MECHANISM

RadiationInduced

Idiopathic

OTHER COMMENTS
Pathophysiologyprogressive demyelination & connective
tissue fibrosis
Onset insidious occurring weekly to years after radiation
Directly proportional to total dose of radiation given
Most prevalent with radiation thrapy for breast CA
Most common initial symptom median nerve paresthesia
Most common motor finding intrinsic hand muscle weakness
Distal involvement prior to proximal involvement
Prognosis variable
Porradiation fibrosis plexopathy rarely with pain;
primaryfocus of management shoulb be edema control
Please see above discussion ( under Parsonage Turner
Syndrome)

Upper Plexus Palsy (Erb Duchenne Palsy)

Most common
Frequently occur as a result of birth injuries
Involve C5-C6 roots or upper trunk
May have compression, traction or tearing
Paralyzed muscle- deltoid, teres minor, biceps, brachialis, coracobrachialis,
brachioradialis, supinator, infraspinatus, supraspinatus (serratus anterior and
rhomboids if lesion is at the root level)
Movements that are lost and lead to the typical Waiters Tip Position or Porters
Tip position
1. Abduction
2. External radiation
3. Elbow flexion
4. Supination
Description of the Waiters Tip deformity adducted, internally rotated shoulder,
extended elbow and pronated forearm
Sensory loss over deltoid (slight decrease); anterior radial surface of forearm and
hand
Lower Plexus Palsy or Klumpkes Paralysis
Involve C8, T1 roots or lower trunk
Possible causes: compression d/t cervical rib occasionally seen in apical tumors of
the lung
Specific nerves involved ulnar nerve (primarily); median nerve (partially, because
of the C8-T1 contribution coming from the lateral cord; this primarily innervates
muscles of the hand)
Prognosis more favorable unless associated with cancer
Paralysis/atrophy small handmuscles/ flexors of the wris
Can also present with Clawhand deformity (partial)
Ulnar type sensory loss
Edema, cyanosis, trophic changes common
Horners Syndrome if sympathetic rami of T1 involved (ipsilateral miosis, narrowed
palpebral fissure, enophthalmos andabsence of sweating and increased
temperature face and neck)
Middle Plexus Type (C7)
Rare by itself

Triceps paralysis and weakening of extensors of wrist and hand (similar to a radial
nerve palsy as far as the wrist and hand are connected)
Potential Mechanisms Resulting in Lumbar Plexopathy
MECHANISM
COMMENTS
Diabetic
Diabetic plexopathy more common in lumbosacral plexus
than brachial plexus
Predominantly proximal sx
Also called proximal diabetic neuropathy, diabetic lumbar
plexopathy, diabetic myelopathy, diabetic mononeuropathy
multiplex, diabetic femoral neuropathy, diabetic myopathy
and diabetic amyotrophy
Most common clinical presentation: anterior thigh pain
progressing to proximal LE weakness especially the
quadriceps
Sensory loss less pronounced
Patellar hyporeflexia or areflexia
Later see atrophy and weight loss
May be initial sign of diabetes
Unilateral weakness may progress to become bilateral
Potentially reversible; maximum improvement may take a
year
Glucose control result in significant by incomplete recovery
of muscle weakness
Pathomechanism unclear; may be infarct, demyelination,
axonal degeneration
Most important aspect of treatment; control of the
hyperglycemia
Traumatic
Lumbosacral plexus well protected from direct impact
Sacroiliac joint fracture may cause ipsilaterla L5-S1
impairments
Fracture-dislocation of hip may cause traction injury to
plexus
Neoplastic
Causes of lubosacral plexopathy by direct extension of a
neoplastic lesion most commonly seen with colorectal CA;
also seen with uterine, prostatic & ovarian tumors
Metastatic invasion of the plexus seen with breast, thyroid,
testicular cancers and lymphomas, myelomas and
melanomas
Neoplastic plexopathies usually manifest with unilateral pain

Hemorrhagic

Radiation

Iatrogenic

Lumbosacral plexopahty may occur with retroperitoneal

hemorrhage d/t compression of the plexus at the iliac or
psoas muscles
Femoral nerve compression may occur with hematoma of
the iliacus musclemanifest with groin pain aggravated by
hip hyperextension; and quadriceps weakness
Upper lumbosacral plexus may also be compressed by a
psoas hematoma affecting both femoral & obturator nerves
Above hemorrhagic problems usually occur in patients with
bleeding disorders or on anticoagulation therapy

Insidious onset of from 1-31 years after radiation

Bilateral, slowly progressive weakness that is predominantly
distal
Paresthesis and numbness less common
May be caused by blunt trauma from surgical retraction and
forceps deliverymost commonly affect femoral and
obturator nerves
Hip arthroplasty may cause direct traquma, stretching or
thermal injury of the femoral, obturator and sciatic nerves
Epidural anesthesia, perioperative and retroperitoneal
hemorrhage can result in femoral nerve injury
Cord infarction d/t anterior spinal artery occlusion may occur
Hypodermic injection usually affect lateral sciatic nerve
Prolonged or tight hip flexion during the dorsal lithotomy
position may stretch or compress the sciatic nrve
Common peroneal nerve at fibular head also predisposed to
compression injury during or after surgery

NEUROMUSCULAR JUNCTION DISORDERS

Myasthenia Gravis
An autoimmune disorder
Acetylcholine receptors on the post junctional membrane and antibodies to these
receptors interfere with nerve impulse transmission
More likely in young adulthood
Sex predilection: female>male
Incidence: one in 50,000
o Clinical manifestation:
Fluctuating bulbar palsy eyes (diplopia, ptosis)
o Speech slurring, nasal twang
o Muscles of mastication & swallowing
o More pronounced late in the day, temporarily relieved by rest
o Later on affect large muscle groups: neck, arm
Physical examination should assess
o Cranial Nerves III, IV, and VI for the Extraocular Muscles

o Speech breathy dysarthria

o Smile transverse, snarling
o Mouth hanging
o MMT neck and UE muscles
Diagnostic Studies
o Edrophonium chloride test (anticholinesterase)
o Electrodiagnostic test which will show & decremental response
Treatment: Anticholinesterase, Steroids, Immunosuppresants

Ossermans Classification of Myasthenia Gravis

Neonatal
Seen in 10-15% of babies born to
myasthenia gravis mothers
Type I (Ocular Myasthenia)
15-20%
Type IIA (Mild, Generalized Myasthenia)
30% (slow progression with no crisses;
responsive to drugs)
Type IIB (Moderately Severe Generalized) 25% (severe skeletal and bulbar
involvement but no crises; less
satisfactory drug response)
Type III (Acute Pulminating Myasthenia)
15% (rapid progression of severe sx
with respiratory crises and poor drug
response; high incidence of thymoma;
high mortality)
Type IV (Late Severe Myasthenia)
10% (same as Type III but progression
over 2 years from Class I to II)
Myasthenia Syndrome (Eaton-Lambert)
Often found in association with Bronchial Carcinoma
Failure of release of acetylcholine & neuromuscular junction
Begins in middle age
Sx: proximal weakness or fatigue, dry mouth, sexual dysfunction, areflexia,
occasional bulbar signs
Electrodiagnostic: Marked facilitation in response to repeated stimulation and
exercise
NEUROLOGICAL EVALUATION
Different levels of consciousness
Stupor
Patient less alert than usual but can be stimulated into
responding
Response to noxious stimuli
Orientation
Appears to be asleep most of the time when not
stimulated
Respond to noxious stimuli
Comatose
Unconscious and does not respond to any stimuli
Vegitative Stage
Continued decreased levels of consciousness after coma
Eyes open and close, may track objects , swallow and
chew but
Not respond to auditory stimuli
Not appear to sense pain, hunger or other stimuli
Have arousal but no awareness
Delirium
Disturbance of consciousness accompanied by a
change in cognition that cannot be better

Post-traumatic
Amnesia

accounted for by preexisting or evolving

dementia
Time between injury and the time when patient
can again remember ongoing events

Hydrocephalus
Definition: increased CSF fluid in the ventricles
Communicating or non-obstructive hydrocephalousmeans there is communication
bet. The ventricles and subarachnoid space
Non-communicatingno communication bet. Ventricle and subarachnoid space so
most likely due to an obstructive causes
Two major types: developmkental hydrocephalous and normal-pressure
hydrocephalous
Developmental hydrocephalous
Present at birth
Often due to congenital block in CSF; increased production rare
Have increased intracranial pressure
Normal Pressure Hydrocephalus
Adult-onset
Due to imbalance bet. Production and Resorption of CSF
Communication bet. Ventricles and subarachnoid space intact but
Communication bet. Subarachnoid space and arachnoid villi and granulations not
intact so that not efficiently transferred to superior sagittal sinus
Still causes enlargement of ventricles and not pressure on outer structures
Triad: progressive dementia, gait disturbance (slow, unsteady and wide-based) and
urinary incontinence
Above findings due to compression of brain tissues surrounding the gradually
enlarging ventricles
Various neurological tests
Marcus Gunn Syndrome
Activation of levator palpebrae upon
using muscles of mastication usually
with congenital ptosis on affected
side
Elevation of ptotic eyelid on
movement of jaw to contralateral
side
Occur with lesion of facial nerve as
exit pons
Jaw Reflex
Tap with reflex hammer over finger
placed at middle of patients chin
with mouth slightly openedhave
contraction of masseter and
temporalis bilaterally
Test trigeminal nerve and pons
integrity
Marin Amat Test
Inverted Marcus Gunn
Closing of eyes when patient opens
mouth forcefully and maximally
Occur after CN VII palsy

Chvostek Test

Bells Phenomenon

Grading of Spasticity
ASHWORTH SCALE
0 Normal tone
1 Slight hypertonus, catch

1
+
2
3
4

Mild, limb moves easily

Moderate, passive movement difficult
Severe, rigid limb

Upper vs. Lower Motor Neuron Sign

UMN Signs
Hypertonicity (spasticity)
Hyperreflexia
(+) Babinski, clonus

Tapping over parotid gland results in

spasmodic contraction of ipsilateral
facial muscles
Sign of tetany
Have hyperexcitability of facial nerve
Eyeball rolls upward when eye is
closed
MODIFIED ASHWORTH
Normal
Slight increase, manifested by catch
and release or by minimal resistance at
the end of ROM when part flexed or
extended
Slight increase in tone, catch followed
by a minimal resistance throughout the
remainder (less than half) of the ROM
More marked increase, moves easily
Considerable increase, movement hard
Rigid in flexion or extension

LMN Signs
Hypotonicity (flaccidity)
Areflexia
No pathologic reflexes
Fasciculations (for anterior horn cell
diseases)

Type of Diplopia Based on Paralyzed Extraocular Muscle

PARALYZED RIGHT
No movement of RIGHT EYE to the
EOM
Lateral Rectus
RIGHT

Medial Rectus

LEFT

Inferior Rectus

DOWNWARD when turned to the

RIGHT

Superior Rectus

UPWARD when eyes turned to the

RIGHT

Superior Oblique

DOWNWARD when eye turned to

the LEFT

Field defect
HORIZONTAL homonymous
diplopia increasing on looking
to the RIGHT
HORIZONTAL CROSSED
diplopia increasing on looking
to the LEFT
VERTICAL diplopia (image of
right eye lowermost) on
looking to the RIGHT & DOWN
VERTICAL diplopia (image of
right eye uppermost)
increasing on looking to the
EYE FINDINGS IN BRAIN
CONDITIONS and UP
VERTICAL diplopia (image of
right eye lowermost)
increasing on looking to the

Inferior Oblique

UPWARD when eyes turned to the

LEFT

LEFT & DOWN

VERTICAL diplopia (image of
right eye uppermost) when
looking to the LEFT & UP

Eye Findings in Brain Conditons

Frontal Lobe Lesion
- eye is turn to side of cerebral LESION or far from the PARETIC side
- when the lid is closed the eye moves to the side of hemiparesis and NOT upward
- gaze paralysis of central origin are not accompanied by strabismus and diplopia
Midbrain Lesions affecting the pretectum
- Interfere with conjugate movement in vertical plane; Ex. Parinaud or dorsal
midbrain syndrome
- Upward gaze affect more than downward gaze
- (+) mydriasis, (-) convergence, (-) pupil light reflex
- Occasionally (+) Collier sign or lid retraction
Dolls head
- Forced flexion of head results in reflex upward deviation of the eye
Bells phenomenon
- Forced closure of the eye results in upward movement of the eye
Dolls and Bells phenomenon will suggest a supranuclear lesion when present
STRABISMUS (Squire) Muscle imbalance that results in misalignment of the visual axes of
the two eyes
DIPLOPIA see image as double
Difference Between Rigidity &Spasticity
RIGIDITY
Physiolog
y

Clinical
Test

1. Overdischarge of motor
neuron
2. Influence from higher
centers
3. Influence from peripheral
afferents

Alpha

SPASTICITY
Gamma

Extrapyramidal

Pyramidal

Limited

Important

4. Temperature changes

Less sensitive

More sensitive

5. Sleep

Less changes

Released

1. Range of hypertonicity

Whole ROM, lead

pipe resistance
Unchanged or
decreased
Diffuse
Less

Initial movement

Anticholinergic,
dopamine

Spasmolytic

2. DTR
3. Muscle involvement
4. Affected by postural
change
5. Drug treatment

Increased
Anti-gravity muscles
More

Differences between upper and lower motor neuron paralysis

Upper Motor Neuron or Supranuclear
Lower Motor Neuron or Nuclear-Infranuclear
Paralysis
Paralysis
Muscles affected in groups, never individual Individual muscles may be affected

muscles
Atrophy slight and due to disuse
Spasticity with hyperactivity of the tendon
reflexes and extensor plantar reflex
(Babinski sign)

Fasciccular switches absent

Normal nerve conduction studies; no
denervation potentials in EMG

Atrophy pronounced up to 70 to 80% of

total bal
Flaccidity and hypotonia of affected muscles
with ____
Of tendon reflexes
Plantar reflex, if present, is of normal flexine
type
Fascicular twitches may be present
Abnormal nerve conduction studies
denervate potentials (fibrillations,
fasciculations, positive_____ waves) in EMG

Clinical differences between corticospinal and extrapyramidal syndromes

CORTICOSPINAL
EXTRAPYRAMIDAL
Character of the alteration
Clasp-knife effect
Plastic, equal throughout
of muscle tone
(spacticity)
passive movement (rigidity),
or intermittent (cogwheel
rigidity); hypotonia in
cerebellar disease
Distribution of hypertonus
Flelxor of arms; extensors of Flexors (predominantly) and
legs
extensors of all four limbs;
flexors of trunk
Shortening and lengthening
Present
Absent
reaction
Involuntary movements
Absent
Presence of tremor chorea,
athctosis, dystonia
Tendon reflexes
Increased
Normal or slightly increased
Babinski sign
Present
Absent
Paralysis of voluntary
Present
Absent or slight
movement
Tests for the different Cranial Nerve
Olfactory Nerve Familiar, non-irritating odors in small bottles are placed under
each nostril (tested separately) for identification
Optic Nerve visual acquity; perimetry; color blindness tests; fundoscopic
examination
Oculomotor, Trochlear and abducens Nerves visual field test; prism test; diplopia
testing (for oculomotor only light reflex, accommodation, consensual light reflex)
Trigeminal Nerve Sensory test of the face; corneal wink, conjuctival reflex, jaw jerk
reflex, sneeze
Facial Nerve MMT of facial muscles; taste for anterior two-thirds of th etonguel
corneal or wink reflex; conjuctival and lid reflexes
Acoustic or Auditory Nerve
Coclear Function hearing acuity tests; Webers test; Rinnes test; Bings
test; otoscopic exam; audiometry

Vestibular Function Caloric Test

Glossopharyngeal Nerve Pharyngeal or Gag reflex (for sensory component);
Vernets Rideau phenomenon; carotid sinus reflex; taste for posterior third of the
tongue
Vagus Nerve Gag reflex; oculocardiac reflex, carotid sinus reflex; laryngoscopic
examination
Spinal Accessory Nerve MMT for trapezius and Sternocleidomastoid muscles
Hypoglossal Nerve strength of tongue muscles; tongue deviation
Cranial Nerve Examination
CN I: Olfactory Nerve
Smell
Familiar, non-irritating odors in small bottles are placed under each nostril
and are tested separately for identification
CN II: Optic Nerve
Include tests for visual acuity and color blindness
Pupillary reactions
Visual fields and perimetry
fundoscopy
CN III: Oculomotor Nerve
Tests for oculomotor nerve function alone includes the light reflex;
accommodation and consensual light reflex
Extraocular muscles (eye movements) except for the lateral rectus and
superior oblique
CN V: Trigeminal
Sensation of the face
Corneal Reflex or corneal wink; conjuctival reflex
Jay jerk reflex; sneeze reflex; and tests for mastication or chewing ability
CN IV: Trochlear Nerve
Superior oblique muscle
CN VI: Abducens Nerve
Lateral Rectus muscle
CN VII: Facial Nerve
Facial symmetry; MMT of the muscles of facial expression
Taste anterior two-thirds of tongue
Also needed in the corneal or wink reflex; conjunctival and lid reflexes
CN VIII: Auditory or Acoustic Nerve
Cochlear Function-houring acuity tests; Webers and Rinnes test; Bings Test;
audiometry
Vestibular Function calorie test or tests for vestibular balance; nystagmus
CN IX: Glossopharyngeal Nerve
Taste for posterior third of the tongue
Both IX, X Gag Reflex; hoarseness: Carotid Sinus Reflex
CN XI: Spinal Accessory Nerve
Strength of sternocleidomastoid and trapezius
CN XII: Hypoglossal Nerve
Tongue deviation and mobility
Other
1.
2.
3.

neurological test that will elicit a Babinski like response:

Chaddocks Toe Sign stroke the lateral malleolus
Gordons Leg Sign squeeze the calf muscles
Openheims Sign firm downward stroking of the tibia and tibialis anterior muscle

4. Gonda Reflex press one of the other toes downward and releasing it with a snap
5. Schaefers sign squeeze the Achillles Tendon
6. Stransky Reflex vigorous abduction of the little toe for 1-2 seconds with
subsequent sudden release
Evaluation of Cerebellar Function and Coordination
1.
Clinical manifestation suggestive of lesions in the VEERMIS or MIDLINE
CEREBELLUM
1.1disturbance of equilibratory coordination mainly in the head and trunk
1.2TRUNKAL ATAXIA present when patient is sitting, standing and walk-in; most
severe in tandem gait; have swaying, staggering and titubation when
walking; present whether the eyes are open or closed
1.3STATIC ATAXIA Coarse, tremor of the head, neck, or entire body when the
patient attempts to sit up or stand
2.

Manifestations of Lesions in the Cerebellar Hemispheres

2.1ASYNERGY OR DYSSYNERGY loss or lack of coordinated action between
various groups of muscles resulting in DECOMPOSITION OF MOVEMENT
2.2DECOMPOSITION OF MOVEMENT movements is jerky, irregular and
inaccurate (like a robot or puppet)
2.3DYSMETRIA loss of the ability to gauze the distance, speed or power of a
movement tested through the finger-to-nose test
2.4DYSDIADOCHOKINESIA or ADIADOCHOKINESIS disturbance in the reciprocal
innervation of agonist and antagonist; tested through the performance of
rapid alternate movements
2.5REBOUND PHENOMENON loss of the check reflex due to failure of the
agonist to relax and antagonist to contract rapidly on time to prevent a
rebound movement
2.6Hypotonia
2.7INTENTION Tremor
2.8PAST-POINTING
2.9Nystagmus

3.

Test for Coordination

3.1Rombergs Test
Starting Position: stand erect with the feet together
Procedure:
1. With the eyes open note whether patient sways
2. With the eyes closed note tendency to sway
Positive Test: no swaying with the eye open; (+) swaying with increasing
unsteadiness with the eyes closed
Interpretation: rule out dorsal column lesion

3.2Tandem Gait patient is asked to walk with one foot placed in front of the
other both with the eyes open and closed
3.3Walking on a straight line test
3.4Test for Dysynergia Circle Drawing Test
Patient is asked to draw circles about a foot in diameter, in space using his finger;
Shape and size of the circles are drawn irregularly in zigzag manner
3.5Tests for Dysmetria
3.5.1 Finger-to-Nose Test
3.5.2 Nose-Finger-Nose Test
3.5.3 Heel-to-Knee-To-Toe Test
Interpretation:

HYPOMETRIA patient stops before he reaches the target

BRADYTELEOKINESIA patient completes the act slowly and
unsteadily
HYPERMETRIA patient overshoots the target usually going
toward the side of the lesion and he brings the limb to his target
with too much force and speed
4.

Tests for Dysdiadochokinesia

4.1Pronation-Supination Test
4.2Knee-putting Test
4.3Rapid Tapping of the forefinger on the thumb

5. Test for Past-Pointing BARANYS POINTING TEST

Starting Position: patient sits facing the examiner holding his arm forward
horizontally so that the index finger touches upon the tip of the examiners index
finger;
Procedure: Without the examiner moving his index finger;
1. Patient moves his arm up vertically then back to the examiners finger;
2. The above procedure is repeated this time horizontally (right and left) and
there is the frontal place (toward and away from the patients trunk)
3. These are done with the eyes open and closed
Positive Test: patient will miss his target with deviation to the involved side
6. Test for Rebound Rebound Test of STEWART-HOLMES
Starting Position: sitting or standing with shoulder flexed 90 degrees, elbow slightly
flexed, forearm supinated and hand fisted
Procedure:
1. Ask patient to flex the elbow against the resistance applied by the
examiner
2. Examiner suddenly releases the resistance (examiner makes sure he
blocks the hand)
Positive Test: patient is unable to voluntary stop the rebound of the arm and will end
up holding himself if the hand is not blocked
Reflexes
1. Muscle Stretch Reflex (Deep Tendon Reflexes)
Refer to deep tendon reflexes or myotatic reflex
Includes the jaw reflex; biceps, brachioradialis, triceps, quadriceps and tendon
of Achilles reflex and finger flexor reflex (Hoffmann Sign)
The grading system is as follows:
0 or - Not Elicited even after reinforcement
+
Present but sluggish and diminished
++
Average response
+++ Increased but not necessarily to a pathologic degree
++++ Markedly hyperactive; put (CI) when there is associated clonus
The JENDRASSIK MANEUVER can be used when it is difficult to get the patient
to relax particularly when eliciting the knee jerk. This maneuver is the most
common example of REINFORCEMENT. The use of reinforcements is a
technique that creates a diversionary spiral are at a level above the reflex
segment being tested and therefore blocks cortical suppression. To do the
Jendrassik maneuver the patient clasp both hands together with shoulders in
90 degrees of abduction. Patient pulls on both hands while examiner elicits the
knee jerk.

2. Superficial Reflexes
Examples: corneal, nasal, pharyngeal, superficial abdominal, cremasteric,
superficial anal and plantar reflex
Also called exteroceptive reflexes
Usually have a protective function
3. Other Reflexes
Blink Reflex
Trigeminofacial reflexes
Late response to a tap on the brow which is lost in Parkinson and
enhanced in pseudobulbar palsy
Glabellar Reflex -> also tests the facial nerve; tapping of the glabella
causesboth eyes to blink
Palmomental Reflex
Tapping or stroking of palm causes contraction of ipsilateral mentalis
muscle
Seen in pyramidal diseases
Help diagnose a central palsy of the facial nerve
Four Levels of Function in the Hierarchy of Sensibility of Hand Sensation:
1. PUNCTATE TOUCH ability to detect punctuate stumulus such as a pinprick
2. DISCRIMINATION ability to distinguish between two different stimuli such as twopoint discrimination
3. QUANTIFICATION ability to detect the variation or changes in the degree of tactile
stimulus; most common test is to ask the patient to distinguish from the roughtest,
most irregular and smoothest surface
4. RECOGNITION is the final and most complicated sensibility level; refers to the
ability to recognize objects through touch or STEROGNOSIS
Definition of Some Relevant Terms related to Sensation
1. ANESTHESIA complete loss of all forms of sensation
2. DISSOCIATE ANESTHESIA loss of some forms of sensation (usually pain and
temperature) with preservation of others (tactile) as in syringomyella
3. HYPESTHESIA diminished sensation
4. HYPERESTHESIA increased tactile sensibility
5. PARESTHESIA consists of abnormal sensations, numbnest, tingling and formication
6. FORMICATION sensation of insects crawling over the skin
7. SYNESTHESIA (SYNCHIRIA) with a single stimulus two sensations are perceived,
one that is well localized and one that is distant
8. ANALGESIA complete loss of pain sensation
9. HYPALGESIA diminished sensibility to paon
10.HYPERALGESIA increased sensibility to pain
11.ASTEREOGNOSIS inability to recognize familiar objects by the sense of touch
(anesthesia not being present)
12.ATOPOGNOSIS inability to localize tactile stimuli
13.AGRAPHESTHESIA inability of the patient to recognize numbers traced lightly on
the skin usually in the palm of the hand
Notes

on Electromyography
EMG applies to entire spectrum of tests including: EMS, NCV, RNS, SSEP
Powerful, sophicticated, sensitive
It provides vital diagnostic and prognostic information for a wide variety of
neuromuscular conditions including peripheral nerve injuries.
Evaluates: motor & sensory physiology of both the DNS & PNS

Electromyography shows FUNCTIONAL DEFICITS; this is in contrast to ANATOMIC

DEFICITS which is derived from the CT scan and MRI diagnostic tests
Specific information that can be elicited through EMG include
o Normal and abnormal conduction/transmission
o Distribution and extent of pathology/injury; including whether the injury is
complete or incomplete; localized or generalized
o Nature of the pathology; myopethic vs. neuropathic
o Site of injury; whether proximal or distal, peripheral nerve; nerve root or
plexus
o Time of onset; severity; course; whether it is improving or progressing
Conditions: diseases in neuromuscular transmission,, radiculopathy, carpal tunnel
syndrome & other compression and entrapment neuropathies, peripheral nerve
injuries, generalized weakness, myopathies
Special test:
o H-reflex for SI nerve root
o F-wave to assess proximal transmission
o Blink reflex for pathologies involving CN V and VII

On Nerve Conduction Velocities

1. Axonal potential conduction velocity is related to axonal diameter in a roughly linear
fashion
2. Fastest conducting axons determine the conduction velocity
3. Conduction velocity of peripheral; nerves tend to decrease in a proximodistal
manner
4. Conduction velocity decreases significantly with decreased temperature and distal
latencies become correspondingly prolonged
Distal limb temperature more critical
NCV drop by 1.5 - 2.5m/secoC
5. AMPLITUDE tends to INCREASE w/ decreased temperature
6. Conduction velocities in newborns are approximately those in mature adults;
even lower in premature babies
7. Adult values reached at 3-5 years old. At 1 year old have 80% of adult value.
8. Conduction velocities decrease slightly after 30-40 y/o.
9. Maximum decrement approximately 10m/sec at 60-80 y/o.
Causes of Decreased Sensory/Motor Conduction Velocity
1. Diffuse demyelination
2. Loss of large, myelinated fibers
3. Focal or Multifocal demyelination
4. Marked axonal stenosis
AKATHESIA involuntary movements
LOCUS COERULESIS major ascending source of norepinephrine in the forebrain areas

SPEECH AND LANGUAGE DISORDERS

(A continuation from pages 326 to 332)

Systems Involved in Communication

1. Nervous System
2. Respiratory System

 Generate required air pressure

Respiration is the power source for voice and speech
3. Phonatory System
Generate required vibrating energy for speech so it can be heard at a
distance
Vocal cord adduct to close the glottis temporarily blocking flow of air from
trachea to larynx resulting in phonation
Have two types of phonation: voicing and whispering
4. Articulatory System
Expands and contracts the vibrating energy rapidly so that the shaped
sounds of speech will fade quickly and not blur into each other
Primary articulatory structures; soft & hard palate, pharynx, tongue, tooth,
lips, cheeks and mandible
5. Auditory System
Transform acoustic waves of speech sounds into neural signal so it can be
interpreted
Vocal Parameters
1. Pitch sound frequency measured in hertz.
Average pitch in men 125 Hz
Average pitch in women 200 Hz
2. Loudness sound intensity described in decibels
Vocal intensity influenced by amount of glottal resistance and air pressure
beneath glottis
3. Quality
4. Flexibility
Mechanism of Sound &Hearing
Outer ear sound pressure waves of speech in the air
Waves converted to mechanical vibrations by tympanic membrane and ossicles
Mechanical vibrations converted by cochlea into fluid vibrations or hydraulic
vibrations
Nerve endings in cochlea covert hydraulic vibrations into nerve impulses
Nerve impulses sent to brain through auditory nerve

Five Apects or Dimensions of Language

Phonology rules on the way the sounds of a language are organized
Semantics rules on the meaning of words and word combinations
Morphology rules on how words are formed
Syntax rules on how words are combined into larger meaningful units of phrases,
clauses and sentences
Pragmatics rules on the use of language in context
Definition
TERMS
Value
Dyspho
nia
Aphonia
Mute

of terms Related to Normal & Impaired Communication

DESCRIPTION DEFINITION
Audible sound produced by phonation
Abnormal voice
May be a problem with pitch, loudness, quality and or flexibility
Absent definable laryngeal tone; voice secretly breathy or whispered
Absent phonation and articulation

Phonem
es
Fluency
Prosody

Stutteri
ng

Sound patterns
Smoothness with which sounds, syllables words and pleases are joined
together during oral language with lack of hesitations or repititions
Includes rate, rhythm, loudness and pitch contours that signal stress and
therefore carry additional meaning beyond individual speech sounds;
words or sequences of words
A disorder of fluency; Presents with gaps, prolongation, or involuntary
repetitions of a sound or syllable during speech production.

Nice to know facts about communication

Normal voice and speech are produced during expiration
Average number of words per minute or speaking rate 125
Language a complex and dynamic system of conventional symbols that is used in
various modes for thought and communication
Levels
-

of Language Usage
Automatic ex. Counting, reciting the days of the week, moths of the year etc.
Imitation simple repetition of what is heard
Propositional conveying a message, want or need, or a joke etc.

Muscles Involved in Speech

PHASE OF SPEECH

Respiration
Phonation

Articulation

MUSCLES
Diaphragm
Sternomastoid
Intercoastals
External & internal oblique
Transverse abdominis
Arytenoid muscle &
cricothyroid
Tongue muscles

Masseter
Temporalis
Internal & external pterygoid
Velopharyngeal mechanism
Levator palatini
Tensor paltini
Palatoglottis
Pharyngeal constrictor

INNERVATION
Phonic
CN XI
T2=12 intercostal nerves
T6=12 intercostal nerves
T7=12 intercostal nerves
Vagus nerve
Hypoglossal nerve
Accessory nerve (for
palatoglossis)
Trigeminal nerve
Trunk of mandibular nerve
branch
Vagus nerve
Trigeminal nerve
Accessory nerve
Vagus nerve

Definition of Hearing Problems

1. Hard of Hearing partial impairment in sense of hearing enough to came some
difficulty with comprehension of speech
2. Deafness hearing in nonfunctional for the ordinary purposes of daily life
3. Hearing Loss refers to degree or severity in which hearing is impaired; classified as
follows:
3.1 Normal hearing
- 0-20dB
3.2 Mild hearing loss
- 20-40
3.3 Moderate loss
- 41-55

3.4 Moderately severe

3.5 Severe loss
3.6 Profound Deafness

- 56-70
- 71-90
- >90

Types of Speech Disorders

1. Apraxia of Speech
A sensorimotor disorder of articulation and prosody
Frequentyly accompanies Brocas aphasia
Has volitional programming problems in saying what is meant
Characterized by
- Effortful, trial-and-error, groping articulatory movements, and attempts
at self-correction
- Dysprosody unrelieved by extended periods of normal rhythm, stress
and intonation
- Articulatory inconsistency on repeated production of the same
utterance
- Obvious difficulty initiating an utterance
2. Dysarthria
Collective term for a group of motor speech disorders; language not involved
Due to impaired neuromuscular control of speech, whether central or
peripheral
May be a problem in respiration, phonation, articulation, resonance and
prosody
Subtypes: Flaccid, spastic, ataxic, hypokinetic, hyperkinetic and mixed
dysarthria