Theme: Assessment of the nervous system.

Neuropathology (from greek neuro – nerve, pathos – disease, logos – science) – is a part of clinical medicine, which is involved in nervous diseases and its role in pathology of other organs and systems of human body.

The main structural functional genetic and anatomic unit of nervous system is neuron - nervous cell. Its main function is to accept and carry out impulse.

The main function of nervous system is unification and regulation of different physiological processes. That means that nervous system unites, integrates and subordinates all the parts of human body and provides its connection with environment.

The base of nervous system activity is reflex principle. Reflex – is a reaction of our organism to various outside and inside effects. It is provided by nervous system.

The reflex consists of afferent part (which accepts information), central part (that keeps information), and efferent part (that creates response). As a result we have a circle – like structure - receptor (primary information centre) – programme centre – executive apparatus.

All the reflexes can be divided into different groups - simple and complex, inborn and trained, conditioned and unconditioned.

Unconditioned reflexes.

1. They are inborn ones.

2. They are phylogenetically old, that means they were formed in course of phylogenesis.

3. They are based on certain anatomic structures (segments of spinal cord or brain stem).

4. They exist even without brain cortex influence.

5. They are inherited.

6. They can be regulated by brain cortex.

7. They are basis for the conditioned reflexes.

Conditioned reflexes.

1. They are the result of the individual experience and are formed during ontogenesis.

2. They are unstable, that means they need constant support.

3. They aren’t based on certain anatomic structures.

4. They are fixed in brain cortex.

There are such conditioned reflexes as speaking, writing, reading, calculation, practice.

Neurology studies unconditioned reflexes. That helps evaluate the state of nervous system. Conditioned reflexes are studied by psychiatrists.

Unconditioned reflexes are divided into such groups:

· Superficial and deep

· Simple and complex

· Proprioceptive (stretch, periosteal, articular)

· Exteroceptive (dermal, from mucose membrane)

· Interoceptive (from mucose membrane of internal organs – for example urination in case of internal sphincter irritation)

In clinical practice we evaluate the following reflexes:

Reflex	The group of reflex	Muscles	Nerves	Segments
Subeyesbrow	Deep, periostal reflex	M. orbicularis oculi	N. trigeminus ( V ) – N.facialis (VII)	Medulla oblongata and pons
Corneal (lid)	Superficial, from mucose membrane	M. orbicularis oculi	N. trigeminus ( V ) – N.facialis (VII)	Medulla oblongata and pons
Jaw Jerk (mandibular, chin, masseter) reflex (Bechterev’s)	Deep, periostal reflex	M.masseter	N. trigeminus ( V ) – N.mandibularis (sensory and motor )	Medulla oblongata and pons
Pharyngeal	Superficial, from mucose membrane	Mm. constrictores pharyngis and others	N.glosso- pharyngeus, n.vagus (sensory and motor), 9th and 10th pair of CCN	Medulla oblongata
Palatal (palatine)	Superficial, from mucose membrane	Mm. levatores velli palatini	N.glosso- pharyngeus, n.vagus (sensory and motor)	Medulla oblongata
Biceps	Deep, stretch reflex	M.biceps brachii	N.musculo- cutaneus	C5-C6
Triceps	Deep, stretch reflex	M.triceps brachii	N.radialis	C7-C8
Radial (carporadial, brachioradial)	Deep, periostal reflex	Mm.pronatores flexores, digitorum, brachioradialis, biceps	N.medianus, N. radialis, N. musculo-cutaneus	C5-C8
Scapulo- humeral (scapuloperiosteal) reflex (Bechterev’s)	Deep, periostal reflex	Mm. teres major, subscapularis	N. subscapularis	C5-C6
Upper superficial abdominal	Superficial, dermal	Mm. transversus, obliquus, rectus abdominis	N.intercostales	D7-D8
Middle superficial abdominal	Superficial, dermal	Mm. transversus, obliquus, rectus abdominis	N.intercostales	D9-D10
Lower superficial abdominal	Superficial, dermal	Mm. transversus, obliquus, rectus abdominis	N.intercostales	D11-D12
Cremasteric	Superficial, dermal	M.cremaster	N.genito- femoralis	L1-L2
Knee jerk, or patellar reflex (quadriceps stretch reflex)	Deep, stretch reflex	M.quadriceps femoris	N.femoralis	L3-L4
Achilles (ankle jerk)	Deep, stretch reflex	M.triceps surae	N.tibialis (n.ischiadicus )	S1-S2
Plantar (sole)	Superficial, dermal	Mm. flexores digitorum pedis and others	N.ischiadicus	L5-S1
Anal	Superficial, dermal	M.sphinter ani externus	Nn. anococcygei	S4-S5

Normally the reflexes are lively and the same on both sides. (D=S). Hyperreflexion, hyporeflexion or areflexion are abnormal signs. If the reflexes change on one side we can write down:

D > S; S > D; D = S; D < S; S < D.

Put the pathologic sign always on the first place.

There are quantity of unconditional reflexes is great enough for man. The greatest notice is deserved by that of them, which differ by appreciable persistence. Therefore we shall be limited to treating only of that small part of reflexes, which are permanently researched in neurological practice. In the presentation we shall adhere about research from above downwards, designating the name of a reflex, character of response, reflex arch and technique of calling.

Subeyesbrow reflex is caused by impact of a hammer on subeyesbrow arc territory. Concerns to deep, periosteal (bone) reflexes. Answer response is closering of blepharons (m. orbicularis oculi). Reflex arch: n. Ophthalmic (the first branch of a trigeminal nerve), sensitive nucleus of trigeminal nerve, motor neurons of facial nerve, movement fibbers of facial nerve, m. orbicularis oculi.

Corneal (lid) reflex turns out as a result of a cautious touch by cotton or soft paper to a cornea above the iridescent shell (but not above a pupil); a reflex superficial, from a mucous. The movement response consists in same closering of blepharons; reflex arch same, as of subeyesbrow reflex.

Conjunctival reflex, as frequently absent in norm, large value in research of the nervous system have no. It has such reflex arch as a corneal reflex.

Mandibular (chin, masseter, jaw) reflex (Bechterev’s) jaw relaxed and about half-opened. Finger, pressing downward on chin, is percussed. It is a deep, periosteal (bone) reflex. Answer response is abbreviation (cutting) masseter (m. masseter), causing closering of a jaw (rising of a mandible). Reflex arch: sensitive fibbers of n. Mandibular (the third branch of a trigeminal nerve), sensitive nucleus of trigeminal nerve, its motor neurons in the pons, movement fibbers same third branch of trigeminal nerve. The reflex does not differ by the large persistence in norm and is sharply boosted in pathological cases (at a pseudobulbar paralysis).

Pharyngeal reflex is caused by applicator stick touch to a back wall of pharynx’s; occur swallowing, sometimes cough and gagging. Reflex arch: sensitive fibbers and nucleus of IX and Х nerves (n. glosso-pharyngeal and n. Vagus), motor neurons and fibbers of IX and Х nerves.

Pharyngeal and palatal (palatine) reflexes do not differ by the large persistence and can be absent for the healthy persons. The one-sided lowering or absence of reflexes is the diagnostic valuable. Therefore it is necessary to concern separately right and left sides of a mucous soft palate and fauces. Both reflexes concern to number superficial, from mucous.

Biceps reflex from a tendon of m. biceps is caused by impact of a hammer on a tendon of the two-chapter muscle in an Ulnar fold. Answer response is abbreviation (cutting) the called muscle and inflection in an Ulnar joint. Reflex arch: n. Musculocutaneous, V and VI cervical segments of a spinal cord. It is a tendon (deep) reflex.

Triceps reflex from a tendon m. triceps, it turns out as a result of impact by a hammer on a tendon of the three-chapter muscle, that causes its abbreviation (cutting) and extension of a forearm in an Ulnar joint. The impact is put on 1,5 — 2 sm above olecranon. Reflex arch: n. radial, VII and VIII cervical segments of a spinal cord. It is a tendon (deep) reflex.

Radial (carporadial, brachioradial) reflex is caused by impact of a hammer on ргос. stiloideus a beam and consists in bending in Ulnar joint, pronation and bending of fingers. Not all named reactions turn out constantly: it is most clearly usually expressed pronation. Reflex arch: mm. Pronatores, flexores digitorum, brachioradial and biceps: nn. Median, Radial and Musculocutaneous; V, VI, VII and VIII cervical segments of a spinal cord. It is a deep (periosteal) reflex.

Scapulohumeral (scapuloperiosteal) reflex (Bechterev’s) turns out at impact of a hammer on internal edge of scapular: reduction and rotation a shoulder which freely should hang down thus is marked. It is a deep (periosteal) reflex. Reflex arch: mm. Teres major and Subscapular: n. Subscapular, V, VI cervical segments of spinal cord.

Superficial abdominal reflexes are caused by shaped irritation of a stomach skin: below the costal arch – epigastric reflex, at a level an umbilicus – midlamdominal reflex, above pupart sheaf – hypogastric reflex. Shaped irritations should be fast render a little bit pointed subject (a goose feather). A direction of strokes and places of their drawing are represented on fig. 2. Reflex arches: the top belly reflex - VII and VIII chest segments; on the average - IX and X; bottom - XI and XII. Response is reduction of muscles belly press. Reflexes are dermal, superficial. 

There reflexes usually cannot be elicited if the abdomen is obese, distended, or overly flaccid, or if the patient is unable to relax. Proper relaxation seems best obtained when the patient lies supine with knees comfortably drawn up and supported, arms hanging loosely at the sides, and eyes closed.

Cremasteric reflex causes shaped irritation of a hip internal surface skin. Reflex contraction of the cremasteric muscle with elevation of the testicle is observed. Reflex is constant, but sometimes and in norm non-uniform (apparently, because of unequal smartness testis). Reflex arch: n. Genitofemoral, I-II lumbar segments. It is a superficial, cutaneous reflex (see fig.).

Knee jerk, or patellar reflex (quadriceps stretch reflex), turns out at hammer impact on patellar tendon lower than patella. As a result of that there is a reduction of m. quadriceps femor and extension of shins. Reflex arch: n. femoral, II and IV lumbar segments. It is deep, tendon reflex.

Achilles (ankle) reflex is caused by impact of hammer on Achilles tendon; there is a reduction of m. triceps sure and extension of stops. Reflex arch: n. Tibial (a branch of n. Sciatic), I and II sacral segments. It is a deep, tendon reflex.

Plantar (sole) reflex is the normal flexion of the toes that result from stimulation of the sole of the foot. The direction of a stroke may be from below upwards or from the top downward (fig. 3); it is better to carry spend a stroke with some pressing, with his strengthening by the end of irritation. Response is bending fingers stops. Reflex arch: n. Sciatic, V lumbar and I sacral segments of a spinal cord. A superficial reflex.

Plantar reflex is inherent in the intact nervous system of the person who has reached age of 1-3 years. At small children exists, and at patients with damaged of pyramidal system (dissociation with a brain) arises Babinski phenomenon (great-toe reflex).

Anal reflex is caused by an injection of a skin about back pass; his circular muscle (m. sphincter ani externus). A reflex arch: nn. anococcygei, IV and V sacral segments. It is a superficial, dermal reflex.

Final Touches of Examination

The examination should be concluded by the performance of several observations that may add to the total picture of the patient's disability.

Changes of reflexes

Reflexes may change aside:

1) downturn or losses of them,

2) increases

3) distortions.

Classically, the stretch reflex will be exaggerated when normal function of the pyramidal tract above the lower motor neuron is chronically suppressed or destroyed. Thus, enhanced response in the reflex arc may mean disease of spinal cord, brain stem, or hemispheres and is a basic characteristic of the spastic state. Sometimes other muscles stretched slightly by the maneuver may visibly respond also – spend of response also typical of the spastic state.

Discretion must be used in evaluating the meaning of uniformly “decreased” or “increased” stretch reflexes, using one’s knowledge of normal range as a guide. The normal range is broad. Differences between upper and lower extremities and between the two sides are much more safely regarded as evidence of dysfunction than is the general reflex tonus. At times it may be difficult to decide whether a reflex response is enhanced on one side or decreased on the other. One looks for other evidence of disordered function, e.g. sensory deficits, atrophy, poor motor performance, and the Babinski sing, to integrate with the stretch reflex response in constructing a concept of pathologic change.

In pathological conditions there may be new reflexes which are not caused.

Loss or downturn of reflexes (areflexia and hyporeflexia) results from infringement of an integrity and conductivity of a reflex arch in its any department (afferent, combinative, and efferent). Symmetric downturn and even loss of reflexes sometimes is not an attribute of defeat of nervous system. So, some reflexes at healthy persons are caused hardly or fail at all.

Belly reflexes, both skin, and deep, go down or disappear not only at defeat of their reflex arches, but also at dissociation of the spinal segments appropriate to them (About VII-XII) with cortex of brain, at lesion of pyramidal tract. Belly reflexes are not congenital, and are developed in connection with development of brain cortex and pyramidal systems during individual life. Occurrence of them coincides with time of development at the child of vertical position of a body. Belly reflexes stimulate by brain cortex and consequently disappear at dissociation with it. Clearly, that they die away as well at a break of their reflex spinal arches.

Hyperreflexia specifies increase of reflexes strengthening of reflex activity of the segment device (a spinal cord, a brain stem). More often the reason of increase of reflexes is lesion of pyramidal tract - systems which transfers braking influences of a brain cortex on segment spinal reflex mechanisms. Hyperreflexia signifies an upper motor neuron lesion along the neuraxis from cortex to lateral columns of the spinal cord. Symmetric increase of reflexes at absence of other pathological symptoms not always speaks about presence of organic disease; high reflexes may be and at healthy persons, may be observed at neurotics, at some intoxications etc. A good rule is that hyperactive reflexes in the presence of downgoing toes are usually normal. If the hyperactive reflexes truly reflect pyramidal tract disease, the toes should also be abnormal. A unilaterally upgoing toe or hyperactive reflexes on one side implies damage to one side of the nervous system.

Extreme displays of increase tendon reflexes are clonuses. Clonuses represent itself rhythmic reductions of any muscle arising as a result of a stretching of its sinew.Continued applied stretch will cause repetitive reflex responses interrupted by brief “silent periods” in the muscle. As a result, an oscillation can be set up that may continue indefinitely. This phenomenon named clonuses. Sustained clonuses usually indicate disease. It is based on hyper synchronization in a poorly inhibits reflex arch. The most often clonuses are clonuses of the jaw, wrist and patella. As against organic clonuses, clonuses at neurosis, physiological increase of reflexes etc. There is not enough rack, are always in regular intervals expressed from both sides and are not accompanied by other organic symptoms.

Clonuses on the upper extremities are observed seldom; more often others it happens clonuses a brush, arising as a result of sharp rhythmic reductions of it.

Non-uniformity of reflexes always specifies organic disease of nervous system. Non-uniformity of reflexes (anizoreflexia) arises or as a result of downturn of reflexes on one side (lesion of a reflex arc in a nerve, roots or horns of a spinal cord), or its increases on another (lesion pyramidal tracts).

Motor system

This system provides conduction of nervous impulse from brain cortex to muscles. The way of this impulse is known as motor way or tractus corticomuscularis. It consists of two neurons:

1. central

2. periph

Upper and lower extremities, neck, trunk and perineum muscles’ innervation.

The first (central) neuron is called tractus corticospinalis.

The second (peripheral) neuron is called tractus spinomuscularis.

The fibers of tr.corticospinalis are of Betz cells origin. Most of its fibers originate from anterior central gyrus, posterior parts of upper and middle frontal gyri and paracentral lobe (area 2,4,6). The Betz cells in central anterior gyrus are presented vice versa to the parts of the body:

in upper part the muscles of lower extremities are presented;

in middle part - the muscles of upper extremities are presented;

in lower part – the face muscles are presented.

There is crossed innervation of muscles .The axons of Betz cells that create tr. corticospinalis go through corona radiata to internal capsula via its anterior 2/3 of posterior crus. Then the axons of motor way go through the peduncles, pons to medulla oblongata to form pyramides.

80 % of all fibers make decussationon the border between medulla oblongata and spinal cord. The crossed fibers go to the lateral foniculus of spinal cord on the opposite side and create tr. corticospinalis lateralis. The last provides lower and upper extremities muscles innervation.

The rest – 20 % of all fibers aren’t crossed. They go to foniculus anterior and create tr. corticospinalis anterior ( fasciculus Turka ). This one provides neck, trunk, perineum muscles innervation.

The fibers of tr. corticospinalis are finished in motorneurons of spinal cord anterior horns.

The second neuron – peripheral - tractus spinomuscularis.

Neurons of C1-C4 anterior horns innervate neck muscles, C5-Th1-2 – muscles of upper extremities, Th2-Th12 – trunk muscles, L1-S2 – muscles of lower extremities, S3-S5 – muscles of pelvic organs.

The second neuron originates from anterior horns alphamotorneurons of spinal cord. Axons of these neurons go within anterior roots and then join with posterior ones to form the spinal nerve. Each spinal nerve gives 4 branches:

1. ramus anterior ( together they form plexus – cervical, brachial, lumbar and sacral)

2. ramus posterior (it is spinal nerve, which innervates posterior trunk muscles)

3. ramus meningeus

4. ramus comunicante albi.

Thus, the motor impulse goes from anterior horns through anterior roots, spinal nerve, plexus and peripheral nerves to muscles.

That’s the reason to make following conclusions:

1. The muscles of upper and lower extremities have unilateral cortical innervation from contralateral hemisphere

2. The muscles of neck, trunk and pelvic organs have bilateral innervation from both hemispheres. In case of unilateral pathologic focus these structures do not suffer.

Face, tongue and pharynx muscles innervation.

This way is called tractus cervicomuscularis.

The first central neuron is called tractus corticonuclearis.

The second peripheral one is called tractus nucleomusculares.The first neuron cells are situated in the lower part of anterior central gyrus. The axons go through corona radiata, the knee of internal capsula to brain stem (that means peduncles, pons and medulla oblongata). There are nuclei of CCNs in brain stem.

And one more peculiarity – the fibers of tractus corticonuclearis make decussation above all the nuclei. This decussation is incomplete. The only exception is lower nucleus of VII CCN and nuclei of XII CCN. In this case decussation is complete.

The second neuron is situated in motor nucleus of CCNs. This way to face muscles is called tractus nucleomuscularis.

Thus we can make the following conclusions:

1. The face muscles have bilateral cortex innervation except the mimic muscles and tongue muscles that have unilateral innervation from the opposite hemisphere.

2. The muscles of upper and lower extremities, lower mimic muscles and tongue muscles have unilateral cortical innervation.

3. All the other muscles (the muscles of neck, trunk, perineum, m. oculomotorial, m. masseter, pharyngeal and palatal muscles) have bilateral cortical innervation.

Movements disturbances.

In case of complete lesion of motor way (tractus corticomuscularis)paralysis (plegia) occurs. That means the absence of active movements

In case of incomplete lesion of motor way paresis occurs. That means active movements disorders – hemi-, tetra-, mono-, tri- and paraparesis.

Paralysis is divided into

· Central ( spastic )

· Peripheral ( flaccid )

Central or spastic paralysis is caused by the lesion of central neuron and its fibers (tr. corticospinalis or tr. corticonuclearis).

Peripheral or flaccid paralysis is caused by the lesion of peripheral neuron (tractus spinomuscularis or tractus nucleomuscularis).

main features of central or spastic paralysis are:

1. It is a diffuse paralysis.

2. There is spastic hypertonus of muscles

That means

· Tonus is increased in the group of flexors in upper extremities and in the group of extensors in lower extremities

· “ clasp – knife “ symptom

· in course of evaluation tonus decreases

3. Hyperreflexion of stretch and periostal reflexes.

4. There are pathologic reflexes.They are considered to be reliable signs of central paralysis.

All the pathologic reflexes on lower extremities are divided into flexing and extensing.

To flexing ones belong Rossolimo (pic)

Jukovski (pic)

Bechterev’s, Mendel – Bechterev’s reflexes. The response is reflex flexing of II -V fingers (pic).

To extensing reflexes belong Babinski (pic)

Oppenheim’s (pic)

Gordon’s (pic)

Shtrumpel, Grossman, Sheffer (pic)

Chaddock’s, Pusep’s and Redlich reflexes. The abnormal response is dorsiflexion of the great toe and fanning of the others (pic).

There are following pathologic reflexes on upper extremities:

1. Bechterev’s sign This is simply a muscle-stretch reflex of bending of fingers obtained by tapping the back of hand with a reflex hammer.

2. Jukovski sign. This is caused by hammer impact on a palm under fingers; response is reflex flexing of II-V fingers.

3. Rossolimo ( Venderovych ) reflex: This is simply a muscle-stretch reflex obtained by tapping the palmar surfaces of the fingers with a reflex hammer; the response is reflex flexing of II-V fingers.

4. Tremner reflex . This is simply a muscle-stretch reflex obtained by tapping the palmar surfaces of the nail-phalax of II – V fingers. The response is fingers flexing.

5. Jakobson – Laske reflex. This is caused by hammer impact on processus styloideus ; the response is reflex flexing of II-V fingers.

6. Klipel – Veil reflex. This is caused by passive bending of II – V fingers. The response is thumb flexing.

5. Protective reflexes (the reflexes of spinal automatism ).

They also are one of signs of lesion of motor way. They are especially clearly expressed at cross lesion of a spinal cord (dissociation of underlaying segments of the last from a brain). The result is squeezing of foot, and also an injection or sharp plantar flexion of toes (V.M.Bechterev). The response reflex flexion of paralyzed extremities, flexion in femoral, knee and talocrural joints (shortly reaction); opposite extremities thus straightens, being unbent in joints (long reaction). Serial putting irritations on one and the other leg, can result in imitation of automatisms of walking.

6. Pathologic synkinesis

are involuntary movements in paralysed extremity . They are observed while moving by healthy extremity. Synkinesis are divided into

· Global

· Coordinatory

· Imitating

Peripheral ( flaccid, atonic ) paralysis.

It occurs at lesion of tractus spinomuscularis or tractus nucleomuscularis.

The main features of peripheral paralysis are :

1. Areflexion or hyporeflexion

2. Atonia or hypotonia

3. Muscular atrophy

4. Fasciculation of muscles

5. It is limited paralysis

6. There is reaction of degeneration.

The Basic Neurological Examination of Movements

Gate

Volume of active movement and Muscular weakness

Muscular tone

Muscular stretch

Reflexes

The energy, speed, and agility with the patient rises and walks about provide important initial clues to his general health, his mood, and the status of his musculoskeletal and nervous systems. Maintenance of upright posture and walking bring into action a substantial portion of the nervous system, both motor and sensory. To see the patient get up and move about is as important in general orientation as the background history. Prior to the formal assessment of gait, it is worthwhile to observe the patient as he walks to the examining room. Often more can be learned while the patient is unaware that his gait is under scrutiny.

Examination of Gait and Station

The patient is asked to walk across the examining room while the examiner observes the gait. The patient should have normal posture. The feet should be a normal distance apart, and there should be good associated movement of the arms. A loss of associated movement of the arm on one side indicates the early development of either spasticity or rigidity in that limb. Particular attention should be given as the patient turns; this movement is likely to produce slight ataxia or a shuffle indicating early dyspraxia of gait. After the patient has walked back and forth several times, the examiner demonstrates tandem gait and

asks the patient to walk toward the examiner, with one foot placed in front of the other, the heel touching the toes at each step (Fig. 1-22). This is normally performed without any undue unsteadiness or sudden lateral placement of one foot to maintain balance, which would indicate the presence of ataxia. The patient is then asked to walk across the examining room on his heels and return on the toes. These maneuvers not only tend to accentuate ataxia but can also disclose unexpected weakness in the lower limbs. The ability to perform heel walking and toe walking indicates good strength in the dorsiflexors and plantar flexors of the feet.

Walking is not a delicate function, however, and compensatory mechanisms can mask deficiencies. Moreover, disorders of gait caused by no neurological conditions, especially joint disease, may be misleading. Nevertheless, close observation of walking may yield important evidence of dysfunction of the nervous system. Ask the patient to walk back and forth several times and observe successively his posture, balance, arm swinging, and leg movement. As in almost any aspect of the examination, allowance must be made for age and obvious no neurological disability. If the gait seems unusually slow and cautious, encourage the patient to walk more rapidly since this may uncover subtle abnormalities not seen when he is moving at a slower pace. Common sense must be used in asking an ill or decrepit patient to walk. Sometimes it is fitting to assist a partially disabled patient to walk when this can be done safely.

The normal person progresses with only casual observation of the floor and a brief survey of the range of the area. Balance is normally achieved with no apparent attention or correction, with appropriate arm swinging, and with slightly flexed posture of elbows and fingers, palms facing thighs. 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 though is kept at right angles to clear the floor, and the pelvis remains parallel to the floor without tilting. The “springiness” of this normal gait is recognized as a sing of health and energy. Observe the hands for tremors and disturbed posture (dystonia), which may become more evident when the nervous system is occupied with the task of walking.

A cautious, short-stepped gait may be due to weakness, pain, disturbed sense of balance, disease of basal ganglia, or diffuse cerebral disease. A waddling gait results from weakness of the glutei, usually due to muscular dystrophy. A scraping toe may be due to footdrop of central or peripheral origin, in which case elevation of the leg to swing through is accompanied by a slapping of the foot. The spastic leg is characterized by limited swing, tendency to adduction, and loss of free joint movement.

In case of spastic paraparesis, the legs of the patient may actually scissor and tend to trip him. The unilateral spastic leg in patients with hemiparesis may be pulled forward, with outward circling (circumduction) and stiffness and with dragging of the toe. Parkinsonism is characterized by stooped posture, loss of free swinging of the arms, a turning in one piece (en bloc) with stiff trunk and neck, and, often, shuffling. The depressed patient’s slumped shoulders and slow gait may simulate Parkinson’s disease. In patients with disease of the cerebellum, upright posture may be maintained only with difficulty, and often the excessive corrections for threatened loss of posture result in reeling and staggering. The hysterical patient may adopt bizarre postures and progression, often with dramatic values.

Accumulated deficits from lesions in several parts of the nervous system contribute to loss of function. The free-swinging, springy gait of youth may give way in the aged to stiffer and slower, even shuffling steps. Arthritic joints and loss of musculature add further to the decrepitude.

Ask the patient to turn rapidly as he walks. The face and head should lead, and balance should be well maintained. Ataxia may be betrayed by missteps or lunching. Failure to swing the arm and to turn head and trunk successively suggests Parkinsonism or spinal arthritis. Running is more demanding, but it is usually neither possible nor wise to test this. Inquiry about this ability in the young is always appropriate.

Hopping in place on either leg is one of the best screening tests for function that can be used for the ambulatory patient. Obviously it should not be requested of those whose general state of health or apparent disability makes attempted hopping unwise. Elderly, arthritic, or obese patients would not perform well and might find the exercise impossible. Use caution and common sense in deciding which patients should perform this test, and routinely steady those who perform by holding one elbow lightly.

Hopping with agility required intact function on much of the nervous system. If the patient can hop well on either foot, springing up and down in one spot on his toes while maintaining balance, he has little dysfunction of the long motor and sensory tracts, the cerebellum, the basal ganglia, the peripheral nerves, or the muscles of the hip and lower extremity. Hitting the heel hard, losing balance, being unable to get off the floor, or landing more than a few inches from takeoff serve notice of some disorder. A low, heavy, flat-footed hop is typical of upper motor neuron disorders. Slight awkwardness in hopping on one side often will be the only functional evidence of early paresis due to a lesion of cord or brain. Hopping may occasionally be done well in the presence of pathologic hyperreflexia and the Babinski sing if the patient is young and athletically accomplished. In patients with ataxia of posterior column or cerebellar origin, the performance will be awkward, with a poor springing action and in ability to drop the foot at the point of takeoff. The cautious patient may refuse to perform, while the more cooperative and less judicious (e.g., occasionally a patient with multiple sclerosis) may try, with rather wild and frightening incoordination.

Although hopping is an excellent screening test for function, analysis of difficulties in performing this act can give only a general idea of the nature of the functional disorder.

While the patient is on his feet, it is convenient to proceed to other examinations of function of the legs, especially those testing the strength of muscle groups. These can instead be deferred to the time of examination of the lower extremities. However, some of the muscle groups are so strong originally that in the early stages of disease weakness will not be directed on direct examination. Hence, whenever possible, test the strength of the leg muscles while the patient is standing upright and bearing weight.

Even though the musculature that extends the knee has already been tested in hopping, it is good to stress it more vigorously by requesting a shallow squat and rise, with the patient bearing the entire weight on one leg. The squat is then repeated on the other leg. This is the best and safest way to discover minor degrees of weakness. It is at the same time a test of the musculature that stabilized the pelvis and that extend the thigh on the hip while engaging the back and hip-girdle musculature and hamstrings in the activity light support at the patient’s elbow is appropriate. The normal person can easily squat and rise on the leg with only a little help in balance. Any differences between the performances of the right and left sides will be readily apparent. Difficulty in rising indicates weakness, and if the quadriceps is very weak, the patient will collapse to the floor. Arthritis, deformity of knee or ankle, primary muscle weakness, or lesion at any level in the nervous system will interfere with performance of this maneuver. A less demanding test that is more suitable for the elderly patient is to have him step up on a footstool. In cases of patient with proximal muscle weakness it loss useful to observe the patient’s attempt at squatting on both legs simultaneously.

When weakness is apparent, look for atrophy that may signify a lower motor neuron lesion or muscular disorder. However, disuse of a muscle from any cause – pain, immobilization, or paralysis of central origin – will result in some loss of muscle mass. The quadriceps, for example, is notoriously prone to disuse atrophy.

The patient who hops well does not have serious weakness of the gastrocnemius. This is a strong muscle and difficult to evaluate by direct testing. Watch the patient walk on his toes as he supports his entire weight on first one foot and then the other. Weakness will be evident if the heel drops in walking. Observe the contours of the musculature for atrophy and for hypertrophy. The patient who has suffered a stroke and has a moderate degree of spastic and increased tone in antigravity muscles may still be able to rise on his toes. When weakness is evident on attempting this maneuver, look first for a primary disorder of root, nerve, or muscle.

Having the patient walk on the heels is an especially valuable screening test, since dorsiflexion of ankle and toes is weakened in many muscular and neural disorders. (Help the patient to maintain balance if necessary.) The normal person can hold the anterior foot and toes off the floor, strongly dorsiflexion the great toe as he walks on his heels. If he can do this, he dose not have footdrop. He could, however, still have some minor weakness of the muscles of the anterior compartment, and these should be tested directly. Footdrop may be of either central or peripheral origin. The severe footdrop of peripheral origin is clearly revealed by the abnormal nature of the gait and by an observable loss of dorsiflexion of the ankle and toes. If footdrop of peripheral origin (lower motor neuron) has been present several weeks, shrinkage and softness of the anterior compartment also will be apparent. When the leg is shaken, as in the test for alternating motion rate, the foot will be unstable and flop about. The foot a less floppy in central disorders (upper motor neuron lesion) and may be relatively fixed in plantar flexion. The toes of the spastic leg, when dorsiflexion of ankles and toes is weak, are dragged in walking. Before the examiner concludes that there is weakness of dorsiflexion, the foot should be passively dorsiflexed to be certain that previous weakness, now healed, did not permanently shorten the gastrocnemius.

The introductory tests serve as a valuable survey for screening in the ambulatory patient. The same principles should be applied throughout the examination. Elicit as much movement as is possible and sensible, patterned movement as well as isolated movement. Test strength against gravity whenever possible and applicable.

The term “upper motor neuron paralysis” refers to supranuclear disorders in which weakness, slowness, incoordination, and incompleteness of movement are due to lesions above the lower motor neuron. Atrophy of muscle can result from disuse but is seldom conspicuous. Stretch reflex pathways remain intact, and reflex responses are often exaggerated. The Babinski sign is usually present. The motor system is so complex that the pattern of malfunction may vary greatly depending on the location and multiplicity of lesion. However, typical patterns can be found in conditions such as hemiplegia and spinal paraplegia.

In lower motor neuron paralysis, weakness of movement is, by definition< due to a lesion of the motor cell or its axon, and diminished tonus is characteristic. The muscle shrinks and becomes soft and the reflex arc is interrupted, resulting in diminished or absent stretch reflexes. The Babinski sign is not present. Fasciculation of muscle may be present. This pattern of main function is seen in poliomyelitis, motor neuron disease, peripheral neuropathy, and peripheral nerve injuries.

In some conditions, notably amyotrophic lateral sclerosis and some spinal cord neoplasm, upper and lower motor neuron paralysis may coexist, and the clinical sing of each are found together, sometimes even in the same extremity.

Muscular weakness is a cardinal sign of dysfunction in many parts of the nervous system. The degree of weakness present can be judged about as accurately as most other abnormalities, but experience must be gained in learning what is normal strength for men, women, and children of various ages, states of health, and responsiveness. Pain and fear of pain will inhibit maximum effort, and anxiety, indifference, hysteria, and, rarely, malingering may cause reduced effort. Strength of the extremities is tested by directly opposing the action of various muscle groups, as well as by utilizing various functional tests. Cajole or tease the patient, as appropriate, to maximum exertion, but use restraint and consideration in testing the injured, debilitated, or elderly.

Evaluation of the central nervous system is concerned with patterns of movement rather than contraction of isolated muscles. For application of maximum strength of a muscle or muscle group, contraction of many other groups must occur contemporaneously to provide a stable base for the movement being studied. In analyzing peripheral nerve and root lesions, one may attempt to appraise the involvement of a single muscle, but this is not appropriate in most disorders.

The method of quantization of muscle strength most commonly employed is based on an index of 0 to 5:

5. Normal strength

4. Full normal movement possible, but strength of contraction can be overcome by examiner

3. Normal range of movement against gravity but not against added resistance

2. Movement when gravity does not act in opposition

1. Flicker of movement only

0. No movement

A plus or minus is often used to indicate a score in between these grades.

Always observe and palpate the musculature being tested. Often dysfunction is immediately proclaimed by odd posture or loss of normal muscle contour. Atrophy is difficult to evaluate in the aged or malnourished patient; when it is asymmetric or restricted to a specific area or muscle group, then disorder of the nervous or muscular system should be strongly suspected-unless local pain, joint disease, or immobilization provides a possible explanation.

Test the patient's ability to hold the arms against gravity and fixed in the some postures shown in Figure with his eyes closed: first with his arms extended straight in front, fingers together, and hands flat, parallel, and separated by one to two inches (A), then with his arms extended above the head, hands flattened and facing forward (B). These postures should be well maintained for 20 to 30 seconds. Observe the musculature for symmetry and tone. Especially look for drooping of an arm or for tendency of an arm and hand to flex and rotate internally, one of the earliest signs of paresis of central origin. Strength on direct testing may be normal despite the existence of these postural disorders. Weakness of peripheral origin will also cause poorly maintained posture and inability to support the limb, especially at the shoulder. Consistent disturbances in maintenance of posture serve notice disorder requiring further attention.

Ability to hold the arms extended above the head (fig 25, A) is impaired early in hemiparesis or in weakness of the shoulder girdle from any cause. Try to force the patient’s arm down against his resistance. The deltoid is the principal muscle tested in the exercise shown in Figure 25, B. Observe the muscle for firmness and contour. Impairment in function of the trapezius, Serratus anterior or other muscles stabilizing the shoulder girdle may compromise the ability of the deltoid to hold this position against the examiner’s downward pressure. Painful disorders of the shoulder joint that limit movement will seriously interfere with performance of there tests. Be cautious in diagnosing a neurogenic lesion when the patient has a painful, atrophic shoulder.

Test for scapular winging by depressing the arms while the patient holds them outstretched in front of the body (Fig 25,C) and lateral to the body (fig 25,B). When the Serratus anterior is weak, the lower angle of the scapula will wing out and be displaced medially and up. Weakness of the deltoid interferes with testing in this manner, so scapular winging should be looked for by having the patient push against the wall with outstretched arms, first one arm and then the other. If winging is absent, the scapula will remain closely applied to the chest wall. Weakness of the trapezius may also result in scapular winging, which will be displayed by downward and lateral displacement of the scapula on lateral abduction of the arms.

Test strength of flexion at the elbow as shown in Figure 25,D. The principal muscles concerned here are the biceps brachii (Musculocutaneous nerve), and brachioradial. The brachioradial plays a larger role in flexion of the elbow when the palm faces inward. This muscle is innervated by the radial nerve, which mediates both flexion and extension at the elbow.

Extension at the elbows is mediated by the triceps muscle, which is innervated by the radial nerve. An excellent way to test this function is to resist extension while standing behind the patient, as in Figure 25,E. The strength of the two arms is easily compared.

Dorsiflexion of the wrist is a vulnerable function and is impaired early in disease of central motor pathways, in radicular compression, in radial nerve paresis, and often in peripheral neuropathy. Ask the patient to make a tight first and hold it immobile against your attempt to bend the wrist ventrally (fig26, A).

A common way to gauge strength is by the force of the grips (fig 26, B) two or three fingers may be offered to the patient, two fingers for small hands to give the patient an advantage, and three fingers to powerful hands to reduce discomfort for the examiner. Test the grips of right and left hands simultaneously for easy comparison chide the patient into maximum effect and make the test an opportunity for the patient to express a bit of hostility and competitive spirit. Try to withdraw the grasped fingers by twisting and pulling.

Some additional estimate of strength and function of arms and shoulders is thus possible. The patient’s wrist should not deviate; if it does, weakness of a muscle group in the forearm is probable and effectiveness of the grip is reduced. Strength of the grip can be inhibited by pain anywhere in the extremity. Remember that the grip is largely a function of forearm musculature, which should be observed for contour, symmetry, and tone.

The grips may be strong, even though intrinsic hand muscles are weak. Observe closely for atrophy of these muscles and their distribution. The thenar eminence will give evidence of atrophy in median-nerve disorders, the first dorsal interosseous muscle, in early Ulnar-nerve paresis. The intrinsic muscles lose mass diffusely in cases of arthritis or other debilitating disease and in cases of disuse or old age. However, strength is retained unless inhibited by pain. In general, loss of strength will accompany visible atrophy if denervation or myopathy is directly responsible for the atrophy. Diffuse atrophy with weakness is seen in patients with some types of neuropathy, myopathy, certain root disorders, and motor neuron disease. However, a lesser atrophy of disuse is common in cases of paresis of upper motor neuron origin, and this finding may be confused with that of atrophy from the other causes just listed. Central lesions producing weakness and secondary atrophy of disuse usually cause hyperreflexia.

Abduction of the fingers is a function that readily loses strength in either central or peripheral disorders, especially Ulnar-nerve lesions. To assess the strength of this function, attempt to force the patient’s fingers together as shown in figure 26, C. strength of opposition of the thumb and fifth digit, abduction of the thumb, and flexion of the fingers are tested by pulling one’s thumb through the apex of a firmly held cone formed by the patient’s digit (fig 26, D) in most healthy people the fingers will snap back into position.

Rapid tapping of the forefinger on the thumb is a good test. Demonstrate the desired movement for the patient. It can be made more demanding by asking him to tap out a specific rhythm.

Agility of the hands and fingers is impaired by many disorders. Rapid touching of each finger in succession to the thumb (Fig 28,A) effectively tests this function. Ask the patient to button and unbutton his jacket with the eyes closed (Fig 28,B) or have him pass a safety pin through his pyjamas or a sheet, closing and opening it with one hand (Fig28,C). Such movements are notoriously clumsy when sensation is reduced, as in cases of peripheral neuropathy or demyelization of the posterior columns.

These functions are impaired to various degrees by any motor disorder. The loss of finger dexterity is sensitive indicators of motor or sensory disorder. Further examination is necessary to identify the nature of the deficit.

Direct testing is necessary for estimating strength of the lower extremities and hip girdle in the nonambulatory patient and for certain functions in the ambulatory. The movements most vulnerable to impairment are flexion at the hip and dorsiflexion of ankles and toes. Extension of the knee and plantar flexion of the ankle are strong movements mediated by massive musculature and are part of the antigravity functions. An excellent test is shown in Figure 29, A for determining strength of flexion of the thigh on the abdomen when sitting. This movement is mediated largely by the Iliopsoas muscle and is not a strong function. Weakness here is one of the early signs of dysfunction of central motor pathways.

To test flexion of the hip in the supine position, ask the patient to kick, with his knee extended, the examiner's hand held 2 ft above the extremity. Hold your hand so that it will be struck by the shin. The quickness and smartness of such a blow are an accurate index of the strength of the Iliopsoas. The patient should also be asked to elevate the leg and hold it against the examiner's downward pressure (Fig 29, B).

Flexion of the knee is largely a function of the hamstring muscles and the sciatic nerve. It is tested as shown in Figure 29, C, with the patient's knee flexed and foot held firmly to the bed while the examiner attempts to straighten the leg. Instruct the patient to hold the foot down. Extension at the knee is tested in the supine position as shown in Figure 29, D. Mild degrees of weakness may not be discerned because of the inherent strength of these muscles.

Plantar flexion of the ankles and toes may be weakened, yet this weakness may not be easily detected in direct tests of strength. Ask the patient to step down on your hand (Fig 29, E). This function is even better tested by having the patient walk on his toes, as previously described. Dorsiflexion of ankles and toes is tested as shown in Figure 29, F. Most patients understand the instruction to "cock back" the foot. The AMR of the legs is evaluated by having the patient, if he is able, elevate the leg and shake the foot. The best position to test this function is shown in Figure 30, A. The maneuver can also be done with the patient standing on one leg or sitting. The desired rapidity and amplitude are often best communicated to the patient by asking him to "shake your leg as though you were shaking water off it." Lesions of corticospinal pathways reduce this ability more than do peripheral lesions. However, strength must be fairly well preserved for this test to be done.

The reflexes. Sudden stretch of a skeletal muscle results in a reflex contraction of that muscle mediated by a simple and usually monosynaptic reflex arc. The afferent side of the arc begins with 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 brain stem. The efferent side of the arch is the motor neuron with its axon and terminal structures that innervate the muscle. When a tendon is tapped, the resulting distortion applies a sudden stretch to the muscle. The response is directly related to the degree of the distortion and its velocity. Slowly applied stretch will cause no detectable response, so the use of a hammer is appropriate since it enables the examiner to place a sudden and well-controlled stimulus.

The elicitation of a motor response means that the arc is intact and conducting impulses. Yet the absence of a response does not have the converse meaning, since normal or abnormal neural influences may suppress the reflex. There is a wide variation in normal amplitude of response with which the student must become acquainted. Moreover, there is ixiation in response to the same person in both health and disease from time to time.

Because the reflex response is largely beyond voluntary control (when properly elicited), it takes on special value as a manifestation of isolated function subject to objective appraisal. Not only does the presence of involuntary muscle contraction in response to stretch indicate intactness of the arc, but, since the arc itself has a fairly constant path and locus of central connections, the presence or absence of the reflex is helpful in locating the peripheral pathways and vertical levels within the neuraxis.

The loss of a reflex in a painful extremity may well mean that nerves or roots innervating the painful area are being impinged. A consistent difference between the two sides of the body in the presence of a disease affecting the reflex arc is evidence of asymmetric involvement and lateralizes the area of greater involvement.

Classically, the stretch reflex will be exaggerated when normal function of the pyramidal tract above the lower motor neuron is chronically suppressed or destroyed. Thus, enhanced response in the reflex arc may mean disease of the cord, brain stem, or hemispheres and is a basic characteristic of the spastic state. Sometimes other muscles stretched slightly by the maneuver may visibly respond also—a spread of response also typical of the spastic state.

Discretion must be used in evaluating the meaning of uniformly "decreased" or "increased" stretch reflexes, using one's knowledge of normal range as a guide. The normal range is broad. Differences between upper and lower extremities and between the two sides are much more safely regarded as evidence of dysfunction than is the general reflex tonus. At times it may be difficult to decide whether a reflex response is enhanced on one side or decreased on the other. One looks for other evidence of disordered function, e.g., sensory deficits, atrophy, poor motor performance, and the Babinski sign, to integrate with the stretch reflex responses in constructing a concept of pathologic change.

The following system is useful for estimating vigour of reflex muscular contraction to stretch:

4+ Very brisk responses — evidence of disease and associated with clonus

3+ A brisk response, possibly indicative of disease

2+ A normal, average response

1+ A response in low-normal range

0 No responses and possibly evidence of disease, depending on the circumstances.

When examining the reflexes, position the patient so that he is sitting or reclining with a minimum of effort necessary to maintain balance or position. Then place the extremities in symmetric posture with the muscles to be tested moderately stretched. If the patient is contracting the muscle to be tested, the reflex will be suppressed or absent. Therefore, distract the patient's attention from the region being examined.

Tap lightly but quickly. Use free finger and wrist movement (Figure 32,A). Don't chop with the hammer. The free-swinging movement illustrated in Figure 32 gives a well-regulated, easily duplicated blow of rapidly applied force.

When muscle stretch reflexes are difficult to elicit, determining whether the reflex arc is intact assumes primary importance, especially since many healthy people are hyporeflexic or are flexic to ordinary testing.

Conduction in the arch may be facilitated by isometric muscular contraction elsewhere in the body. Commonly this is done by having the patient lock the fingers of the two hands and pull one against the other while the reflexes of the lower extremities are being elicited (Jendrassik's maneuver; Fig 32,B). For best facilitation of the reflex, the tendon should be struck the moment that suddenly applied tension is detected by the examiner. This can be done if the examiner is holding the patient's arm or the interlocked fingers with one hand and is ready to swing the hammer with the other. The moment that tension is sensed the hammer should be swung. Figure 32 C shows a maneuver that may be employed when testing the upper extremity. The patient is instructed to perform some maneuvers with the opposite hand, such as squeezing his thigh or making a fist. (He may, of course, unknowingly influence the reflex response by tensing his muscles)

The position shown in Figure 33, A is satisfactory for eliciting the biceps stretch reflex. The degree of flexion of the elbow may be varied for best response. Place the thumb on the biceps tendon and strike the thumb. The reflex contraction will be felt by the thumb and should be visible. Note whether contraction of the biceps is indeed responsible for flexion of the elbow, since the brachioradial, if stretched, also produces this movement. The biceps and the brachioradial are innervated from the same spinal segments but from different branches of the brachial plexus, the biceps by the Musculocutaneous nerve and the brachioradial by the radial nerve. The C-6 root is primarily involved in this reflex.

A commonly used position for eliciting the triceps reflex is shown in Figure 33, B. This reflex is sometimes difficult to obtain, probably because the disposition of the tendon makes stretching by a laterally displacing force inefficient. The degree of flexion at the elbow should be adjusted for best response, and the triceps should be observed for visible contraction. If the patient can stand, another useful test is to have him place hands on hips with arms akimbo as you stand behind him and strike the triceps tendon 1 to 2 inchesabove its insertion. The two sides are then easily compared. The C-7 root is primarily involved.

The Hoffmann sign is sought by positioning the patient's hand and wrist, the wrist extended a bit beyond the physiologic position of rest. Flick the terminal phalanx of the third digit as shown, snapping it between your thumb and first finger. This maneuver is a convenient way to cause sudden extension of the middle finger, thus eliciting a stretch reflex. The positive sign is said to be present when the patient's thumb and forefinger flex in response. Often the other fingers will flex as well. The Hoffmann sign is often incorrectly considered the upper-extremity equivalent of the Babinski sign. The Babinski sign is a pathologic reflex, whereas the Hoffmann sign is simply a hyperactive stretch reflex. It has the same meaning as hyperactivity of other stretch reflexes and should be interpreted accordingly. Another way of eliciting the same reflex response in the thumb and fingers and is known as Tromner's sign.

The patellar reflex or quadriceps stretch reflex is easily elicited with the patient's feet flat on the floor (Figure 34, A). Hold one hand on the distal thigh and strike the tendon just below the patella. The response is both seen and felt. This reflex can be obtained while the patient sits on the edge of the examining table, the response judged from the rapidity and extent of leg movement. The latter method provides an opportunity to observe the poorly damped (pendular) knee jerk of cerebellar disease, but the former method ensures better relaxation. The femoral nerve and the L2, L3, L4 spinal segments and nerve roots are involved. This reflex is obtainable when the patient is supine, as shown in Figure 34, B. The degree of knee flexion varies. If the patient will not relax, ask him to press his heels into the bed.

An excellent way to evoke on each side the Achilles reflex or gastrocnemius and soleus stretch reflex is shown in Figure 34, C. While one hand is positioned as shown to stretch the muscle slightly, tap quickly and gently with the other. A satisfactory horizontal position for obtaining this reflex is seen in Figure 34, D. The sciatic (its Tibial branch) nerve and the L-5 and S-1 nerve roots and spinal segments, chiefly the latter, are involved.

Syndromes of motor disturbances, lesion of Cortical-spinal Tract on different levels

The main symptoms of motor way lesion on different levels

1. The lesion of anterior central gyrus

usually cause monoplegia ( or monoparesis ) on the opposite side . If the focus is situated in upper part of anterior central gyrus , paralysis of lower extremity occurs.

If it is in middle part of anterior central gyrus, we can observe paralysis of upper extremity. If it is in lower one, face suffers. In case of anterior central gyrus irritation Motor Jackson takes place. Motor Jackson is a set of local seizures that can cause generalized seizures.

2.The lesion of corona radiata

usually cause central hemiplegia on the opposite side ( that means that arm, leg, lower mimic muscles and tongue muscles are involved ). By the way, if the process is much more expressed in upper part of corona radiata, paralysis in lower extremity dominates. If the process is much more expressed in middle part of corona radiata , paralysis in upper extremity prevales. If the process is much more expressed in lower part of corona radiata, paralysis in face muscles dominates.

Besides hemianesthesia can join hemiplegia.

3. The lesion of internal capsula part of motor way

can cause hemiplegia on the opposite side, central paresis of tongue muscles and lower mimic muscles . Hemihypesthesia often joins all the other symptoms. Vernike – Mann posture is typical for this lesion.

4. The lesion of brain stem

cause central paralysis on the opposite side and peripheral paralysis of face muscles on the side of lesion. It is known as alternating syndrome. The last are divided into peduncle, pontine and bulbar ones.

5. The lesion of pyramidal decussation part of motor way

usually cause central paralysis of upper extremity on the side of lesion and paralysis of lower extremity on the opposite side . Sometimes tetraplegia or triplegia is observed.

6. The lesion of motor way in lateral foniculus of spinal cord

cause central paralysis below the level C1-C4, C5-Th1, Th1- Th12, L1-S2.

7. The lesion of anterior horns or motor nucleus of CCNs

cause peripheral paralysis of certain muscles . At chronic process we can observe fasciculation of muscles. Also there are early atrophy and degenerative reaction.

8. Anterior roots lesion

cause also peripheral paralysis . In most of cases it is observed only when several roots are damaged.

9. The lesion of nerve plexus

cause peripheral paralysis , pain, sensory and autonomic disturbances.

10. The lesion of peripheral nerve

cause peripheral paralysis of the muscle , innervated by this nerve. There is also pain, sensory and autonomic disturbances.

Students’ practical Study Program

1. Clinical anatomy of spinal cord. Spinal reflex arche. Reflexes and methods of examination

Step I. Aim: To research patient’s reflexes. For this purpose it is necessary:

1. To cause all superficial and deep reflexes.

2. To check up presence or absence of pathological plantar reflexes: flexing (Rossolimo, Jukovski, Bechterev’s, Mendel – Bechterev’s reflexes) andextensing reflexes (Babinski, Oppenheim’s, Gordon’s , Shtrumpel, Grossman, Sheffer, Chaddock’s, Puusepp’s and Redlich).

Step II. Aim: To describe unconditioned reflexes: living, hyperreflexia, torpid, presence of pathological reflexes, foot and patellar clonuses.

Step III. Aim: 1.To formulate output about presence or absence pathology according to patient’s reflexes.

2. To make recording about uniformity of reflexes or anizoreflexia.     

3. To make output about a level of lesion of nervous system (sectional or subsectional)

2. Active movements, types of paralysis, syndromes of movement disturbances

Step I. Aim: To determine presence or absence of disturbance of movements in patients. For this purpose it is necessary:

1. To collect the patient’ complaints (limitation of active movements, weakness of the extremities).

2. To examine strength of muscles and volume of active movements, volume of passive movements.

3. To cause all superficial and deep reflexes.

4. To check up presence or absence of paresis (paralysis) in patient.

Step II. Aim: To determine character of paralysis (paresis). For this purpose it is necessary:

1. To examine patient’s neurologic status.

2. To carry out data of analysis of inspection, using the given below criteria:

3. To make output about presence of flaccid or spastic paresis.

Step III. Aim: To find level of lesion of Pyramidal tract.

Step IV. Aim: To make the topical diagnosis. In topical diagnosis it is necessary to point character of paralysis (spastic or peripheral), level of Pyramidal tract lesion.

3. Syndromes of lesion of Cortical-Muscular Tract on different level

Step I. Aim: To determine presence or absence of paresis or paralysis in the patients. For this purpose it is necessary to hold examination, stipulated by the first stage of the methodical instruction.

Step II. Aim: To determine character of paralysis (paresis) in patients. For this purpose it is necessary to hold examination, stipulated by the first stage of the methodical instruction.

Step III. Aim: To find level of lesion of Pyramidal tract.

Step IV. Aim: To make the topical diagnosis. In topical diagnosis it is necessary to point character of paralysis (spastic or peripheral) and level of lesion of nervous system.