N E U R O L O G I C A L E X A M I N A T I O N

2013
Page 1 of 16


E XAMI NAT I ON o f C E RE B E L L UM












































FUNCTIONS OF THE CEREBELLUM

I. FLOCCULONODULAR LOBE
Modulates equilibration and orientation of head and eye
movements
Has connection with vestibular nuclei
Lesions of flocculo nodular node produce:
1. TRUNCAL DYSTAXIA
Can sit but, unable to stand and walk
Cant ambulate even without paralysis
2. NYSTAGMUS
Jerky movements of the eye (persistent)
Normal: initially jerky but will disappear for a while
Caudal vermis syndrome
Very common in pediatrics
Neoplasm
Medulloblastoma, ependymoma, astrocytoma

II. ANTERIOR LOBE (ROSTRAL VERMIS)
Concerned with posture gait and truncal tone (stand & walk)
Lesions
Unsteady walking
GAIT ataxia (tutummba-tumba)
Elicited by doing tandem walk (like crossing in a straight
string)
Hypotonia
Affected by Alcoholism and nutritional status
Vit. E for cerebellum

III. POSTER LOBE HEMISPHERE
For coordination of skilled action
Lesions
LIMB ataxia
Dysnetria
dysmetria failure to control, or meter the muscular
contraction that set the distance

Tremor
Dyssynergia
Affected by Infarct, hemorrhage, neoplasm, abscess, trauma


EFFECT OF CEREBELLAR LESION ON SPEECH

Due to lesion on VERMIS (midline of cerebellum)
Dysarthria consists of:
Slowness, slurring of words
Scnanning speech
Dysarthria
Difficulty in production of sound
Voice varies from a low volume to a high volume
Failure to meter and modulate the strength of muscular contraction that
produce the speech sounds
Nystagmus
Easiest to examine
Dysmetria of saccades
Cant follow movement without moving the head
Jerky pursuits
Slowness in initiating eye movements


CLINICAL TESTS FOR CEREBELLAR FUNCTION

I. TESTS FOR DYSTAXIA OF STATION & GAIT
Swaying when standing even with eyes open
Broad based gait and stance
Impaired tandem walking


II. TESTS FOR ARM DYSTAXIA
Postural tremor
tremor even without fine movements
Intention tremor
tremor while doing fine movements
Dysmetria on finger to nose test
Undershoot or overshoots target
DYSDIADOCHOKINESIA
Dystaxia dysmetria of rapid alternation movement
Test performed:
1. Thigh patting test
Patting the thigh by pronation and supination
Must elicit an audible sound with each pat
2. Finger tapping test

III. OVERSHOOTING AND CHECKING TEST OF THE ARMS

A. WRIST TAPPING TEST
Patient stand with eyes closed
Patient holds the arms extended out front
Examiner strikes back of the patients wrist with a sharp blow
strong enough to displace arm
Normal/ negative: patient arm must bounce back
Positive: arm dont bounce back to original place

B. ARM PULLING TEST
Examiner pulls hard against the patients flexed arm
Examiner suddenly releases the patients arm
Positive (cerebellar patient)
failure to check arms flight
Masusuntok ang sariling face


IV. TESTS FOR LEG DYSTAXIA

A. HEEL TO SHIN TEST
Patient supine or sitting
Patient to place one heel precisely on the opposite knee
Patient run the heel in a straight line precisely down to shin
Normal: precise movements without awkwardness

B. HEEL TAPPING TEST
Patient to place one heel over the other shin and tap the shin
with heel as rapidly as possible on one spot
Normal: rapid alternating movements


N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 2 of 16



OTHER MANIFESTATION OF CEREBELLAR DYSFUNCTION

I. DECOMPOSITION OF MOVEMENT
Movement #1 Lifts arm at the level of the nose
Movement #2 Brings fingertip to the nose
Normal: movement should be smooth and not robotic like

II. HYPOTONIA
Floppy posture
Rag doll gait
Pendulous MSRs

III. MILD ASTHENIA


SUMMARY

Observe spontaneous activity
gait speech
eyes extremity movements
Formal tests
Eye movements
Sustained posture
Upright stance
Arm suspension

Gait
Free walking
tandem walk
Finger to nose test
Alternating movements
Overshooting
Heel to shin, heel tapping
Hypotonia
Passive movement
Pendulous reflexes




E XAMI NAT I ON o f RE F L E X E S

PHYSIOLOGY OF THE MSR (MUSCLE STRETCH REFLEX)

Muscle contractile engines
Stretch causes contraction of the entire receptors muscle spindles
Muscle spindles
Made up of small muscle fibers (intrafusal)
Has afferent and efferent axons that maintain constant tension
Skeletal muscles
Extrafusal muscle fibers
Only have efferent axons























EFFECTS OF THE STRETCH ON THE MUSCLE SPINDLES

The muscle fibers of the spindle originate and insert into the perimysial
connective tissue, which is connected with the tendon
Extension of the joint pulls on the perimysium and stretched the muscle
spindle
Flexion of the joint relaxation of the muscle spindles
To maintain stretch sensitivity:
Joint EXTENSION (JE) muscle spindle LENGTHENS
Joint FLEXION (JE) muscle spindle CONTRACTS
REFLEXES

I. DEEP TENDON REFLEXES (MSR)

Upper extremities
Biceps reflex (C5, C6)
Triceps reflex (C6-C8)

Lower extremities
quadriceps femoris reflex/KNEE JERK/patellar reflex
Femoral nerve (L2-L4)
triceps surae reflex (ANKLE JERK)
Achilles reflex
Tibial nerve (L5-S2)

INTERPRETING MSR
Wide variation of normal
Asymmetry most important
Look for accompanying abnormalities





























TECHNIQUE ELICITING MSR
Holding the percussion hammer and delivering the blow
1. Taylor tomahawk hammer
Short, convex side
2. Hammer swinging
Have the patient sit or recline
Part to be tested places at rest
Strike a crisp blow
Try reinforcement

LESIONS AT VARIOUS SITES OF THE REFLEX ARC
Paralysis
LMN lesions
myopathies
Denervation atrophy
LMN lesions
Loss of sensation
Dorsal root (of spinal cord) lesion
Absence of MSR
Dorsal root lesion
LMN lesion
Myopathy

II. SUPERFICIAL REFLEXES
Types:
1) Abdominal reflex
Upper quadrants (T8-T9)
Lower quadrants (T11-T12)
Beevors sign umbilical migration
Scrape the skin toward the umbilicus
movement of the umbilicus toward the direction of the
stimuli

2) Cremasteric reflex (L1-L2)
Scratching the skin of the medial thigh from above
downwards

G R A D I N G O F MS R
G R A D E I NTERPRETATI ON
0 Areflexia
1 Hyporeflexia
2 Normal
3 Hyperreflexia
4 clonus
N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 3 of 16



3) Anal pucker reflex (S2-S5)

Abnormalities
Abdominal reflex:
Absent in:
infants < 1 y/o
deep sleep (coma, anesthesia)
Increased in:
Parkinsonism
Tension
Absent reflex in:
Abnormality in spinal cord or cortex

















































































































PATELLAR REFLEX
FEMORAL NERVE (L2-L4)
ACHILLES REFLEX TIBIAL
NERVE L5 S2
movement of the umbilicus toward the direction of the stimuli
SUPERFICIAL ABDOMINAL REFLEX
Biceps reflex (C5, C6)
patient lying down
Triceps reflex (C6-C8)
N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 4 of 16



PATHOLOGICAL REFLEXES

I. PYRAMIDAL TRACT RESPONSES
Hoffmans Babinski reflex and its variations
Chaddocks
Oppenheim
Gordons

II. NON LOCALIZING PRIMITIVE REFLEXES
Palmomental reflex
Snout reflex
Grasp reflex
Suck reflex





































PRIMITIVE REFLEXES

1) Palmomental reflex
Stroke proximodistally over patients thenar eminence

2) Snout reflex
With patients eye closed
Tap phitrum several times at medium rate

3) Grasp reflex
Stroke patients palm from the hypothenar eminence toward the
junction of the patients thumb and index finger

4) Suck reflex
With patients eye closed
Stroke the patients lip from the center of the crevice to the
sides
















E XAMI NAT I ON o f MOT OR S Y S T E M

CORTICOBULBAR TRACT (CBT)
Cerebrm to brainstem
Affect brainstem, thus also the cranial nerves
CN VIII thus no fibers coming from the CBT

LATERAL CORTICOSPINAL TRACT (LCST)
to localize & lateralize
terminate in the lateral folliculus of spinal cord
decussate in the medulla
above the decussation lesion contralateral
below the decussation lesion lateral

UPPER MOTOR NEURON (UMN)
Corticospinal tract (CST) lesion
Cerebrum to lateral folliculus (level of ventral horn cells)

LOWER MOTOR NEURON (LMN)
Ventral horn cells to muscles

INTERNAL CAPSULE
Very important because the fibers are very close to each other,
Thus, if there is a lesion in the internal capsule, the
manifestations are significant

DENSE HEMIPARESIS
Zero strength both upper and lower extremities
Due to lesion in internal capsule

BASAL GANGLIA (globus pallidus + putamen)
Most common location of cerebral hemorrhages
Greater significant manifestation
Very hard to recover (0-3); normal = 5


EXAMINATION OF THE MOTOR FUNCTION
1) Stance or posture gait
Ask patient to stand & walk
2) Strength
3) Tone
4) Volume or size
Use tape measure to find signs of muscle atrophy
5) Coordinated performance of motor acts
6) Involuntary movements


SENSORY & LOWER MOTOR GAIT DISORDERS

A. STEPPAGE GAIT
Excessive flexion of hips 7 knee with every step
Parang umaakyat ng stairs kahit hindi naman

B. WADDLING GAIT
Weakness if hip muscles cause drop of hip & trunk tilting to the side
opposite foot placement
Kumekendeng kendeng

C. VESTIBULAR ATAXIA & VISUAL ATAXIA
Broad base of support
Example, drunken gait

D. VEST ATAXIA
Veer or fall to side of lesion (ipsilateral

E. VISUAL ATAXIA
Tentative steps
Foot not certain where to put itself





TYPES OF PARALYSIS/WEAKNESS

A. MONOPLEGIA
Weakness or paralysis of all the muscles of one leg or arm
Term should not be applied to paralysis of isolated muscles or groups
of muscles supplied by a single nerve or motor root
Evidence of
lesion in
pyramidal
system or
CST
N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 5 of 16



B. HEMIPLEGIA
The commonest form of paralysis or weakness seen
Involves the arm, leg and sometimes the face on one side of the body
(half of the body is weak)
Attributable to a lesion of the corticospinal system on the side
opposite to the lesion (contralateral)
Spinal nerves or plexus problems

C. PARAPLEGIA
Indicates weakness or paralysis of both legs.
Level of thoracic cord injury
Polyneuropathy
Common cause of neuropathy is DM
Most often the result of disease of:
thoracic spinal cord
cauda equine (cauda equine syndrome)
peripheral nerves
both medial frontal cortices (rarely)
start of brainstem infacrtion paraplegia (sudden) then hemiplegia
because basilar artery is affected

D. QUADRIPLEGIA (tetraplegia)
Denotes weakness or paralysis of all gour exteremities
May result from the disease of:
LMN
Peripheral nerves
Muscles
Myoneural junctions
Gray matter of the spinal cord
Upper motor neuron bilaterally in:
Cervical cord
e.g. Whiplash incidence of cervical vertebra))
Brainstem
cerebrum
forms:
DIPLEGIA
special form of quadriplegia
legs are affected more than arms

TRIPLEGIA
Occurs most often as a transitional condition in the
development of or partial recovery from tetraplegia


GAIT DISORDERS OF CENTRAL ORIGIN

A. SPASTIC GAIT
Base of support is narrow
Leg externally rotated at the hip
Knee extended and stiff
Foot flantar flexed
Common in STROKE patient
tone of extensors of leg & flexor of upper extremities

B. CEREBELLAR GAIT
Similar to gait of vestibular ataxia but also,
Have irregular timing, cadence of leg movement

C. PARKINSONIAN GAIT
Rigid trunk
Slow & short steps
Knee flexed
Extrapyramidal gait
Involve basal ganglia
Lakad hukluban



MUSCLE STRENGTH (BMRC)












5= parang naghihilaan ang patient at examiner
2 = cant move against gravity (hindi maitaas ang arm pataas)
DIFFERENCES BETWEEN UMN & LMN PARALYSIS




MUSCLE TONE RESISTANCE UPON PASSIVE FLEXION

H Y P E R T O N I C
RI GI DI TY SPASTI CI TY
resistance upon passive flexion
throughout the range of motion
Matigas/mahirap
imanipulate all throughout
Initial FREE interval
Tendon reflexes are NORMAL MSR
Limb DOES NOT resume its
original position
Original position RESTORED
+3 or +4 +2


CLINICAL DIFFERENCE BETWEEN CORTICOSPINAL & PYRAMIDAL
SYNDROMES






UMN
(supranuclear paralysis)
LMN
(nuclear-infranuclear paralysis)
Muscle affected in groups
Never individual muscles
Individual muscles may be
affected
Atrophy slight & due to disuse
(comes later)
Atrophy pronounced
Up to 70% of total bulk
Spasticity with hyperactivity of
the tendon reflexes & extensor
plantar reflex ( BABINSKI
SIGN)
Flaccidity & hypotonia of
affected muscles with loss of
tendon reflexes (NEGATIVE
BABINSKI)
Plantar flex if present, is of
normal flexor type
Fascicular twitches ABSENT
Fascicular twitches may be
PRESENT
NORMAL nerve conduction
studies
NO denervation
potentials in EMG
ABNORMAL nerve conduction
studies
Denervation potentials in
EMG:
Fibrillations
Fasciculations
sharp waves
MUSCLE GRADE DESCRIPTION
0/5 No response
1/5 Trace movements
2/5 Movement without gravity
3/5 Movement against gravity
4/5 Movement against slight resistance
5/5 normal
CORTICOSPINAL EXTRAPYRAMIDAL
Character of the
alteration of
muscle tone

Spasticity
Clasp-knife
effect
Rigidity
Plastic, equal throughout
passive movement

Cogwheel rigidity
Intermittent movement
Distribution of
hypertonus
Flexor of arms
Extensors of legs
Generalized but predominates in
flexors of limbs and of trunk (seen in
parkinsonism)
Involuntary
movements
Absent

Presence of:
Tremor
Chorea
Athetosis
Dystonia

Tendon reflexes Normal or slightly
Babinski sign Present Absent
Paralysis of
voluntary
movement
Present Absent or slight
N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 6 of 16



MUSCLE GROUPS & SEGMENTS TESTED

SEGMENTAL LEVEL MUSCLE GROUP
C2 C3 Flexors & extensors of neck
C4 Diaphragm
C5 Deltoid arm abductor
C6 Biceps arm flexor
C7 Triceps arm extensor
C7 C8 Wrist flexor & extensor
C8 T1 Intrinsic hand muscles
T1 T8 Chest expansion
T9 T10 Upper abdomen
T11 T12 Lower abdomen
L1 L2 Thigh adductor & hip flexor
L3 L4 Quadriceps leg extensor
L5 S1 Hamstring, leg foot movements




































































TECHNIQUE OF ELICITIN MSR

1) Holding the percussion hammer & delivering the blow
a. Taylor tomahawk hammer short, convex sides
b. Hammer swinging

2) Have the patient sit or recline
3) Strike a crisp blow
4) Try reinforcement


SAMPLE CASES

1) CASE #1
RIGHT hemiplegia
babinski reflex

LEFT side cerebral lesion
UMN paralysis

2) CASE #2
3) Crossed motor/sensory syndrome
IPSILATERAL cranial nerve deficit RIGHT brainstem lesion
CONTRALATERAL hemiparesis Babinski
IPSILATERAL limb ataxia
Internuclear opthalmoplegia
Median longitudinal fasciculus syndrome



cerebral lesion (CONTRALATERAL) CT scan





Brainstem lesion (IPSILATERAL) MRI




MOTOR SYSTEM
UMN
Spinal cord
Definite level of sensory deficit
Autonomic dysfunction (bladder & bowel)
Bilateral movement

SPINARL CORD LESION
Numbness CONTRALATERAL to lesion
Weakness IPSILATERAL to lesion
3) CASE #3
LMN
Anterior horn cells (spinal cord)
Peripheral nerves
NMJ
Muscle

peripheral nerve problem
distal motor & sensory deficit



muscle problem
proximal motor & sensory deficit



















N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 7 of 16


EXAMI NATI ON of the SENSORY SYSTEM

Lateral Spinothalamic tract (LST)
Pain & temperature (trunk and extremities)
CN VII for pain and temp of Face
branches travel for a distance of one or two segments of the
spinal cord andform the posterolateral tract of Lissauer
axons of the second-order neurons now cross obliquely to the
opposite side in theanterior gray and white commissures within
one spinal segment of the cord,ascending in the contralateral
white column as the lateral spinothalamic tract
upper cervical segments of the cord:
sacral fibers lateral
cervical segments medial
contralateral if the lesion is below the decussation
thalamus - 3
rd
order neuron
all senses reach the thalamus EXCEPT olfaction

Anterior Spinothalamic Tract
Light (crude) touch & pressure

Lateral Corticospinal tract
Decussate at medulla
Example: Lesion from outside of the cord (UMN type lesion)
Mass compressing the cord from outside to inside

1
st
: ipsilateral leg weakness & numbness

Last: upper extremities & neck

Extramedullary lesion if outside the cord type of lesion
Neurological deficit: from foot neck

Example: lesion in ventricles of brain
Descending pattern: upper ex. lower ex.
Contralateral Weakness & numbness

Example: spinal edema
Bigger lesion
Two (2) sides of the spinal cord are affected

Sensory
Lesion in cervical vertebra
Quadriplegia
Highest lesion of quadriplegia is the cervical
vertebra
Extra or intramedullary lesion
To spinal spinal cord always ipsilateral
Intramedullary hands first
Extramedullary foot first


SENSORY MODALITIES

1. Light touch
2. Temperature discrimination
3. Pain perception
4. Vibration perception
5. Position sense
6. Astereognosis
7. Romberg
8. Directional scratch test


GENERAL PRINCIPLES
If no sensory complaint, test only vibration/position sense in the fingers toes
and pinprick over the face, trunk, and extremities in the symmetric areas
PINPRICK
Use to confirm if the patients sensory loss is true
Should be symmetrical
Done if no sensory complaint
Done on both upper & lower extremities
3 tusok, 2 galaw galaw daliri

Proceed exam from are of reduced sensation to normal sensation
Make patient familiar with stimulus
Cotton stimulus: mapurol
Aspile stimulus: matulis
Take note: eyes should be closed to concentrate on the stimulus

Weakness (anterior horn of spinal cord)
SACRAL SPARRING
Because the farthest location in spinal cord is sacrum
Patient numb and weak in upper extremities & trunk, BUT anal
wink is intact thus sacral sparring
DEFINITION OF PROPRIOCEPTION
Sense of movement, of position and of skeletomuscular tension provided by
deep mechanical receptors in muscle joints, connective tissue & the
vestibular system
Along with touch vision & touch provides with a sense of equilibrium &
verticality
Position sense & vibration sense
Rombergs


DORSALCOLUMNS MEDIATED SENSATION
Sense of position or posture
Sense of movement of joints and body (KINESTHESIA) & of something moving
on the skin
Vibration (PALLESTHESIA)
Two point discrimination
Sense of pressure
Texture
Touch localization (TOPOGNOSIA)
Sense of weight (BARESTHESIA)
GRAPHESTHESIA sinisulat sa balat tapos alam kung ano yung sinulat
STEREOGNOSIS identifying object by touch


TESTING SENSORY SYSTEM:

A. TECHNIQUES FOR TESTING DIGITAL POSITION TEST
Graspthe digit by its side & wiggle it up and down, stopping
randomly in one direction or the other
Patient eyes closed
Hold laterally on the distal interphalangeal joint (IPJ)
Signal patient if start
NORMAL patient know if the finger is shifter upward or
Downward
In foot, toes is tested instead
Separate the digit being tested so that you do not touch the other
digits
Use the 4
th
digit (ring finger) in testing position sense
Work distally then proximally

B. TESTING POSITION SENSE BY THE SWAYING (ROMBERG) TEST
Ask the patient to stand with the feet together, note whether the
patient sways
Then ask the patient to close the eyes and note wether the swaying
increases
Stand behind the patient with arms held up ready to cath the patient
(but dont touch the patient)
Narrow the base & increasing the stress on balance
Removing visual clues for balance
Open eyes feet closed together observe swaying
Closed eyes (no visual clues) observe swaying
Compare the swaying with eyes open and closed
POSTIVE Romberg swaying more prominent at CLOSED eyes

C. SENSORY VS. CEREBELLAR ATAXIA

SENSORY DYSTAXIA CEREBELLAR DYSTAXIA
Loss of position & vibration sense
Areflexia
Reflex is part of sensory
because of 1 receptor in
spinal cord
Hypotonia
Dystaxia (milder ataxia) much
worse with eyes closed
Nystagmus
Hypotonia
Overshooting on release


D. TESTING FOR LOSS OF VIBRATION SENSE (PALLANESTHESIA)
Do test with the patient with eyes closed
Holding a tuning fork (128 or 256 cps or cycles per second) by the
round shaft & strike the tines a crisp blow against the ulnar side of
the palm to set the for vibrating
Apply free end of the shaft to the nails or just proximal to the
nailbed
Place your finger against patients finger pad & serve as control
Check by alternating presence & absence of vibration

E. TESTING OF TACTILE SENSATION
Usually done with wisp of cotton
Von frey hair (bend hair)
Cornified areas vs. noncornified areas
Moving contractual stimulus vs. stationary

SUPERFICIAL
DEEP SENSORY
N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 8 of 16



F. TESTING OF PAIN PERCEPTION
Usually assessed by pinprick
Delivered at about one per second
Pinwheel used to apply constant pressure
Small differences in intensity can be discounted


ORIGIN OF ABERRANT SENSATIONS


NOMENCLATURE IN THE DESCRIPTION OF PAIN & ABNORMAL
SENSATION

DYSESTHESIA
Any abnormal sensation described as unpleasant by the patient (di
mapakali, not tolerated)
Opposite of parasthesia

HYPERALGESIA
Exaggerated pain response from a normally painful stimulus
Usually includes aspects of summation with repeated stimulus of constant
intensity & aftersensation
Opposite of allodynia

HYPERPATHIA
Abnormally painful & exaggerated perception of pain from normally non
painful stimulus
Related to hyperalgesia

HYPERESTHESIA (HYPESTHESIA)
Exaggerated perception of touch stimulus
Example: touch with cotton exaggerated response

ALLODYNIA
Abnormal perception of pain from normally nonpainful mechanical or
thermal stimulus
Usually has elements of delay in perception & aftersenation
Example: konting kalabit lang exaggerated response

HYPOALGESIA (HYPALGESIA)
sensitivity & threshold to painful stimuli

ANESTHESIA
perception of all sensation (mainly TOUCH)

ANALGESIA
perception of pain stimulus

PARESTHESIA
Mainly spontaeneous abnormal sensation that is not unpleasant
Usually described as pins & needles

CAUSALGIA
Burning pain in the distribution of one or more peripheral nerves

NEUOPATHIC PAIN
Phantom limb syndrome


SUMMARY OF EXAMINATION OF SOMATIC SENSORY SYSTEM

A. Superficail Modalities
Light touch
pain or temperature
discrimination over hands, trunk & feet

B. Deep Sensory Modalities
Position sense
Vibration sense
Astereognosis
Directional scratch test
Ronbergs

C. Determine The Distribution Pattern Of Any Sensory Loss (dermatome)






SYMPTOMS STRUCTURES AFFECTED
Paresthesia, tingling, buzzing large fibers (in nerve or posterior columns)
Burning, heat, cold Small fibers
Pricking pain Combined small & large fiber
Pseudocramp
A type of parethesia
Probably related to large-fiber dysfunction
Band tightness
(parang may nakatali sa kamay)
Lemniscal system dysfunction
Lancinating pain Small-fiber neuropathy & radiculopathy
Hyperalgesia Partial peripheral nerve damage
N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 9 of 16


PAIN & TEMPERATURE PATHWAYS
DISCRIMINATIVE TOUCH, VIBRATORY SENSE, AND CONSCIOUS
MUSCLE JOINT SENSE PATHWAYS
LIGHT TOUCH & PRESSURE PATHWAYS
Figure 2 SENSORY HOMONCULUS
Figure 1. spinal cord showing the segmental arrangement of the
nerve fibers within major tracts. On the left side are indicated the
sendory modalities that appear to be mediated by two main
ascending pathways. C, cervical; L, lumbar; Th, thoracic;










































































































N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 10 of 16




































































The sites of lesions of the characteristic spinal cord sensory syndromes
Shaded areas indicated




































































































N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 11 of 16



EXAMI NATI ON of CEREBRAL FUNCTI ONS


































































































MANIFESTATIONS OF CEREBRAL DYSFUNCTION

1. Disturbed Consciousness
2. Intellectual Deterioration
3. Memory Impairment
4. Dysphasia
5. Dyspraxia
6. Dysgraphia
7. Dyslexia
8. Dyscalculia
9. Seizures
10. Motor/Sensory Deficit
11. Hemianopia
12. Movement Disorders


EVALUATION OF MENTAL AND RELATED FUNCTION

LEVEL OF CONSCIOUSNESS
INTELLECTUAL PERFORMANCE
1. coherence, attention
1. orientation
2. memory
3. fund of information
4. insight ,judgment and planning
5. calculation

EMOTIONAL REACTION
THOUGHT PROCESSES
COMPLEX SENSORY PERCEPTION
PERFORMANCE OF COMPLEX ACTS
SPEECH
HANDEDNESS


DEFINITION OF SENSORIUM AND CONSCIOUSNESS














SUMMARY OF EXAMINATION OF SOMATIC SENSORY SYSTEM

Registers Current Internal (Anxiety, Hunger) And External (Fire, Meeting
Another Person) Contigencies

Relates Current Internal And External Stimuli To Our Memories And To Our
Future Hopes And Desires

Invests The Streams Of Afferent Stimuli With Emotion, Determines Their
Significance, And Assigns Priority That Results In Neglect Or Attention

Proposes Various Actions And Their Consequences

Directs The Motor System In The Actual Behaviors That Achieve Personal
Survival And Satisfaction

Allows Us To Experience Life As A Conscious Process With A Past, Present,
And Future And To Respond Appropriately
N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 12 of 16



LEVELS OF UNCONSCIOUSNESS

CONFUSION
Inability To Maintain A Coherent Stream Of Thought Or Action
Cerebral hemisphere for focus and concentration toward the most
important sensory stimuli

ATTENTION
Ability To Sort Out And Stratify The Many Sensory Inputs And
Potential Motor Outputs So That A Particular Thought Or Action
May Be Completed In An Organized And Logical Fashion

Metabolic/Toxic Derangement
Example: creatinine levels causes confusion

DELIRIUM
Confusional State Plus Excess Sympathetic Activity

DROWSINESS
Ready Arousal, Ability To Respond Verbally, And Fending- Off
Ordinary verbal stimuli can wake the patient up
If left alone, will sleep
Still can be able to respond to stimulus

Movements Induced By Verbal Stimuli

STUPOR
Incomplete Arousal To Noxious Stimuli,No Response To Verbal
Commands, Motor Response Purposeful Fending Off Response
Needs painful or noxious stimuli to wake the patient up
Example: substernal pain midline, thus can serve both sides
Suborbital nerve

LIGHT COMA
Primitive And Disorganized Motor Responses To Noxious Stimuli,
No Response To Attempts At Arousal
Worse than stupor
No motor response (ex. Reflex)

DEEP COMA
Absence Of Response To Noxious Stimuli
Absence even with the deepest stimuli

GLASGOW COMA SCALE






















MECHANISMS OF LOSS OF CONSCIOUSNESS

Most common is ICP which come from the following:

1. Supratentorial Mass Lesions Which Compress Deep Midline Structures
2. Infratentorial Lesions Which Damage Brain Stem Core
Example: infarct or hematoma in brainstem or cerebellum

reticular activating system

3. Metabolic Disorders That Disrupt Cortical Function
Example: blood loss to brain both cereberal hemisphere MUST be
affected to elicit loss of conscousness
4. Psychiatric Disorders
Good diferential diagnostics
CATEGORIES OF COGNITION TESTED IN MENTAL STATUS
EXAMINATION

ORIENTATION
Time, place, person
If for all three, oriented to three spheres
Example: if only 1 out of 3 is oriented to place
Most common or 1
st
disorientation - TIME, 2
nd
place, 3
rd
person

ATTENTION
ask patient to count backwards from 100 by 7. Stop after 5 correct
answers

REGISTRATION
name 3 objects
then ask patient to repeat the 3 objects

COMPLEX TASK
give patient 3 step command

NAMING
REPITITION
ask patient to repeat a sentence
naming & registration is usually done together

RECALL
of the object previously registered

READING
follow written command

WRITING
ask patient to write a simple sentence

COPYING
ask patient to copy overlapping shape

GENERAL INFORMATION
You must also know the answers

ABSTARACT THINKING
Example: What Is The Difference Between A Wheel & Tomato?
Similarities/Dissimilarities/Proverbs
What do you mean by time is gold?

INSIGHT
The Ability To See Into A Situation, Esp. Into Oneself
describe their understanding of their illness
describe how they see themselves
example: ano ang diperensya mo?

JUDGMENT what if
Neutral questions
Example: there is a tree, what will you do?




AGNOSI A


DEFINITION
The Inability To Understand The Meaning, Import, Or Symbolic Significance
Of Ordinary Sensory Stimuli Even Though The Sensory Pathways And
Sensorium Are Relatively Intact
Affects Various Sensory Modality
TYPES OF AGNOSIA

AGRAPHOGNOSIA (AGRAPHESTHESIA)
with patients eyes closed, trace letters or numbers between 1 and ten
on the skin of the palm or fingertips of the patient
use any blunt tip
CONTRALATERAL PARIETAL LOBE
Example: cant recognize written in the R hand, problem is L hemisphere
GRAPHANESTHESIA Destroyed Sensory Pathways

PROSOPAGNOSIA
inability to recognize faces in person or in photos, owned objects
Lesion of RIGHT OR BILATERAL inferomedial temporo- occipital region
Associated with color agnosia





N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 13 of 16



AUTOTOPAGNOSIA (ASOMATOGNOSIA)
Can be evaluated in ages 4yrs up
Inability to locate, identify and orient ones body parts (body scheme
agnosia)
a) tactile finger agnosia and R-L disorientation
identify fingers, assign numbers
touch your right hand to your left ear
touch my right shoulder with your left hand (more
complex)
b) place a part in one position and ask patient to duplicate the
position with eyes closed
example: lift the patients hand then the patient should also
lift his hand alone
LEFT ANGULAR GYRUS LESION

ANOSOGNOSIA
Inability to be aware of his own bodily defect
Ask patient with left hemiplegia if there is something wrong with left
arm. Patient says no.
Patient may grasp examiners hand
RIGHT PARIETAL LESIONS (classic)
If the problem is on the R brain, you test patient for L hemiplegia


OT HE R CE REBRAL SYMPT OMS

LEFT- SIDE HEMISPATIAL INATTENTION
Seen with right parietal lesions
Unilateral neglect;
Aask patient to draw symmetrical figures patient can only draw the
left half

INATTENTION TO DOUBLE SIMULTANEOUS CUTANEOUS STIMULI
Sensory extinction,sensory inattention
Touch patient on one or both sides
RIGHT PARIETAL (COMMON)/LEFT PARIETAL LESIONS
How many kalabit? If simulataneously done, patient can only feel one
kalabit

DYSLEXIA AND ALEXIA
Word agnosia and word blindness
LEFT PARIETAL LESIONS

**Dscs right parietal lesion patient inattends to the left side


APRAXI A

DEFINITION
Inability To Perform A Voluntary Act Even Though The Motor System,
Sensory System And Mental Status Are Intact
Patient Comprehends And Attempts To Cooperate
Patients Previous Skills Were Sufficient To Perform The Act
TESTING THE APRAXIAS

1. BUCCO- FACIAL APRAXIA
Verbally Instruct Patient To Do The Different Tongue Movements
Ask Patient To Act As If Blowing Out A Match Or Sucking A Straw
If Verbal Instruction Fails Try Miming

2. IDEOMOTOR APRAXIA
Ask Patient To Demonstrate Sequential Acts
EXAMPLE: give patient comb then ask patient to demonstate how to
comb

3. CONSTRUCTIONAL APRAXIAS
Draw Geometric Figures
EXAPMLE: ask patient to drawk 3 PM clock

4. DRESSING APRAXIA
if the patient cant dress properly (baliktad)

5. GAIT APRAXIA
No hemiparesis (intact motor) BUT CANT walk

3,4 SEEN COMMONLY IN RIGHT PARIETAL LESIONS
COMMUNI CATI ON

DEFINITION
Speaking And Writing
Reading And Listening
Exclamatory Speech- Emotional State At Particular Moments
Declarative And Propositional Speech
Declarative: THE UMBRELLA IS RED
Propositional: I WANT A RED UMBRELLA

Aphasics Retain Exclamatory Speech And Also Singing And Humming
Can say *SHIT!!*, but the rest of the speech is gone

Left Hemisphere Invests Words With Meaning
Right Hemisphere Prosody Of Speech (Intonation,Melody,Pauses,
Phrasing)

**EXCLAMATORY SPEECH EMOTIONAL STATE OF THE MOMENT

DISORDERS OF SPEECH

THREE (3) GROUPS OF DISORDERS OF SPEECH
1. voice
APHONIA or DYSPHONIA
alteration or loss of voice because of a disorder of the larynx
or its innervation

2. Normal way of production of sound
DYSARTHRIA and ANARTHRIA
A defect in articulation with intact mental functions and
comprehension of spoken and written language and normal
syntax (grammatical construction of sentences).
pure motor disorder of the muscles of articulation and may
be a result of accid or spastic paralysis, rigidity, repetitive
spasms (stuttering), or ataxia

3. Normal way of comprehending words
APHASIA or DYSPHASIA
Loss or impairment of the production or comprehension of
spoken or written language because of an acquired lesion of
the brain


















APHAS I A

DEFINITION

Inability To Understand Or Express Words As Symbols For Communication,
Even Though The Primary Sensorimotor Pathways To Receive And Express
Language And Mental Status Are Relatively Intact
Dysphonia, Dysarthria, Dysprosody, Dysphasia

CLASSIFICATION OF APHASIAS













N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 14 of 16


















TYPE OF APHASIA AND LESION

1. BROCAS APHASIA
LEFT POSTERIOR INFERIOR FRONTAL OPERCULUM
2. WERNICKE S
POSTERIOR PARASYLVIAL, TEMPORAL OPERCULUM
3. CONDUCTION
POSTERIOR PARASYLVIAN AREA
4. TC (Motor)
frontally and superiorly towards the striatum
5. TC (sensory)
parietal and temporal + thalamocortical circuit
6. GOLBAL
entire parasylvian area

** usually the L side of the brain is affected by different types of aphasia



CL I NI CAL MANI F E S T ATI ONS ( L OBE S )

FRONTAL LOBE LESIONS

I. EFFECTS OF UNILATERAL FRONTAL DISEASE, EITHER LEFT OR RIGHT
A. Contralateral spastic hemiplegia
B. Slight elevation of mood, increased talkativeness, tendency to joke
inappropriately (lackof tact, difculty in adaptation, loss of initiative
C. If entirely prefrontal, no hemiplegia; grasp andsuck reexes or
instinctive grasping may bereleased
D. Anosmia with involvement of orbital part

II. EFFECTS OF RIGHT FRONTAL DISEASE
A. Left hemiplegia
B. Changes as in I. B, C, and D

III. EFFECTS OF LEFT FRONTAL DISEASE
A. Right hemiplegia
B. Broca's aphasia with agraphia, with or without apraxia of the lips and
tongue
C. Sympathetic apraxia of left hand
D. Changes as in I.B, C, and D

IV. EFFECTS OF BIFRONTAL DISEASE
A. Bilateral hemiparesis
B. Spastic bulbar (pseudobulbar) palsy
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, utilizationbehavior
D. Decomposition of gait and sphincter incontinence

PSEUDOBULBAR PALSY
manifest brainstem dysfunction
bulbar palsy if unilateral in medulla difficulty in swallowing,
speaking

if cerebral origin MUST be bifrontal lobe difficulty in walking &
speaking


TEMPORAL LOBE DISEASE

I. EFFECTS OF UNILATERAL DISEASE OF THE DOMINANT TEMPORALLOBE
A. Homonymous contralateral upper quadrantanopia
B. Wernicke's aphasia (word deafness; auditory verbal agnosia)
C. Amusia (some types)
D. Impairment in tests of verbal material presentedthrough 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 somecases
C. Impairment in tests of visually presented nonverbal material

III. EFFECTS OF DISEASE OF EITHER (left or right) TEMPORAL LOBE
A. Auditory, visual, olfactory, and gustatory hallucinations
B. Dreamy states with uncinate seizure (complex
C. partial seizure)
D. Emotional and behavioral changes
E. Delirium (usually nondominant)
F. Disturbances of time perception

IV. EFFECTS OF BILATERAL DISEASE
A. Korsakoff amnesic defect (hippocampal formations)
B. Apathy and placidity
C. Hypermetamorphopsia
compulsion to attend toall visual stimuli
Klver-Bucy syndrome
hyperorality
hypersexuality
blunted emotional reactivity










N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 15 of 16



PARIETAL LOBE DISEASE

I. EFFECTS OF UNILATERAL DISEASE OF THE PARIETAL LOBE, RIGHT OR LEFT
A. Corticosensory syndrome and sensory extinction (or total
hemianesthesia with large acute lesions ofwhite matter)
B. Mild hemiparesis (variable), unilateral muscularatrophy in children,
hypotonia, poverty of move-ment, hemiataxia (all seen only
occasionally)
C. Homonymous hemianopia or inferior quadrantan-opia
(incongruent or congruent) or visual inatten-tion
D. Abolition of optokinetic nystagmus with targetmoving toward side
of the lesion
E. Neglect of the opposite side of external space (moreprominent
with lesions of the right parietal lobe

II. EFFECTS OF UNILATERAL DISEASE OF THE DOMINANT (LEFT) PARIETAL
LOBE (IN RIGHT-HANDED AND MOST LEFT-HANDED PATIENTS); ADDITIONAL
PHENOMENA INCLUDE
A. Disorders of language (especially alexia)
B. Gerstmann syndrome (dysgraphia, dyscalculia, nger agnosia,
rightleft confusion)
C. Tactile agnosia (bimanual astereognosis)
D. Bilateral ideomotor and ideational apraxia

III. EFFECTS OF UNILATERAL DISEASE OF THE NONDOMINANT (RIGHT)
PARIETAL LOBE
A. Visuospatial disorders
B. Topographic memory loss
C. Anosognosia, dressing and constructional apraxias (these disorders
may occur with lesions of either hemisphere but are observed
more frequently and are of greater severity with lesions of the
nondominant one)
D. Confusion
E. Tendency to keep the eyes closed, resist lid opening, and
blepharospasm

IV. EFFECTS OF BILATERAL DISEASE OF THE PARIETAL LOBE
A. Visual spatial imperception, spatial disorientation,and complete or
partial Balint syndrome (optic apraxia)



OCCIPTAL LOBE DISEASE

I. EFFECTS OF UNILATERAL DISEASE, EITHER RIGHT OR LEFT
A. Contralateral (congruent) homonymous hemianopia, which may be
central (splitting the macula) or peripheral; also homonymous
hemiachromatopsia
B. Elementary (unformed) hallucinationsusually because of irritative
lesions

II. EFFECTS OF LEFT OCCIPITAL DISEASE
A. Right homonymous hemianopia
B. If deep white matter or splenium of corpus callosum is involved,
alexia and color-naming defect
C. Visual object agnosia

III. EFFECTS OF RIGHT OCCIPITAL DISEASE
A. Left homonymous hemianopia
B. With more extensive lesions, visual illusions (metamorphopsias)
and hallucinations (more frequent with right-sided than left-sided
lesions)
C. Loss of topographic memory and visual orientation

IV. BILATERAL OCCIPITAL DISEASE
A. Cortical blindness (pupils reactive
B. Anton syndrome (visual anosognosia, denial of cortical blindness)
C. Loss of perception of color (achromatopsia)
D. Prosopagnosia (bilateral temporooccipital including fusiform gyrus),
simultanagnosia (parietooccipital)
E. Balint syndrome (bilateral dorsal [high] parietooccipital

































































































N E U R O L O G I C A L E X A M I N A T I O N
2013
Page 16 of 16



EXAMI NATI ON of CRANI AL NERVES
wi th CLI NI CAL CORRELATI ON