THE BASIC NEUROLOGICAL EXAMINATION

History: relevant data given by patient or family concerning:

- PREVIOUS PERSONAL HISTORY:
- personal physiologic and pathologic background
- age, occupation, handedness, residence, marital status, military
service of the patient
- circumstances of gestation and delivery, attainment of standard
landmarks of achievement, childhood diseases, serious illness, trauma
(especially for infants and children)
- menstrual history, parenthood, menopause
- pathological history like other concomitant diseases (diabetes, heart
and lung diseases, hypertension, gastro-intestinal complaints, urinary
function, endocrinological diseases, malignancies, surgical procedures,
trauma and hospitalizations
- previous and current medication
- alcohol abuse, smoking, professional use of toxic substances
- sexual preference and proclivity, use of intravenous drugs (for AIDS
potential)
- EREDO-COLLATERAL HISTORY:
- disorders of parents, ancestors, siblings:
- for diseases genetically transmitted (such as muscular dystrophies,
chronic chorea, spinal ataxias)
- for predisposing circumstances (such as for epilepsy)
- for diseases with nervous system impact (such as hypertension,
diabetes, atherosclerosis, etc.)
- for transplacental transmission (such as syphilis, toxoplasmosis)
- PRESENT ILLNESS HISTORY:
- symptoms and complaints
- onset circumstances: sudden (seconds), acute (minutes, hours),
subacute (days), chronic (weeks, months)
- temporal profile of symptoms (order of onset, concomitance,
persistence, disappearance)
- pain pattern: topography, intensity, character, rhytmicity, drug
response

- COMMON SYMPTOMS OF DISEASE OF THE NERVOUS SYSTEM:

1. Lost of interest, drive and energy
2. Disorders of memory and intellect
3. Headache
4. Seizures with convulsive activity, loss or alteration of consciousness, with
details of aura and character of the episode
5. Visual changes (dimness, diplopia, monocular or binocular changes)
6. Loss of hearing and tinnitus
7. Loss of balance and vertigo
8. Change in speech and difficulty in swallowing
9. Clumsiness or weakness of the extremities, involuntary movements
10. Spinal pain
PATIENT EXAMINATION comprises:
1. GENERAL EXAMINATION
2. NEUROLOGICAL EXAMINATION
The neurological examination is an exhaustive examination in a
precise sequence and which leads to assess objective neurological signs.
Following the neurological examination, one has to be able to answer
the following questions:
- Are there GENUINE neurological signs and symptoms?
- Which is the LEVEL of the nervous system involved?
- supratentorial level ( tentorium = the dural fold that separates the
hemispheres from cerebellum; supratentorial are the cerebral hemispheres)
- posterior fossa level (subtentorial the posterior third of the skull
base that contains the cerebellum, midbrain, pons and medulla)
- spinal level
- peripheral level
- more than one level
- Which is the most likely responsible lesion within the selected:
- FOCAL on the RIGHT side of the nervous system
- FOCAL on the LEFT side of the nervous system
- FOCAL but involving the MIDLINE and CONTIGUOUS
STRUCTURES on both sides of the nervous system
- NONFOCAL and DIFFUSE
- Which is the most likely responsible pathologic lesion for the symptoms?
- some form of MASS lesion
- some form of NONMASS lesion
- Which is the most likely cause of the found lesion?
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- vascular
- degenerative
- inflammatory
- immunologic
- neoplastic
- toxic-metabolic
- traumatic
FOCAL = strictly confined to a single circumscribed area.
DIFFUSE = distributed over a wide areas of the nervous system.
A diffuse lesion may involve only a single level (for example
supratentorial or spinal level) or it may be distributed over multiple levels. A
diffuse lesion involves bilaterally symmetrical areas in the nervous system,
without extending across the midline as a single, circumscribed lesion.
NONMASS = a lesion that is altering cellular function in the area of the
lesion but it is not significantly interfering with neighboring cell
performance. In this type of lesion, the pathologic process is not by virtue of
its size or volume compressing, destroying or damaging nearby structures.
MASS = a lesion that not only alter cellular function in the area of the
lesion, but also is of sufficient size and volume to interfere with neighboring
cell functions by compressing, destroying or damaging the nearby cells.
STEPS OF NEUROLOGICAL EXAMINATION:
1. Particular attitudes.
2. The maintenance of upright posture (orthostatism) and walking (gait).
3. Active motility and segmental force.
4. Passive motility, muscular tone, signs of meningeal irritation.
5. Coordination.
6. Involuntary movements.
7. Reflexes.
8. Trophic and autonomic disorders.
9. The sensory examination.
10. The cranial nerves examination.
11. Speech and praxic disorders.

1. PARTICULAR ATTITUDES
Definition: an abnormal, pathologic position or posture of a part of the body
(segmental level) or the entire body.
Common causes:
- motor deficit (paralysis of paretic or plegic intensity)
- muscular tone dysfunction
- muscular atrophies
- pain (antalgic postures)
- altering of the consciousness state
- involuntary movements (dyskinesias)
Examples:
1. The swan neck posture of the upper arm in the radial nerve
paresis, when the hand is flexed on the forearm and no hand extension is
possible due to the paralysis of the hand extensors.
2. The foot drop from the peroneal nerve paresis (external
popliteal sciatic nerve), as the anterior calf muscles responsible for the
dorsal flexion of the foot are paralyzed.
3. The lateral head rotation in torticolis due to an increased
muscular tone on one side of the neck muscles.
4. The flexed fetal position of the patient with meningitis.
5. The global semiflexed position of the parkinsonian patient: arms,
legs and upper body, with an inexpressive mask-like face and a typical finger
tremor.
6. The posture encountered in the spastic hemiparesis the arm flexed
and the homolateral leg extended.
2. THE MAINTENANCE OF THE UPRIGHT POSTURE
(ORTHOSTATISM) AND WALKING (GAIT)
Orthostatism or upright posture = the maintenance of the vertical station.
It can be influenced by:
- paralysis
- muscle tone dysfunction
- the presence of involuntary movements
- cerebellar disorders
- vestibular system disorders
- proprioception system disorders (position sense or myoartrokinetic sense)

The Romberg test:

The Romberg test assesses the ability of the patient to maintain
upright posture while standing on a narrow base.
The patient must stand erect with feet approximated, arms starched at
90 degrees to the body, with eyes opened then closed (to suppress the visual
substitution of the proprioception system).
Trough this test, the efficiency and integrity of the 3 systems that
achieve station is verified (the cerebellum, the vestibular system and the
proprioception system).
A negative Romberg test implies that the patient can maintain this
posture and doesnt fall.
A positive Romberg test is considered when the patient doesnt
maintain this posture and has a clear tendency of falling.
There are 3 types of positive Romberg tests, due to each of the system
involved:
1. A cerebellar positive Romberg test is when the patient tends to fall on
the side of the affected cerebellum (on the right side when the right
cerebellar hemisphere is affected, on the left side when the left cerebellar
hemisphere is affected, forward in anterior vermis lesions, backwards in
posterior vermis lesions). The tendency to fall is not enhanced by eye
closing.
2. A vestibular positive Romberg test is when the patient tends to fall
towards the affected vestibule; head rotation changes the falling direction as
it changes the spatial vestibular direction. The tendency to fall is enhanced
by the eye closing.
3. A tabetiform or proprioceptive positive Romberg test leads to
swaying and falling tendency in many directions. The tendency to fall is
enhanced considerably by the eye closing.
There are situations when the patient is lying down due to various
other causes and the test cannot be performed (ex. hemiplegia).
Walking (gait) is the next function to be assessed as it reflects the bringing
into action of a substantial portion of the nervous system, both motor and
sensory, and yields important evidence of dysfunction of the nervous system.
The patient is asked to walk forth and back several times and the
posture, balance, arm swinging, leg movement, speed and confidence,
direction maintenance are successively observed.
The normal person progresses with only casual observation of the floor and brief
survey of the range of the area. Balance is easily achieved, no correction is needed, arms
swing leisurely and there is a slightly flexed posture, elbows, palms and fingers facing the

tights. As weight is shifted from one leg to the other, the heel of the weight-carrying foot
lifts from the floor. The other foot swinging through is kept at right angles to clear the
floor and the pelvis remains parallel to the floor without tilting. When he/she is asked to
turn rapidly as he/she walks, the face and head should lead and balance should be well
maintained.

Main causes of pathologic walking:

- paralysis
- muscle tone dysfunction
- the presence of involuntary movements
- cerebellar disorders
- muscular diseases
The patient is asked sometimes to walk on his toes, then on his heels,
to hop and to squat and rise.
Examples of pathologic gait:
1. Spastic hemiparesis the unilateral spastic leg of a hemiparetic
patient is pulled forward with outward circling (circumduction), with
stiffness and with dragging of the toe.
2. Spastic paraparesis the legs of the patient scissor and tend to
trip him as he walks on his toes and cross his knees.
3. Muscular dystrophy (myopatic walk) there is a waddling gait; it
results from weakness of the glutei, usually due to muscular dystrophy.
4. Peroneal nerve paresis there is a foot drop and a scraping toe; the
patient elevates the leg to swing through and there is a slapping of the foot stepping gait.
5. Parkinsons disease there is a stooped posture, a loss of the
swinging of the arms, a turning in one piece (en bloc) with stiff trunk and
neck and shuffling of the steps.
6. Cerebellar diseases the upright posture is maintained with
difficulty and often the excessive corrections for threatened loss of posture
results in reeling and staggering.
7. Lacunar gait - a walk with small staggering steps.
8. Tabetic gait there is a hesitant walk, on the heels, with an enlarged
standing base and a visual control of every step.
3. ACTIVE MOTILITY AND SEGMENTAL FORCE
The examination of the active motility and segmental force aims at
assessing the ability to perform voluntary movements and to uncover motor
deficits (paralysis).

A motor deficit is a deficit of speed, force and amplitude of a

required movement.
To test these parameters, the patient is required to perform movements
on command with different muscle groups (of his arms and legs) in order to
check both, proximal and distal muscle groups fine and course movements.
Both sides have to be checked and respectively compared.
There are also some other tests to uncover a motor deficit:
-a) for the upper limbs the patient is asked to elevate both arms at a
right angle to the trunk and keep them in this posture. A paretic limb will fall
at a speed depending of the magnitude of the deficit, while a plegic limb will
not be able to be elevated (this is the situation when the examiner will raise
the affected limb and let it fall to prove the deficit). This is a static test.
-b) for the lower limbs there are static and dynamic tests as follows:
Static tests:
The Mingazzini test is performed by placing the patient in a supine position
with tights in an obtuse angle to the trunk and calves parallel to the bed so
that a paretic limb will not be maintained in this position and will drop.

_____________________________________________________________
The Barr test is performed to check the motor deficits in the dorsal
muscles of the lower limb and requires to place the patient on a ventral
reclining position and to flex the calves on his tights. The paretic limb will
fall.

_____________________________________________________________
Dynamic tests:
The Vasilescu test - this is the most commonly used test and consists in
asking a supine patient to actively drag backward and forward his heels on
the bed sheets with a concomitant knee flexing movement which will lead to
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uncover the paretic limb as it performs more slowly and it will be left behind
the healthy one.

_____________________________________________________________
A paralysis or a motor deficit arises when the voluntary movement
pathway is somewhere affected.
The voluntary motor pathway comprises 2 neurons:
1. The central motor neuron or upper motor or pyramidal neuron (due to the
microscopic resemblance of its body to a pyramid). Its axon is a part of the pyramidal
tract that crosses the opposite side into the lower medulla; its body is located in the
frontal ascendant gyres.
2. The peripheral or lower motor neuron is located in the motor nuclei of the brain stem
(for the cranial nerves) and in the anterior motor columns of the spine. The pyramidal
tract connects at every level with the assigned lower motor neuron which in turn connects
to muscle fibres in the muscle through a special synapse called the motor end plate.
The synaptic neurotransmitter is Acetyl-choline (A- Ch) and its breaking enzyme
is Acetyl-choline-esterase.
It is worth reminding that one lower motor neuron and the number of muscular
fibres it connects forms a motor unit. Motor units are not equally large, as in muscles
designed for rapid complex movements there are small motor units of 15-20 fibres, while
in muscles placed to support the body there are huge motor units of 400-500 fibres and
even bigger.

A motor deficit can be the result of a upper motor neuron lesion (body
or axon in the pyramidal tract), of a lower motor neuron lesion (body or
axon in the peripheral root or nerve), of a synaptic dysfunction or of a
muscular disease. A good neurological examination can yield clues to the
probable location of the lesion in a motor deficit.
A motor deficit is analyzed and described according to the following
features:
1. Intensity:
- plegia = when no voluntary movement is possible
- paresis = when movements are possible with altered parameters of force,
speed, amplitude
2. Topography:
- monoparesis/plegia one limb (upper or lower) is affected
- paraparesis/plegia both lower limbs are affected
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- hemiparesis/plegia one side limbs, both upper and lower are affected
- diparesis/plegia either upper limbs or other symmetrical muscular
territories are affected
- triparesis/plegia three outs of four limbs are affected
- tetraparesis/plegia all four limbs are paralyzed
- double hemiparesis/plegia there is a successive onset of the tetraplegia
with a temporal gap between the two hemiparesis
3. Muscle tone:
- hypotonic deficit decreased muscular tone
- hypertonic deficit increased muscular tone
4. Anatomo-clinically:
- UPPER MOTOR NEURONE SYNDROME (UMNS):
- there is a motor deficit
- an extended muscular territory is affected
- muscle jerk reflexes are very brisk
- the Babinski sign can be elicited
- there are no muscular atrophies
- LOWER MOTOR NEURONE SYNDROME (LNMS):
- there is a motor deficit
- a restricted muscular territory is affected
- muscle jerk reflexes are low or absent
- muscle fasciculation is present
- there are early muscular atrophies
The muscular force is assessed as the examiner opposes selected movements
of the patient comparing the strength elicited in that particular group of
muscles or even single muscle. Both sides are checked.
4. PASSIVE MOTILITY, MUSCULAR TONE AND SIGNS OF
MENINGEAL IRRITATION
The muscular tone is the basal state of contraction of a muscle (a
resting muscle has an irreducible basal muscle tone).
This basal tone is assessed by passive movements of various
segments performed by the examiner, the patient being relaxed. The
muscular tone is appreciated through its two parameters: the degree of
resistance to passive movements and the amplitude of the induced
movement.
There is also inspection of the examined area and sometimes the
muscle palpation.
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The most common movements performed comprise the flexionextension of the forearm on the arm while palpating the brachial biceps
muscle and its tendon, the flexion-extension of the hand on the forearm and
the passive flexion-extension of the calf on the thigh.
The muscle tone must be assessed symmetrically.
a) HYPOTONIA = low resistance to passive movement and high amplitude
of the movement.
The possible location of a lesion when hypotonia is found includes:
- a muscle disease
- a spinal arch lesion either on the lower motor neuron efferent arch or on the
proprioceptive afferent arch or both
- the initial phase of an upper motor neuron lesion and it is temporally
transient
- a cerebellar lesion
- an extrapyramidal lesion (neostriatal)
b) HYPERTONIA = high resistance to passive movement and low amplitude
to it.
There are 2 main patterns of hypertonia:
- Spasticity (pyramidal hypertonia) in pyramidal lesions. It has
the following features:
- is unevenly distributed, affecting the flexor muscles on the upper limb and
the extensor muscles on the lower limb
- it has elasticity as after the passive movement it tends to regain its
original position
- there is an uneven resistance during the passive movement, higher in the
beginning with a sudden yielding, the so called penknife opening
- other signs consistent with pyramidal lesion are encountered (brisk jerk
reflexes, the Babinski sign, etc.)
- Rigidity (extrapyramidal hypertonia) in extrapyramidal lesions.
It has the following features:
- there is an even distribution of the increased muscle tone, so that all
muscles are affected, with a slight dominance on the flexor muscles
- the whole body seems waxy, with a tendency to maintain longer a given
segmental position
- the cog wheel sign the passive movement of a muscle is done in a
saccadic fashion (3-6 saccadic movements are seen or better felt on the
biceps tendon)

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- the Noica sign (the blockage sign) the examiner performs successive
flexion-extension movements in the wrist articulation while patient is invited
to suddenly elevate his homolateral leg; a sudden increase in the muscular
tone leading to wrist blockage is elicited if rigidity is present. The Noica sign is
due to the fact that voluntary movement enhances extrapyramidal hypertonia.

c) DECEREBRATE RIGIDITY:
Midbrain lesions affecting the red nucleus (which belongs to the
paleostriatal extrapyramidal pathways) lead to a pathologic answer to pain
stimulation.
Pain stimulation (and sometimes even spontaneously) a brisk
extension of the upper limbs in pronation with the extension of the lower
limbs in adduction and internal rotation is elicited.
SIGNS OF MENINGEAL IRRITATION:
Meningeal irritation is due to abnormal substances and cells in the liquor.
Generally, the presence of white blood cells either lymphocytes or neutrophils in the
liquor or the presence of red blood cells, infection of the meninges, chemical irritation
from injected drugs leads to an increased paraspinal muscle tone due to heightened
sensitivity of irritated sensory roots to stretching.

The meningeal irritation is best assessed in the cervical portion of the

spinal cord which is the most mobile.
The best sign is the demonstration of stiffness of the neck on flexion.
The neck must be cradled in the examiners hand and gently flexed with the
chin toward the chest.
In pathological situations a boardlike stiffness can be found.
Fractures of the neck, paraspinal infections or acute spinal arthritis
may also cause stiffness of the neck. Generally, meningeal irritation does not
limit the lateral rotation of the neck, but degenerative arthritis does.
There are Kerning and Brudzinski signs to be looked for.
5. COORDINATION
Coordination is explored in order to assess the cerebellar function.
An efficient voluntary movement is very complex and needs force, speed,
amplitude, harmonically successive muscle contractions.
There is a precise sequence in the way the muscle contributing to a certain
purposeful movement will contract. There are the executing muscles, the agonist muscles
(which help the executing muscles), the antagonist muscles (that oppose the movement)
and the fixing muscles that all enable the perfection of a certain motor action. We omit
here the superior cerebral processes of initiating, planning and accomplishing any given
purposeful movement.
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Even at the basic level of execution, it involves a perfect succession of muscle

contractions in a total harmony between the agonist and antagonist muscles.
Cerebellum is responsible for the achievement of the goal of an harmonically
efficient complex movement (mainly the neo-cerebellar pathways).

Coordination is explored through the following tests:

- finger to nose test the patient has to touch with his index finger the tip of
the nose (with eyes open and closed)
- heel to knee test the patient has to touch the tip of his knee with the
opposite legs heel (with eyes open and closed)
- the adiadokokinesia test Adiadokokinesia is the incapacity to perform
alternate movements such as pronation-supination movements with both
hands.
In cerebellar lesions we encounter a distorted test as the patient cannot
follow the shortest way to the tip of his nose / knee (dysmetria), he surpasses
the target the tip of the nose / the knee (hypermetria) and his movement
ends in oscillating movements of his finger / heel as he approaches the target
(the final intentional tremor).
The adiadokokinesia is present as the successive movements are
clumsily performed.
Asynergia means that complex successive movements cannot be
performed (bending backwards for example).
Ataxia represents the whole coordination disturbances and it is best
seen in walking (a cerebellar walk is that of a drunken person, with an
enlarged sustaining base and oscillating posture. It is also reflected in
writing skills and speech.
Cerebellar lesions are accompanied by muscular hypotonia.
6. INVOLUNTARY MOVEMENTS
These are the movements that appear without the patients will and
therefore he cannot elicit any control upon.
These kinds of movements are produced in the extrapyramidal
pathways and centers and disturb when pathologic the voluntary movements.
The extrapyramidal centers and pathways control involuntary movements,
associated movements to voluntary ones and the muscle tone.

There is a whole range of involuntary movements which has to be

recognized and well understood.
Their analysis consists in inspection, sometimes palpation or even
graphical registration. It has to be found the pattern, the amplitude, the
rhythm, polymorphism or stereotypy, the topography, the temporal profile of

12

the involuntary movements. The involuntary movements are studied at rest,

in posture and during voluntary movements.
1. Tremor it is a rhythmically oscillating movement due to the
alternating contraction of antagonic muscle groups.
1.1. The physiological tremor appears with cold, exhaustion, emotions.
1.2. The parkinsonian tremor is present at rest, in posture and disappears in
voluntary movements. It has a 4-6 Hz frequency and resembles money
counting or paper rolling. It starts unilaterally.
1.3. The cerebellar tremor is course, is present in voluntary movements and
has the final intentional feature.
1.4. The Basedowian tremor appears in hyperthyroidian syndromes, is of
low amplitude and has a 10-12 Hz frequency.
1.5. The alcoholic tremor is fine, irregular and disappears with alcohol
intake.
1.6. The toxic tremor appears in several intoxication syndromes, mainly with
lead, mercury and heavy smoking or coffee abuse.
1.7. The neurotic tremor is variable from one examination to another and has
no precise pattern.
1.8. The hepato-lenticular tremor appears in all circumstances being a
mixture of the parkinsonian and cerebellar tremor.
1.9. The essential tremor is hereditary and has no other accompanying
features. It appears in some families to certain members.
1.10. The senile tremor appears to old aged persons and generally begins at
the head and chin.
2. Choreic movements are relatively rapid, irregularly recurrent,
unpredictable nonrhythmic movements of the trunk, face or extremities. The
condition is generally caused by an abnormality of the neostriatum. It
interferes with voluntary movements being often invalidating.
3. Athetosis consists of slow, twisting, flowing movements, affecting
distal more than proximal muscles and resulting in unusual postures. It is
related either to dystonia (when these movements are sustained) or to chorea
(when they are very brief) and sometimes they are associated to chorea
when they are called choreoathetosis. They are due to lesions in the
neostriatal part of the extrapyramidal system.
4. Pseudoathetosis there are the same movements as in athetosis but
their cause is a lesion at some level in the proprioceptive pathways.
5. Ballism consists in a violent flinging involuntary movement
involving predominantly the proximal muscles of the limbs. Generally it
involves only one side of the body, situation when it is called hemiballism.
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Ballism is usually caused by abnormalities of the subthalamic nucleus

(Luys) or its connections (mainly in stroke).
6. Fasciculations consists in spontaneous, irregular, recurrent
contractions of the muscle fibers belonging to a denevrated motor unit. They
are seen and perceived as twitching in the muscle and are not sufficient to
move the part. Almost any disorder of a lower motor neuron (cell body or
axon) may result in such fasciculations. They are especially prominent and
characteristic of chronic, progressive motor neuron disease.
In this disorder a muscle belly may be constantly agitated by such
fascicular contractions and may be found throughout the body.
They may be elicited by tapping the muscle belly with the reflex
hammer.
In neuronal disorders such as peripheral neuropathy fasciculations are
much less evident. They are also common in contracted muscles of
debilitated patients.
Caution is advised in interpreting fasciculations that appear infrequent
and are not accompanied by atrophy (as they are not necessarily evidence of
progressive disease).
7. Myoclonus is a term applied to rapid, shocklike jerks of a muscle
or part. It can move the limbs or parts of it. Myoclonus can occur in diverse
conditions as encephalopathy (infectious, metabolic), epilepsy and during
normal sleep. Even when pathologic they do not disappear during sleep.
8. Dystonia consists in a prolonged contraction of agonist and
antagonist muscles. When sustained over a long period, a dystonic posture
results; when more brief and recurrent, dystonic spasms are produced.
Examples: spasmodic torticollis - a dystonia of the neck, the writers
cramp a dystonia of the hand and fingers that occurs exclusively during the
act of writing, generalized dystonia of the face, trunk and extremities in
conditions such as dystonia musculorum deformans.
9. Tics are quick movements that are more complex than myoclonus.
A tic is a repetitive and stereotyped movement that can be temporarily
voluntarily suppressed, and sometimes is pseudogestual.
A typical motor tic might consist of eye blinking, licking the lips,
vocalizations of stereotyped utterances or throat clearing, touching of a
specific body part (ex. Gille de la Tourettes syndrome with multiple tics,
motor and verbal).
10. Seizures consist of sudden rhythmically repeated involuntary
movements that move the limbs and are consequence of cortical excitation.
There are generalized tonic-clonic seizures (in grand-mal epilepsy) when
they are preceded by a loss of consciousness and partial (focal) seizures also
14

called Jacksonian seizures that originate in a discrete area of the brain.

They tend to recruit successive muscle groups in contraction and sometimes
can generalize secondarily.
Dyskinesia is the general term indicating an abnormal involuntary
movement. It has to be described.
Bradykinesia is the term used for slowness and poverty of movement
(mainly encountered in Parkinsons disease).
Hyperkinesia is a general term referring to any excessive involuntary
movement.
7. REFLEXES
A reflex is an answer to an excitation and it can be motor, vasomotor
or secretor.
The reflex arch can be monosynaptic, bineuronal (an afferent, sensory
neuron and an efferent motor neuron).
There are the following reflexes types examined:
7.1. Tendon reflexes
7.2. Cutaneous reflexes
7.3. Idiomuscular reflexes
7.4. Posture reflexes
7.5. Triple flexion reflexes
7.6. Archaical reflexes
7.1. TENDON REFLEXES (tendon jerks) :
- to be examined require a tendon hammer
- it is monosynaptic bineuronal
- it is a stretch reflex elicited by tapping the tendon of a muscle or its
insertion on the bone
The afferent neuron of the arc begins with the muscle stretch receptors, the cell
bodies of which are in the dorsal root ganglia; intramedullary fibers of these cells synapse
on the motor neurons in the anterior horns of the spinal cord or on motor nuclei in the
lower brainstem; the efferent side of the arch is the motor neuron with its axon and
terminal structures that innervate the muscle.

In the upper limb there are 4 reflexes currently examined:

- The biceps reflex (bicipital jerk) BJ
- neuromere: C5-C6
- muscle: biceps
- nerve: musculocutaneous

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- arm to forearm at right angle, tapping through the examiners finger

- answer: flexion of the forearm on the arm
- The triceps reflex (triceps jerk) TJ
- neuromere: C6-C7
- muscle: triceps
- nerve: radial
- arm sustained by the examiner, arm to forearm at right angle,
tapping the triceps tendon above the olecran
- answer: a forearm extension on the arm
- The stiloradial jerk RJ
- neuromere: C6-C7
- muscle: the long supinator
- nerve: radial
- tapping the styloid process of the radius in an intermediate position
of the forearm
- answer: a flexion of the forearm on the arm with supination
- The stilocubital jerk CJ
- neuromere: C8-T1
- muscle: pronatus teres and pronatus quadratus
- nerve: cubital
- tapping the styloid process of the cubitus in an intermediate position
- answer: pronation
In the lower limb there are 2 reflexes currently examined:
- The knee reflex / jerk KJ
- neuromere: L2-L3-L4
- muscle: quadriceps
- nerve: femoral
- examined either with the patient sitting, calves at right angle to the
thighs, or in the supine position with calves at an obtuse angle to the thighs
sustained by the examiner, tapping the quadriceps tendon bellow the patella
- answer: the extension of the calf on the thigh
- The Achilles reflex / jerk AJ
- neuromere: L5-S1-S2
- muscle: sural triceps
- nerve: internal popliteal sciatic
- foot at a right angle to the calve, either sitting or lying, tapping the
Achilles tendon
- answer: a plantar flexion of the foot

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Reflexes are examined bilaterally.

They can be:
- normal
- hyporeflexia (low amplitude) in LMNS, lesions of the spinal arch
- hyperreflexia (brisk and high amplitude) in UMNS
- areflexia ( no answer) in LMNS, spinal arch lesions
- polykinesia (more contractions to one tap) in UMNS
- pendular knee jerk in cerebellar disorders (due to hypotonia and
antagonist muscles dysfunction)
- clonus is a variant of hyperreflexia; it is elicited by stretching the muscle
with a brisk movement when repetitive contractions of the muscle occur. It is
usually performed to the quadriceps muscle as the patellar clonus (by
pushing downwards the patella held between the examiners thumb and
index) and the sural triceps muscle as the Achillian clonus (by suddenly
dorsally flexing the foot). Clonus appears in UMNS.
7.2. CUTANEOUS REFLEXES (superficial reflexes):
- they are elicited by scratching the skin
- the response is a muscular contraction
They are polysynaptic involving several levels of the nervous system.

- The plantar reflex (L5-S1):

The plantar skin of the foot is scratched on its external margin, from
heel to first toe (halux).The normal answer is a plantar flexion of all toes.
The pathologic answer is the halux extension with spreading of all other toes
and is called the Babinski sign (it means a pyramidal lesion or a UMNS).
There is also that no answer is obtained (the so called plantar indifference).
The Babinski equivalents are:
- Oppenheim maneuver it consists in pushing downwards the tibial crest
- Gordon maneuver it consist in squeezing the gastrocnemius muscle
- Schaeffer maneuver it consists in pinching the Achilles tendon
- Rossollimo maneuver it consists in tapping the plantar aspect of the toes
with the reflex hammer
The Hoffmann reflex is a Babinski equivalent for the upper limb. It
consists in pinching the medius finger in a semiflexed position. In pyramidal
lesions the thumb adduction with flexion follows.
- The palm menton reflex (Marinescu Radovici):
The thenar eminence is scratched and in pathological cases the
menton contracts. It appears in lesions of both geniculate pathways
(pyramidal).
17

- The abdominal reflexes:

The abdominal skin is scratched from midline outwards at three
levels, on both sides:
- superior abdominal reflex (supraombilical) T7-T8 - under the coastal
ridge
- middle abdominal reflex (ombilical) T9-T10 parallel to the ombilic
- inferior abdominal reflex (subombilical) T11-T12 parallel and above
the inguinal arch
These reflexes are present or are absent and verify the integrity of
their spinal levels
7.3. IDIOMUSCULAR REFLEXES:
A muscle contracts when its belly is tapped with the reflex hammer.
This reflex disappears early in muscular disorders and is preserved in
peripheral neuropathies.
7.4. POSTURE REFLEXES:
They are elicited to prove rigidity if exists.
They consist in nearing the insertion heads of a muscle.
It is best performed on the anterior calf muscle by dorsally flexing the
foot. If there is rigidity (extrapyramidal hypertonia), the position is
preserved longer than normally.
7.5. THE TRIPLE FLEXION REFLEX:
It is a pathological reflex that can be elicited in spinal disorders that
cause a spinal functional or structural transsection, in the phase of spinal
automatism.
It is produced by pain stimuli applied under the section level; it will
lead to a triple flexion (thigh to abdomen, calf to thigh and foot to calf).
Sometimes this reflex is spontaneous.
7.6. ARCHAIC REFLEXES:
These reflexes are normal at some developmental stage, and then they
disappear as the nervous system matures. Their reappearance in adulthood
has a pathological significance.
- Grasp reflex is normal up to 6 month. In adulthood it reflects frontal
lesions. It is elicited by touching with something (i.e. the reflex hammer) the
palm and the patient will promptly and strongly hold the object.
- Sucking reflex touching the lips with an object leads to sucking
movements in adult patients that have frontal lesions.
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8. TROPHIC AND AUTONOMIC DISORDERS

There is a central autonomic headquarter (the hypothalamus) and a peripheral
autonomic system (sympathic and parasymphatic).

- functional autonomic dysfunction:

- breathing pattern (tahy, brady, etc)
- vasomotricity (vasoconstriction, vasodilatation with hyperemia)
- heart rate (tahy, brady, etc.)
- blood pressure (hyper, hypo)
- sweating disorders
- sphincterian dysfunctions (bladder retention/incontinence, anal
retention/incontinence)
- sexual dysfunctions
-trophic autonomic dysfunctions:
- skin changes (thinning or thickening, hair loss, nail changes, skin
ulcers, escars, etc.)
- articular and bone changes (osteo-arthropaties deforming the shape
of the joint, spontaneous fractures, osteoporosis, osteocondensation)
- amyotrophias are trophic disorders, not autonomic
- are muscular atrophies
They can be:
a) primitive or myogenic:
- proximal onset
- symmetrical
- tendon reflexes are preserved
- idiomuscular reflexes are early absent
b) secondary or neurogenic:
- distal onset
- relatively symmetrical
- tendon reflexes are early lost
- idiomuscular reflexes preserved
- fasciculations are present
9. THE SENSORY EXAMINATION
Is the examination of the pathways for all external inputs for which
specialized receptors are available.
There are two main pathways:
- spinothalamic (touch, thermic and pain)
- proprioceptive ( touch, position sense)

19

There are 4 neurons:

1. in dorsal ganglia
2. in posterior horn (spinal) for spinothalamic pathway or in medulla for proprioceptive
Goll and Burdach pathways
3. in thalamus
4. in parietal lobe ascending parietal gyrus, sensitive homunculus
Classification:
-subjective sensations
- objective sensations prothopatic superficial touch
- thermic
- algic (pain)
- proprioceptive myoartrokinetic
- vibratory
- epicritic tactile discrimination
- dermolexia / graphesthesia
- topognosia
- sensory extinction
- morphognosia
- hillognosia
- stereognosia
- somatognosia

Examination technique:
- Light touch: a piece of cotton wool or the doctors fingertips are used to
touch symmetrical areas of the skin at random intervals
- Temperature sensation: symmetrical areas of the skin are touched at
random with two glass tubes containing cold and respectively warm water
and the patient is required to identify the cold or warm quality of the
stimulus
- Pain sensation: using a blunt pin , symmetrical areas of the skin are
pricked eliciting pain
- Joint position sense (myoartrokinetic): the examination is performed
with the patients eyes closed; he has to guess how the examiner moved his
fingers upwards or downwards while the distal phalanx is held between
the two examiners fingers. The direction of the movement must be
randomly chosen.
- Vibratory sense: is examined with a 128 Hz tuning fork. The patient is
with his eyes closed and must perceive the vibrations induced by the tuning
fork while placed on the following locations:
-toe tips, the metatarsal phalangeal joint, the medial malleolus, the tibial
tuberosity, the anterior superior iliac spine
- at the upper limb: the fingertips, each interphalangeal joint, the wrist, the
elbow, the shoulder.
If sensation is normal distally, there is no point proceeding proximally
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- Tactile discrimination (two-point discrimination) refers to the ability to

distinguish two pain stimuli applied simultaneously as such. It depends of
the skin area tested as touch and pain receptors are not evenly distributed
over the body (denser in some skin areas as fingers and face and rarer in
others such the trunk).
- Dermolexia or graphesthesia refers to the ability to recognize the letters
or numbers that the examiner traced on the patients skin.
- Topognosia refers to identifying with eyes closed where on the body the
patient is touched.
- Sensory extinction test refers to a double simultaneous stimulation of two
identical parts on each side of the body (in parietal lesions the patient
neglects and fails to feel the touch on the contralateral side of the lesion).
- Morphognosia refers to identifying the shape of an object by tactile senses
only (without visual control).
- Hillognosia refers to identifying what material an object is made of (glass,
plastic, metal, etc.) by means of touch alone.
- Stereognosia refers to object recognition by means of palpation. The
inability to recognize an object in this manner is called astereognosia.
- Somatognosia refers to recognizing your own body (corporeal schema).
Pathological variants consists in asomatognosia (when the patient fails to
recognize mainly his left hemibody as belonging to him), anosognosia
(mainly failing to recognize his motor deficit called anosognosia for
hemiplegia), anosodyaphoria (the patient is indifferent to the
acknowledgment of his motor deficit).
Topographical analysis has to decide if the sensation disorder is:
- nevritic it respects the distribution territory of a nerve according to the
charts
- radicular it respects a dermatome territory as in the charts
- polyneuropathic it is distributed in a glove and stocking fashion,
being distally placed, with no distinct clear cut limit between the normal and
pathological area
- spinal:
- total section- loss of all sensory modalities both superficial and
proprioceptive under the lesion level (level sensory loss)
- hemisection Brown-Sequard syndrome below the lesion level
there is a homolateral loss of proprioception and motor deficit; contralateral
there is a loss of touch, pain and thermic sensation.
- dissociation patterns: - the syringomyelic type (loss of superficial
sensation and preservation of proprioception)
21

- the tabetiform type (loss of

proprioception and preservation of superficial sensation)
- anterior compression early loss of superficial sensation
- posterior compression early loss of proprioceptive sensation
- brain stem alternate syndromes with contralateral loss of either
superficial sensation or/and proprioception (hemihypoesthesia or anesthesia
or dysesthesia) and homolateral cranial nerves symptoms depending upon
the lesion level in the brainstem.
- thalamic loss of all sensory modalities contralateral to the lesion in a
hemibody accompanied by the thalamic pain.
- cortical loss of either sensory modalities or both in a hemibody
accompanied sometimes by epicritic type of disturbances.
- neurogenic no topographical distribution of the disturbance with
variations in pattern and intensity from one examination to another
- headache / cephaleea pain of the cranial aspect (not the facial aspect) of
the head
- migraine particular type of headache mainly on half of the skull
throbbing.
- causalgia pain and sensitivity in the sensory distribution with
sympathetic overactivity (followed by trophic changes).
10. CRANIAL NERVES
There are 12 pairs of cranial nerves. They are:
-motor
- sensitive
- sensorial
- autonomic (parasympathetic)
-mixed
The cranial nerves are:
I. The olphactory nerve sensorial
II. The optic nerve sensorial
III. The common oculomotor nerve motor and autonomic
IV. The pathetic or trochlear nerve motor
V. The trigeminal nerve motor and sensitive
VI. The abducens nerve motor
VII. The facial nerve motor, sensory, sensitive, autonomic
VIII. The auditory nerve (acoustic and vestibular) sensorial
IX. The glossopharingeal nerve motor, sensorial, sensitive, autonomic
X. The vagus nerve motor, sensitive, autonomic
XI. The accessory nerve (spinal nerve) motor
XII. The hypoglossal nerve motor

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I. The olphactory nerve (sensorial)

- supratentorial nerve
- the olphactory pathway:
- the protoneurons (olphactive cells) are located in the yellow spot of the nasal
mucosa with the axons forming the olphactory nerve that penetrate the base of the skull
through the lamina cribrosa of the ethmoid bone, and their dendrites forming the
olphactory cilli;
- deutoneurons from the olphactory bulb in the anterior cranial fossa at the base
of the skull;
- the third neurons are located in the subcalous gyrus, in the anterior perforated
space, forming the secondary olphactory center;
- the fourth neurons are located in the temporal uncus and amygdale, forming the
tertiary olphactory center;

- most recognizable smells require olfaction; some agents such as ammonia

can be recognized by nasal epithelium and do not require an intact
olphactory pathway
Examination:
- the patient is asked to identify recognizable smells such as orange,
toothpaste, peppermint, camphor, rosewater; each nostril is tested separately
Findings:
- normal smell the patient is able to identify the smells appropriately
- anosmia the patient is unable to recognize scents offered but recognizes
ammonia. It can be unilateral or bilateral (causes: blocked nasal passages as
in common cold, nasal atrophy in cocaine snuffers or in smokers, chronic
rhinitis, nasal trauma with axonal damage of the olfactory nerve, ageing,
meningioma at the skull).
- hyposmia a diminished olphactory capacity (in raised intracranial
pressure, hypophisary adenomas)
- hyperosmia an increased olphactory perception (in hypertiroidia,
pregnancy, migraineous attacks, allergic states)
- parosmia mistaking one smell with another (in epileptical aura)
- cacosmia perceiving all smells as foul and unpleasant (is mainly
psychical, as a remnant overwhelming perception after an actual unpleasant
one)
- olphactory hallucinations smell perceptions in the absence of an actual
excitation (it is caused by an irritative lesion of the temporal cortex in
temporal epilepsy with uncinate crisis in temporal tumors, hallucinatory
delusional psychosis such as schizophrenia, dementia, paranoia).
- hallucination perception without object and with no critic
- hallucinosis perception without object with critic

23

II. THE OPTIC NERVE (sensorial)

- supratentorial
- the most important sensorial pathway from the point of view of the complexity of
information that it conveys, and also very commonly affected as it practically crosses the
skull
- the optic pathway:
- the protoneurons are the bipolar cells in the VI-th layer of retina. It consists in
two kind of cells (the cone cells aimed for colored vision placed in the macula, and the
baton cells aimed for black and white vision scattered throughout the rest of retina).
- the deutoneurons are the multipolar cells in the VIII-th layer of retina. Their
axons gather and form the optic nerve that exits the posterior pole of the ocular globe
through the optic hole of the orbit (optic canal) to enter intracranilly. The optic nerve is
seen in ophtalmoscopic examination of the optic fundi as the papilla.
- the third neuron is placed in the lateral geniculate body, a metathalamic
formation.
- the pathway to the thalamus is known at first as optic nerve, then the two optic
nerves unite to form the optic chiasm, after which the pathways divide again to form the
optic tract.
- the optic chiasm is the location in which the nasal fibers of the optic pathways
cross on the opposite side. Retrochiasmal, in the optic bands, we encounter nasal fibers of
the opposite retina and temporal fibers of the homolateral retina. The middle of the optic
chiasm is in topographical closeness to the hypophysis (the pituitary gland) and the
external margin of the optic chiasm with the internal carotid artery as it exits the temporal
bone to enter the skull.
- the axons of the third neurons form the optical radiations (of Gratiolet) and they
connect to the fourth neurons placed in the occipital lobe along the calcarine fissure
forming the 17-th Brodmanns area.

Neurological examination includes:

a) The visual acuity
b) The visual field
c) The chromatic perception
d) The optic fundi
a) The visual acuity: the keenness of vision, the acuteness of it.
- it is tested for each eye separately, either with the Snellens chart (the
patient placed at 6 meters) or at bedside where the patient has to read a text
(from 50 cm) or to count examiners fingers (from 5 m) or to distinguish
light from dark.
- ambliopia is an inborn visual acuity defect that cannot be corrected by
lenses.
- blindness (amaurosis, cecity) loss of vision (central or peripheral). When
central, it has to involve both left and right occipital cortical areas.
- nictalopia the diminishing of visual acuity during daytime.

24

- hemeralopia the diminishing of visual acuity at sunset (twilight).

b) The visual field: the extent of space perceived with one eye placed
in fix position.
- conventionally, the visual field of each eye is divided in two halves nasal
and temporal, which in turn are divided in an upper half and lower half
respectively.
- the visual field is uneven and has different opening degrees (superior- 60,
inferior - 70, nasal - 60, temporal - 90).
S 60

N 60 T 90

I 70
- There is a digital examination at the bedside and a campimetric one where
charts of the visual field are drawn
- each eye is tested separately, with the other covered. The examined eye
must be kept in a still position and the patient is required to say when he
perceives the examiners fingers that appear in the temporal, nasal, upper
and lower planes
- visual field defects consists in:
- scotomas black spots that appear in the visual fields. They can be
centrally or peripherally placed. The central scotomas are related to macular
lesions, retrobulbar neuritis and raised intracranial pressure. The peripheral
scotomas are due to a retinal or optic pathways lesion.
- concentric visual field narrowing can be regular or irregular. They
are related to disorders such as optic atrophies, glaucoma, double
hemianopia.
- hemianopias the loss of one half of the visual field from each eye,
nasal or temporal.
Hemianopias are heteronymous in chiasmal lesions (bitemporal or
binasal) or homonymous in all retrochiasmal lesions (nasal on one side and
temporal on the other side).
An optic nerve lesion, anterior to the optic chiasm leads to monocular
blindness.
25

The central chiasmal lesions lead to bitemporal heteronymous

hemianopia and the external optic chiasm lesions lead to binasal
heteronymous hemianopia.
The homonymous hemianopias appear in retrochiasmal lesions,
opposite to the affected side.
Double hemianopias lead to cortical blindness in which the patient
ignores his blindness as he is not aware of it (agnosia is given by the
nondominant hemisphere).
Quadrant hemianopias are encountered in lesions of the optical
radiations. They can be in the upper or lower quadrant.
c) The chromatic vision the ability of colored vision.
- it is tested at bedside or with colored charts
- the inability to distinguish certain colors (such as in daltonism) is called
dyschromatopsia.
d) The optic fundi:
- the examination is performed with the ophthalmoscope which allows the
examination of the optic fundi
- the optic disc or papilla and the vessels are examined
- the optic disc is light yellowish and has to be well delimited from the
surrounding retina
- the contour of the optic disc becomes blurred in papillary stasis or
papilloedema (raised intracranial pressure) or papillitis (optic nerve neuritis)
- papilloedema:
- there is an optic disc swelling, humping of the disc margins, arterial
spasms and engorged veins with hemorrhages and exudates
- the visual acuity is preserved, while in papillitis the visual acuity is
early lost
- optic atrophy the optic disc is pale to white (in multiple sclerosis it starts
temporally)
- deep optic cup in chronic glaucoma
- retinal vessels examination:
- in the center of the optic disc two arteries emerge (the central retinal
artery) which divide into two branches superior and inferior, which in turn
divide in temporal and nasal branches
- every artery has an accompanying homologous vein
- arteries are bright red, normally 1/3 from the dark red veins
diameter

26

- arteries have a parietal reflex as normally they are transparent and

the blood column is seen through their transparency; as the arteries are
pathologically affixed, their transparency disappears and the parietal reflex
is heightened or even an arterial opacity is seen (copper or silver wire like
arteries)
- the crossing between an artery and vein is examined for the
tampering of the vein (the Salus Gunn sign) A-V nipping
III. The common oculomotor nerve (motor and autonomic)
IV. The pathetic or trochlear nerve (motor)
VI. The abducens nerve (motor)
The oculomotor nerves must be studied together as they move the
eyeball.
Nerve III:
- midbrain origin
- motor: muscles eyelid lifter (levator palpebralis), the medial rectus (for adduction), the
superior rectus, the inferior oblique, the inferior rectus
- parasympathetic: Edinger Westphal nucleus (for myosis) and Perlia nucleus (for
convergence)
Nerve IV:
- midbrain origin
- motor: the superior oblique muscle (moves the eyeball downwards and outwards)
Nerve VI:
- pons origin
- motor: the lateral rectus (for eyeball abduction)
All three nerves exit through the superior orbital fissure (the sphenoidal aperture)
and travels in the lateral wall of the cavernous sinus.

The examination includes:

a) The eyelids aperture
b) The eyeballs position
c) The ocular motility
d) Ocular convergence
e) The pupil and pupilar reflexes
a) The eyelids aperture:
- lower eyelid position = ptosis (partial or complete). It appears in nerve III
lesion, Horners syndrome (myosis, enophtalmia and palpebral ptosis in
cervical sympathetic lesion)
- higher than normal eyelid = lid retraction in Pourfour du Petit syndrome
(cervical sympathetic irritative lesion)

27

b) The eyeballs position:

- at forward gaze, eyeballs have pupils on the medial line, symmetrical
- oculomotor paresis results in ocular deviation on the opposite side
strabismus
- strabismus can be internal or external, convergent or divergent, congenital
or acquired
c) The ocular motility:
- is achieved through the extrinsic oculomotor muscles action
- examination: the patient follows the movement of the examiners fingers in
all directions while the head is fixed
- oculomotor lesions consists of:
- dyplopia = double vision
- strabismus
- impossibility of muscular movements of the affected nerve
- one oculomotor nerve lesion = partial ophtalmoplegia
- all oculomotor nerves lesions = total ophtalmoplegia
- nerve III palsy:
- dyplopia
- external strabismus
- no movements of the third nerve muscles (adduction, up, down)
- ptosis
- mydriasis
- nerve IV palsy:
- dyplopia (vertical, climbing the stairs)
- strabismus inwards and upwards
- no movement outwards and downwards
- head tilted on the affected side to correct the vision
- nerve VI palsy:
- dyplopia (lateral gaze)
- internal strabismus
- no abducting movements possible
- Parinaud syndrome upwards gaze palsy (collicular lesion)
- Foville syndrome lateral conjugate movements paralysis
d) Ocular convergence :
- consists of eye adduction for near sight and is associated with myosis
- it is a reflex act

28

- it is examined by looking to an approaching object (so that the object can

be caught on the macula)
e) The pupil and pupillary reflexes:
- normal pupils round, equal, regular contour, operating diameter 2-5 mm
- pathologic shape, dimensions and reflexes modifications:
- shape: oval, polygonal, irregular, etc
- anisocoria = unequal pupils in neurolues, anterior pole surgery,
intracerebral haematoma
- dimensions - over 5 mm = mydriasis
- under 2 mm = myosis
Mydriasis sympathetic cervical cilio-spinal center Budge, C8-T2.
Myosis Edinger Westphall third nerve nucleus.

- mydriasis unilateral (Pourfour du Petit syndrome in apical lung

cancer) or bilateral (atropine intoxication, botulinic intoxication,
hyperthyroidism, ethylism)
- myosis unilateral (Horners syndrome) or bilateral (tabes, opiate
intoxication, parathion intoxication, uremia, pontine level coma)
- pupilary reflexes :
- photomotor reflex PMR (pupilar reaction to light) myosis to light
- distance accommodation reflex DAR (pupilar reaction to distance)
- PMR can be normal, slow or absent
- pathological pupilary reflexes:
- Argyll Robertson PMR -, DAR+ (in neurolues)
- inverted Argyll Robertson PMR+, DAR- (in coma, encephalitis,
meningitis, intoxications)
- the false Argyll Robertson PMR-, mydriasis (in epyphisary
tumors)
- pupilar rigidity PMR-, DAR- (in neurolues)
- pupilotonia PMR-, anisocoria (Adie syndrome)
V. Trigeminal nerve (motor and sensory)
- pontine nerve
- three branches:
- ophthalmic (enters the skull through the superior orbital fissure) - sensory
- maxillary (enters through the foramen rotundum) - sensory
- mandibular (enters through the foramen ovale) sensory and motor
- anatomy:
- first neuron in Gasser node (top of the temporal bone)

29

- second neuron in pons

- third neuron in thalamus
- forth neuron in parietal cortex
- V1 sensory territory:
- vertex to frontal region, genian, temporal, back of nose, superior eyelid
- cornea and ocular globe conjunctiva
- the mucosa in the frontal, ethmoydal, sphenoidal sinuses
- dural sinuses in the anterior cerebral fossa
- falx cerebri anterior
- tentorium
- the longitudinal superior sinus
- V2 sensory territory:
- infraorbitar, inferior eyelid, nasal wing, upper lip
- the palate
- teeth of upper maxillary
- maxillary sinus mucosa
- V3 sensory territory:
- temporal, masseterin, mentonier region
- bucal vestibule mucosa
- teeth of inferior maxillary
- tongue in 2/3 of the tongue
- V3 motor territory:
- mastication muscles: temporal muscle, masseter, external and internal
pterigoidian muscle (lift the mandibula)
- myloidian muscle, anterior segment of digastric muscle (lower mandibula)
- pterigoidian muscle unilateral contraction (lateral movement of mandibula)

- sensory examination touch of the symmetrical trigeminal territories

- motor examination movements of the mandibula, tonus and trophicity of
the masseter muscle (palpation)
- cornean reflex:
- pontine level
- afferent branch V1 (light touch of cornea with cotton wool)
- efferent branch facial nerve (eyelid closure ocular orbicular
muscles)
- masseterin reflex (jaw jerk) taping the mentonier region through the
examiners thumb contracts the masseter muscle lifting the mandibula (in
atherosclerosis)
VII. The facial nerve (motor, sensory, sensorial, autonomic)
- pontine nerve
- it includes the Wrisberg nerve (VII bis)
- face, ear, taste, tear

30

- motor territory for the facial mimic or expression (the facial skin muscles, the eyelid
and lip orbiculars), the stapedius muscle in the inner ear, the posterior belly of the
digastric muscle
- sensory territory the retroauricular region, the ear and first third of the external
auditory meatus
- sensorial taste in the anterior 2/3 of the tongue (sweet, sour, salty)
- parasympathetic:
- saliva (the sublingual and the submaxilar gland)
- cephalic arteries
- lacrimal secretion (tear production)
- anatomy: from pons through the internal auditory canal (exits the skull through the
internal acoustic porous) the Fallopian canal where the geniculate node lies and exits
through the stylomastoid hole, goes through the parotid gland to divide in two branches:
temporo-facial and cervico-facial;

- sensory examination: symmetrical touching of the sensory territory

- taste examination: tongue touching with cotton wool dipped in sweet, sour
or salty solutions
- pathological taste perceptions:
- aguesia no taste perception
- hypoguesia diminished taste perception
- dysguesia distorted perceptions
- motor examination:
- inspection: face symmetry, physiological folders (forehead,
nasogenian, nasolabial), mimic, movements, eyebrow lifting, sniffing,
laughing, teeth showing, cheek blowing, whistling
a) peripheral type of facial palsy:
- hemiface hypomimia, smooth skin no forehead folds, no nasogenian and
nasolabial folds, the lip corner is fallen
- no eye closure (lagophtalmia), the lower lid is everted tears running down
the face (epyphora)
- the Charles Bell sign is present the impossibility of eye closure discloses
the physiological upward eyeball movement at eye closure attempt
- no blinking on the affected side
- smiling movements uncovers teeth only on the healthy side (tennis racket
shape mouth)
- labial consonants are pronounced with difficulty (b, m, p)
- distorted mastication on the affected side as food tends to gather between
cheeks and teeth
- the cornean reflex is absent
- intolerance for high pitched noises (hyperacusia)
- involuntary movements accentuate the facial asymmetry (better exposes it)
31

b) central type facial palsy:

- the upper half of the face is spared (due to bilateral innervation)
- the patient can close the eye and lift the eyebrows
- the lip corner is fallen
- smiling movements uncovers teeth only on the healthy side
- involuntary movements (such as laughing, crying) attenuate the asymmetry
- difacial paresis in poliradiculonevritis
- facial hemispasm after a facial palsy, the synkinetic contraction of the
muscles (eye closure is accompanied by lip corner lifting)
- crocodile tears syndrome excessive tear production when eating (due
to a dysdirectional aberrant regeneration as salivary fibers connect to the
lacrimal gland)
VIII. The auditory nerve (acoustic and vestibular)
- sensorial
- pontine origin
- has two components: auditory and vestibular
- the excitant:
- the sonic vibrations for the auditory component
- head movements and head position change for the vestibular component
- anatomy auditory nerve:
- first, receptor neurons the auditory cells or the Corti organ in the inner ear
cochlea; their axons form the auditory nerve that travels through the temporal bone, in the
inner auditory conduct together with the facial nerve, the Wrisberg nerve or the VII bis
nerve and the vestibular nerve
- the second neuron is in the pons (two nuclei ventral and lateral)
- the third neuron in the geniculate body (metathalamus)
- the fourth neuron in the temporal lobe (the transverse circumvolution of
Herschel corresponding to Brodmann area 41 and 42)
- anatomy vestibular nerve:
- the receptors in the utricula, sacula and the three semicircular canals, the first
neuron in the Scarpa ganglia; their axons form the vestibular nerve that travel through the
temporal bone in the internal auditory canal
- the second neuron the vestibular nuclei in the fourth ventricles floor
- they connect to cerebellum (archicerebellum), the reticulate substance, the
oculomotor nerves, the spine and cortical areas in the temporal and parietal lobe

a) auditory nerve:
- examination:
- phonic acumetry each ear has to be tested separately to hear
whispered voice from 5 m

32

- instrumental acumetry a vibrating tuning fork or a diapason (64128 Hz) is approached to one ear and the patient with eyes closed has to
announce when he perceives the vibrations
- audiometry the most reliable examination; an electromagnetic
audiometer emits sounds of different frequencies 64-8000 Hz (0-125
decibels); depending on what the patient hears an auditory chart or map is
drawn
- Pathological changes of the auditory function:
1. deficit type disorders:
- hypoacusia the diminishing of the auditory acuity
- hyperacusia the exacerbation of the auditory acuity (in migraine, facial
nerve palsy the stapedius muscle is paralyzed, pregnancy, epileptic aura)
- anacusia, deafness loss of auditory acuity
Causes of deafness:
- othogenic (transmission deafness): in external and middle ear lesions
(othitis, othosclerosis)
- neurogenic (perception deafness): in inner ear lesions (Corti organ lesion,
auditory nerve lesion, central pathways lesions such as acoustic
neuropathies, temporal bone fractures, tumors in the ponto-cerebellar angle,
basal meningitis)
- mix deafness both middle and inner ear lesions
Differential diagnosis between a transmission and perception disturbances:
- the Weber test: a vibrating tuning fork is placed on the patients vertex; normally the
vibrations are equally perceived in both ears;
- in transmission disorders, vibrations are better perceived in the affected ear (a
lateralized Weber test in the sick ear)
- in perception disorders, vibrations are better perceived in the healthy ear ( a lateralized
Weber test in the healthy ear)
- the Rinn test: the bone transmission is checked by placing the vibrating tuning fork on
the mastoid process(BC bone conduction); when the patient doesnt perceive the
vibration anymore the tuning fork is moved in front of the ear (AC air conduction);
- if the patient perceives the vibrations for another 20-30 seconds (a prolonged aerial
transmission) the test is positive
- in transmission deafness the bone transmission will be longer than the aerial one and the
test will be negative
- the Schwabach test: the vibrating tuning fork is placed on the vertex; a normal
perception time for the vibrations is 20 seconds
- a shortened perception time means a perception disorder
- a prolonged perception time means a transmission disorder

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2. irritation type disorders:

- accuphenes amorphous noises that the patient perceives called tinnitus
(in external and middle ear disorders, toxic acoustic neuritis, raised
intracranial pressure, head trauma)
- auditory hallucinations abnormal perceptions of words, sentences,
melodies, voices (in temporal lobe tumors, epilepsy, psychiatric disorders)
- the perception of arterial pulsations (in carotid aneurysm, angiomas,
dural shunts, atherosclerosis); normally the blood circulation doesnt
produce noise in ears as the blood pulsation is attenuated by the arterial
walls elasticity
b) the vestibular nerve:
- is examined by the following procedures:
- the Romberg test
- the walk test
- the test of holding the arms in a fix position
- oculomotricity for nystagmus
In vestibular disorders the patient has the following symptoms:
- vertigo is a subjective rotatory feeling of the surrounding things with
head movement or a floating sensation; it has a variable intensity sometimes
leading up to impossible orthostatism
- vegetative symptoms are of variable intensity; they accompany the
vertigo and consist in sweating, hypotension, pallor, nausea, vomiting (due
to vestibule-reticulate connections)
- tonic disorders with an increase of the muscle tone in the muscles of the
affected side which lead to a so called tonic deviation of the body or parts
of it (uncovered by the Romberg test, the arms deviation test and a star
deviation pattern deviation walk, nystagmus)
- nystagmus represents an involuntary permanent rhythmic movement of
the eyes in lateral, vertical and sometimes even straightforward look
- when present, it means a vestibular lesion
- nystagmus has two components or phases: a slow one (towards the
affected vestibule) and a rapid compensatory one (opposite to the affected
vestibule) which defines the sense of the nystagmus; so it can be horizontal,
vertical, rotator clockwise or anti-clockwise
- nystagmus is examined like oculomotricity or registered by a
nystagmograph
- there is a normal fixation nystagmus in extreme lateral gaze, an
optokinetic nystagmus (when looking to moving objects) and congenital
nystagmus
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There are vestibular provoked tests to perform:

- the rotation test
- the caloric test
- the galvanic test

There are two clinical vestibular syndromes:

1. The peripheral vestibular syndrome (armonic):
- in vestibular and vestibular nerve lesions
- all signs point to the same vestibule (the tests)
- there is a proportion between the intensity of vertigo and the amplitude of
the accompanying autonomic symptoms
- nystagmus is unidirectional (frequently horizontal)
2. The central vestibular syndrome (dysarmonic):
- in lesions of the pontine vestibular nuclei and all pathways beyond them
- the tests show vestibular dysfunction but do not precisely point one
vestibule
- there is no proportion between the intensity of vertigo and the
accompanying autonomic symptoms
- nystagmus is multidirectional or vertical
IX. The glossopharingeal nerve (motor, sensory, sensorial, autonomic)
X. The vagus nerve (motor, sensory, autonomic)
They are studied together as they have a common medullar origin (the ambiguous
nucleus), they exit the skull base through the same jugular foramen and innervate the
motor muscles for swallowing and phonation.
- the glossopharingeal nerve:
- motor - innervates the superior pharyngeal constrictor muscles (help to swallow
solid food)
- sensory innervates the amygdalian (tonsilar) loge, the pharynx, the posterior
part of the palate, the posterior 1/3 of the tongue, the middle ear
- sensorial taste in the posterior 1/3 of the tongue (bitter)
- autonomic the salivary glands (parotid)
- the vagus nerve:
- motor innervates the middle and inferior pharyngeal constrictor muscles (help
to swallow liquid food) and the palate elevators, the uvula elevator, pharynx, larynx (via
recurrent laryngeal)
- sensory tympanic membrane, external auditory canal, external ear
- autonomic afferents from carotid baroreceptors, parasympathetic supply to and
from thorax and abdomen

In IX th and X th lesions:
- the uvula is deviated towards the healthy side and the palate is lowered on
the affected side

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- saying ahh will not elevate the affected palate and will deviate uvula on the
opposite side
- dysphonia and dysphagia
- hypoesthesia in the affected territory
- aguesia in the posterior 1/3 of the tongue (for bitter)
-gag reflex afferent- the glossopharingeal nerve; efferent the vagus nerve
- touch the pharyngeal wall behind the pillars of the fauces
- watch the uvula as it should lift following the stimulus
- ask the patient to compare the sensation between two sides
- if f uvula moves to one side upper or lower motor lesion of the X th
nerve
- if uvula does not move on saying ahh or gag bilateral palatal muscle
paresis
- if uvula moves on saying ahh but not on gag, with reduced sensation of
pharynx lesion of the IX th nerve rare
XI. The spinal (accessory) nerve (motor)
- arises from the medulla (the internal branch) and has contributions from the spinal route
rising from C2 to C4 (the external branch)
-motor the larynx (the internal branch) - voice
the sternocleidomastoid and the trapezius muscles (the external branch)

- examination:
- the sternocleidomastoid muscle ask the patient to turn his head to
one side, the examiner pushing against this movement; watch the opposite
sternocleidomastoid
- the trapezius ask the patient to push his head back as the examiner
opposes this movement; watch the trapezius
- in sternocleidomastoid paralysis :
- weakness of the sternocleidomastoid muscle
- hypotonia
- atrophy of the muscle
- in bilateral paralysis the patient cant move his had forward
- in trapezius paralysis:
- weakness of the trapezius muscle
- hypotonia
- atrophy of the muscle
- lowering of the shoulder
- the patient cant shrug his shoulder on the affected side

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XII. The hypoglossal nerve (motor)

- origin medulla
- motor intrinsic muscles of the tongue

- examination: look at the patients tongue and then ask him to put out his
tongue
- unilateral lesions:
- atrophy of the affected half of the tongue
- fasciculations
- the tip of the tongue is diverted towards the healthy side when in the
mouth and towards the affected side in protrusion (protrusion is done by the
genioglossal muscles which are crossed muscles) the tongue in protrusion
shows the side of the lesion
- bilateral lesions:
- mastication troubles
- phonation and swallowing problems
- wasting of the tongue with fibrillation

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