality law
atrophy applies to the decussations
Present Absentof all long sensory and motor
pathways:
Response One cerebral
to light Nonehemisphere
(neither directreceives
nor most
Veryof itsdirect
slow somatosensory
and consensualand visual
sensory information from the contralateral side of
consensual) the body
response; remains ormyotonically
the contralateral
con-
tracted if light is removed
half of space and in turn controls the motor activity of the contralateral side of
Response to dark No pupillodilation Slow pupillodilation; delayed constriction
the body (Louis, 1994). on re-exposure to light
2.Response
Using toa colored pencil, superimpose the pyramidal
Constricts Constrictspathway
very slowlyofandFig. 2-29 onto
remains
Fig. 2-28. Then mentally trace a nerve impulse from
accommodation a somatic
myotonically sensory
constricted receptor
after relax-
to the cerebral cortex and back to the motoneurons ationvia the pyramidal tract while
of accommodation
Response
notingtothemydriatics Poor or none
decussations. Responds normally
Other neurologic features Virtually pathognomonic of Benign disorder, often associated
3. Table 2-15 summarizessyphilis; the clinical correlates
if tabes dorsalis is of lesions
with at various
absent muscle stretch sites in the
reflexes;
motor system. present, the patient will have no dorsal column signs: Adie’s
dorsal column signs and no syndrome
muscle stretch reflexes
Sex predeliction More men than women have 70% women/30% men
BIBLIOGRAPHY . Contralaterality neurosyphilis

JS, Chung JP, Sang Ha. Isolated weakness of index finger due to small cortical infarction.
Kim
Neurology 2002;58:985–986.
LAWS OF NYSTAGMUS
3. Check the direct and consensual pupillary light reflexes.
Louis ED. Contralateral control: evolving concepts of the brain-body relationship. Neurology
1. a.Jerk nystagmus
Instruct the Pt to look at a distant point across the room. Beam a flashlight
1994;44:2398–2400.
a.slowly
Central and peripheral vestibular lesions may cause jerk nystagmus.
in from the sides to illuminate each eye separately. Observe whether
b.bothUnidirectional jerk nystagmus is always vestibular in origin.
pupils constrict promptly and equally to unilateral illumination. After
c.the Acquired bidirectional horizontal nystagmus is almost always central in origin and usually indicates a brainstem lesion or toxic/metabolic
prompt initial constriction, the pupils normally dilate slightly.
state.
i. Direct constriction of the pupil in the eye stimulated by light is called the
d.direct light reflex.
Alexander’s law: Looking in the direction of the fast phase of a jerk nystagmus increases its amplitude.
ii.e.TheJerk and pendular nystagmus may have a rotatory component.
consensual constriction of the opposite pupil when light stimulates only
2. Peripheral versus central origin of nystagmus
one eye is the consensual light reflex. Normally, the direct and consensual
a.pupillary responses are equal.
The two cardinal features that distinguish peripheral from central vestibular nystagmus are unidirectionality and inhibition of peripheral
b. Do nystagmus by visual fixation. Fixation has little effect on central nystagmus.
not shine the flashlight abruptly into the Pt’s eyes from directly in front,
b.for two reasons:nystagmus, particularly when vertical has a torsional component, but a pure vertical or pure torsional nystagmus, is always
Peripheral
central in origin.
i. The Pt will automatically look at the light and accommodate for near vision.
c.ii. The
Acquired pendular nystagmus usually is caused by brainstem or cerebellar strokes, neoplasms, or multiple sclerosis.
bright light will cause discomfort, particularly if the Pt has photopho-
d. bia,
Positional nystagmus may occur with peripheral vestibular or central lesions.
mental retardation, or dementia.
4. Fore. theAcquired peripheral nystagmus is short lasting, and central is long lasting.
swinging flashlight test, alternately swing the light from one eye to the
3. Nystagmus with posterior fossa/cerebellar disease
other and hold it on the new eye for 3- to 5-second intervals. Watch for equal
a. Cerebellar
reactions lesions Ifor
of both pupils. thedrugs
Pt hascharacteristically
an afferent defectcause bidirectional
in one optic nerve gaze-evoked
(e.g., nystagmus, deficient smooth pursuit, impaired saccadic
due to accuracy, and slow initiation of saccades.
optic neuritis), the pupils will dilate as the light swings from the normal
tob.the Visual suppression of nystagmus is minimal or absent with cerebellar as with any central nystagmus.
affected eye (Marcus-Gunn pupil or relative afferent pupillary defect)
rather than maintaining
c. Flocculus the same degree
and paraflocculus of constriction.
lesions cause downbeat nystagmus-deficient smooth pursuit, gaze-evoked nystagmus, and rebound
5. While nystagmus.
the room is dimly lit, do the ophthalmoscopic examination.
6. d. Upbeat and downbeat nystagmus, especially in the primary position, indicate a posterior fossa lesion
Whenever a question exists about the duration of an ocular finding, such as aniso-
e. orDownbeat nystagmus, characterized by slow upward drifts and fast downward phases, may indicate a foramen magnum lesion such as
coria ptosis, ask the Pt to bring in an old facial photograph.
7. Rehearse the Chiari malformation
the foregoing steps of the pupillary examination (steps V-A-3 and 4 of
thef. Standard
Torsional nystagmus may arise from medullary lesions.
NE).
4.
8. InMiscellaneous laws
recording the pupillary   reactions, many Ex’s write PERLA as shorthand for “pupils
a. and
equal The react
characteristics
to light and inof accommodation.”
the nystagmus do
Wenot differentiate
often congenital
find that PERLA nystagmus without afferent defect from nystagmus with afferent
actually
means defect.
“pupillary examination really lax.” But if the note says, “pupils 3 mm, equal,
centered, react to light and in accommodation and dilate promptly in dim light,”
b. Gaze-evoked nystagmus may occur with CNS or neuromuscular lesions that cause weakness of eye movements.
thec. reader can trust in a meticulous examination. Such a baseline note in the chart
Some types of nystagmus stay horizontal on upward gaze: congenital, peripheral vestibular, and periodic alternating.
is d.
indispensable for the acutely ill hospitalized Pt whose neurologic signs may change
Cold water irrigation of the horizontal canal of one ear reproduces the effect of an acute vestibular lesion on that side, e.g., fast phase
abruptly and for the chronic Pt whose signs may change subtly over time.
and vertigo to the opposite side, the Romberg fall, and past-pointing to the same side


amination
10. Mnemonics for remembering CrN VII functions: At first glance, mastery of CrN
VII seems hopeless. See Fig. 6-5.
Greater superficial Lesser superficial Zygomaticotemporal nerve (V2)

petrosal nerve petrosal nerve
Lacrimal nerve
Internal carotid artery and gland
Midbrain and sympathetic plexus
Deep petrosal nerve
Pterygopalatine
G1 (vidian)
Pons F1 canal and nerve
G3
Medulla
Stapedius muscle
V3
Eardrum
F2 Palate
Facial nerve: G2
Chorda tympani
Intermediate nerve Tongue
Motor root
Trunk
G4
Facial canal
F3
Lingual nerve Sublingual gland

Submandibular gland
Parotid gland
F: F1 = internal acoustic foramen. F2 = foramen ovale.
F3 = stylomastoid foramen.
G: G1 = geniculate ganglion. G2 = otic ganglion. G3 =
pterygopalatine ganglion. G4 = submandibular ganglion.
V: V2 = maxillary branch of CrN V. V3 = mandibular branch
of CrN V.

205
A B
FIGURE 6-5. Diagram Secretomotor
of the complete distributionLacrimal
(GVE) of cranialnerve
nerve VII.gland
and (Reprinted with permission
from DeMyer W. Neuroanatomy,
component2nd ed. Baltimore: Williams
Greater superficial& Wilkins, 1998.)
Brachiomotor (SVE) component petrosal nerve
G1 V2
F1
CHAPTER 6
G3
Midbrain
Geniculate a. Salvation comes from considering CrN VII as three nerves, a bran-chiomotor
ganglion (G1) Chorda tympani
nerve (Fig. 6-6A), a secretomotor G2 nerve (Fig. 6-6B), and a taste nerve
Pons F1 (Fig. 6-6C). Eardrum
Examination of the Motor Cranial Nerves V, VII, IX, X, XI, and XII
G4 Palatine nerve
Medulla Stapedius muscle Sublingual gland
F3 Submandibular
Chorda tympani C gland
Facial nerve:
Taste (SVA) component
Intermediate nerve
Motor root
Trunk G1 V2
Facial canal F1
G3
F3
Chorda tympani
G2
Eardrum
Parotid gland
Lingual
nerve G4
Sublingual gland
F3 Submandibular
Taste pathways (SVA) gland

FIGURE 6-6. Diagram of cranial nerve VII as composed of three nerves: (A) a branchiomotor nerve,
(B) a secretomotor nerve, and (C) a taste nerve. (Reprinted with permission from DeMyer W.
Neuroanatomy, 2nd ed. Baltimore: Williams & Wilkins, 1998.)
b. Remember that, in addition to moving the face, CrN VII innervates:

i. Tasting: taste from the anterior two-thirds of the tongue via the geniculate
ganglion
ii. Snotting: parasympathetic axons to the nasal mucosa via the pterygopala-
tine ganglion
iii. Tearing: parasympathetic axons to the lacrimal gland via the pterygopala-
tine ganglion
iv. Salivating: parasympathetic axons via the submandibular ganglion.

Mnemonic summary of the clinically important functions of CrN VII: It tears,
snots, tastes, salivates, moves the face, and dampens sounds.
TABLE 2-2 . Segmental Innervation of Spinal Reflexes
Deep (muscle Superficial Segment(s)

stretch) reflexes reflexes Methods of elicitation Normal results traversed
Biceps Tap biceps tendon Flexion of the forearm at the elbow C5 to C6
Triceps Tap triceps tendon Extension of the forearm at the elbow C6 to C7
Brachioradial Tap styloid process of the radius, with Flexion of the forearm at the elbow C5 to C6
forearm held in semipronation
Finger flexion Flick palmar surface of the tip Flexion of the fingers C7 to Tl
of the finger
Abdominal muscle Tap lowermost rib, tap finger Contraction of the abdominal T8 to T12
stretch reflexes placed on rectus abdominis or wall or, when the symphysis is
tap symphysis pubis tapped, adduction of the legs
Abdominal skin- Stroke skin of the upper and Contraction of the abdominal T8 to T12
muscle reflexes lower abdominal quadrants muscles and retraction of the
umbilicus to the stimulated side
Cremasteric Stroke skin of the upper Upward movement of the LI to L2
and inner thigh testicle
Adductor Tap medial condyle of the tibia Adduction of the leg L2 to L4
Quadriceps Tap tendon of the quadriceps femoris Extension of the lower leg L2 to L4
Triceps surae Tap Achilles tendon Plantar flexion of the foot L5 to S2
Plantar Stroke sole of the foot Plantar flexion of the toes S1 to S2
Anal Prick skin of the perianal region Constriction of the anal sphincter— S4 to Co1
”anal wink”
Bulbocavernous Prick skin of the glans penis Contraction of the bulbocavernosus S3 to S4
muscle and constrictor urethrae
E. Segmental composition and motor distribution of the major peripheral

nerves from the spinal plexuses
Note: Study Sections E-1 to E-3 but learn only the principal movements served
by the major peripheral nerves. This material is not programmed, but you need to
know it.
1. Motor distribution of the cervical plexus: Roots C1 to C4.

a. This plexus innervates:
i. The neck muscles that turn the head and open the jaw
ii. The trapezius muscle in conjunction with CrN XI
iii. The diaphragm
b. The phrenic nerve is the single most important nerve in the body because it
innervates the diaphragm. It arises from C3 through C5. C4 usually supplies
most of its axons. The nerve may be pre fixed (C2–C4) or post fixed (C4–C6).
2. Motor distribution of the extremity nerves of the brachial plexus (roots C5 to
T1): This plexus innervates a number of proximal muscles of the shoulder girdle
and issues five major terminal nerves for the arms, as follows:
a. The axillary or circumflex nerve (C5–C6) is the elevator nerve of the arm
because it innervates the deltoid muscle.
b. The musculocutaneous nerve (C5–C7) is the flexor nerve of the arm. It flexes the
brachium on the shoulder and the forearm on the brachium. The only arm flexor
muscle not innervated by the musculocutaneous nerve is the brachioradialis
muscle, which is innervated anomalously by the radial nerve, an extensor nerve.
c. The radial nerve (C5–C8) is the extensor nerve of the arm (elbow, wrist, and
fingers), but it does not extend the distal phalanges. It also supplies the brachio-
radialis, which flexes the elbow.

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DEMYER’S

TECHNIQUE OF THE NEUROLOGIC EXAMINATION 1

MENTAL STATUS EXAM and HIGHER COGNITIVE FUNCTIONS B. Cover-Uncover Test

• Alterations of level of consciousness

II. CN II OPTIC NERVE MENTAL STATUS EXAMINATION

MEDRANO NEURO NOTES 1

Hallucination : false sensory perception not based on a natural

2 MEDRANO NEURO NOTES

D e M yer ’s The Neurologic Examination

MEDRANO NEURO NOTES 3

Examination of the Face and Head

Examination of the Face and Head

increased intracranial pressure? _______________.

MRI is almost always superior to CT in diagnosing intracranial lesions, except in

BIBLIOGRAPHY . Abnormalities of Head Size and Brain Size

IX. THE GENERAL RULES FOR THE NEUROLOGIC

A. Operational rules for the neurologic examination

SENSORY EXAMINATION (Tertiary Neuron) parietal lobe

MEDRANO NEURO NOTES 5

D e M yer ’s The Neurologic Examination

INCLUDES the angle of the SPARES the angle of the

• C5, C6, C7, C8 and T1: arms 3

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EXAMINATION OF THE SOMATIC MOTOR SYSTEM MOTOR STRENGTH TESTING

Fasciculation Giant polyphasic The total number of the units is

8 MEDRANO NEURO NOTES

Middle crus of cerebri Gives rise to RUBROSPINAL TRACT fibers that

MEDRANO NEURO NOTES 9

• The examiner then releases the phalanx suddenly, allowing it

strikes the Achilles’ tendon

• Change the mechanical tension on the muscle

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• Use a broken tongue blade, key, or butt of a reflex hammer

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MEDRANO NEURO NOTES 13

time, do not present the stimulus (done as safeguard for

PAPILLEDEMA midline, about 50 cm away, at station 1. Request the patient to

Retinal patient’s nose. Observe for convergence and the accompanying

Examination of the Peripheral Ocular Motor System

Examination of the Central Ocular Motor Systems

Motor Part of CN V Conductive Hearing Loss – impedance in the conduction of sound

o Diagnosis of MG: Antibodies against AchR or IgG

o Chew, yawn, swallow reflexively but cannot do these

Motor cortex Thalamocortical Clinical findings after destructive lesions

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Preparation fo r the Tex t

WOF: Hypoxia, Hypotension, Hypoglycemia, Hyperthermia, and

VI. SELECT THE SAFEST AND MOST CRITICAL TESTS TO

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A Brief Review of Clinical Neuroanatomy

Size HEMISPHERIC SENSORY AND MOTOR CONNECTIONS

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Greater superficial Lesser superficial Zygomaticotemporal nerve (V2)

Deep petrosal nerve

Lingual nerve Sublingual gland

b. Remember that, in addition to moving the face, CrN VII innervates:

MEDRANO NEURO NOTES 21

TABLE 2-2 . Segmental Innervation of Spinal Reflexes

Deep (muscle Superficial Segment(s)

E. Segmental composition and motor distribution of the major peripheral

1. Motor distribution of the cervical plexus: Roots C1 to C4.

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