Lesson N1

Theme: Introduction on Neurology.

General principles of nervous function

Sensitivity and sensory tracts. The peculiarities of face sensory innervations. Syndromes of sensory disorders

Motor functions. Reflexes and their changes. Method of examination. Movements and their disturbances. Central and peripheral paralysis

 

    Neuropathology (from greek neuro – nerve, pathos – disease, logos – science) – is a part of clinical medicine, which is involved iervous 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:

 

 

 

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 ieurological 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).

 

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.

 

                                 

 

Conjunctival reflex, as frequently absent iorm, large value in research of the nervous system have no.

 

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 iorm 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 iorm 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 wheormal 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 phenomenoamed 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.      peripheral

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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).

 

 

 

The 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

 

 

 

Jukovski

 

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

 

 

 

    To extensing reflexes belong Babinski

  

 

               

 

Oppenheim’s

 

 

Gordon’s

 

Shtrumpel, Grossman, Sheffer

            

 

 

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

        

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 (Fig 28,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 iormal 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 wheormal 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 inches above 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.

 

 

 

 

Students’ practical Study Program

 

1. Clinical anatomy of spinal cord. Spinal reflex arches. 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) and extensing 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.         

 

 

Sensitivity and sensory tracts. The peculiarities of face sensory innervations. Syndromes of sensory disorders

 

Sensation and reception

Sensation is an ability of an organism to accept stimuli from external and internal environment.

 Reception is a set of all afferent systems, which accept stimuli from external and internal environment and carry them out to the center.

Reception is wider concept, than sensation. One doesn’t not feel everything he accepts.

Sensation is a part of reception, which one feels and can analyze by certain structures of his brain. It means that sensation is closely connected with activity of analyzers.

 

Analyzers and its structures

 

Analyzer is a sole functional system that consists of three parts:

1.  Receiving apparatus (receptors) – receptor part

2.  Sensory explorers – conductive part

3.   Part of cortex, which receives information, analyzes and synthesizes it.

 

The main function of Analyzer is to accept and analyze stimuli. We distinguish the following analyzers:

–         Visual

–         Acoustical

–         Sensual

–         Testate

 

Reception apparatus

 

Receptors are sensitive structures that have ability to accept different changes of external and internal environment and transmit them as impulse.

    

Receptors are divided into:

1. Exteroreceptors (in skin and external mucose membrane)

2. Proprioreceptors (in muscles, tendons, joints)

3.  Interoreceptors (in inner organs, in vessels)

There are also telereceptors in ears and eyes.

 

1.    Exteroreceptors accept superficial sensitiveness (light touch (tactile), pain and temperature sense). They are divided into mechanoreceptors (touch, pressure), thermoreceptors (cold, hot), nociceptors (accept pain).

     The tactile sense is perceived by tactile Меrkеl’s bodies on fingers tips.

     Меysnеr’s bodies on palms, soles, lips, on the end of the tongue are very sensitive to any touch.

     Fater-Pachini’s bodies in deep layers of skin perceive sense of pressure.

    Cold receptors are situated in flasks Krause’s.

    Thermal receptors are located in Puffin’s bodies.

     More fibers react to cold stimuli than to thermal ones.

     Pain is accepted by free nervous endings between epidermal cells.

 

2.    Proprioreceptors are situated in deep tissues (muscles, joints, tendons). The muscular receptors are variable. The most important of them are nervous – muscular cords. They react to tension of muscles. They are covered by a connective tissue case and are situated intra- and extrafusally between the fibers of striated muscles.

The Goldie’s and Matson’s bodies accept joint feeling. They are situated between muscles and tendons.

Besides, there are also osmoreceptors, chemoreceptors, baroreceptors and others.

     The impulse is transmitted from the receptor apparatus to the cerebrum by means of nerve fibers. The last are axons of unipolar cells of dorsal root ganglia.

 

There are 3 types of fibers:

1.  Type A – thin myelin fibers, which  carry out deep and light touch sense; the speed of impulse transmission by these fibers  is 40-60  m/s

2.  Type B – myelin fibers, which carry out pain and temperature sense; the speed is 10-15 m/s

3.  Type C – without myelin fibers, which carry out diffuse pain sense with speed 1-1,5 m/s.

 

Classification of sensation

Depending on the special interest of the investigator, sensation may be classified in many different ways. The neurologist, in his search for the location and cause of neurological disease, finds it convenient to classify sensation into: superficial and deep.

Each of the main groups includes different modalities which will be discussed separately. There are different classifications of sensation.

 

І. Classification, which is based on the place of originating of stimuli. According to this classification sensation is divided on:

1. Exteroceptive

2. Interoceptive

3.  Proprioceptive

 

ІІ. Classification, which is based on biological principle of originating of sensation. According to this one sensation is divided into:

1.    Protopatical (vital, nociceptive, thalamic). This ancient sensation is typical for the primitive nervous system of our ancestors.

2.    Epicritical sensation is connected with cortex and it is based on the differentiation of stimuli according to their modality, intensity, localization etc.

 

III. In clinical practice usually we use classification, which is based on the kind of stimuli.   According to clinical classification sensation is divided into:

1. Superficial

2. Deep

3.  Complicated

 

Superficial sensation 

This term includes the modalities of light touch, pain and temperature.

1. Light touch (tactile) sensation – is feeling of touch, which may be examined by touch of cotton, end of hammer, paintbrush;

2. Superficial pain – is a feeling of pain, which may be tested with a corsage pin or pinwheel (acutely or bluntly, pricks or does not prick);

3. Temperature sensation – is feeling of cold or hot, which may be tested by application of glass tubes filled with iced (10⁰ C) and hot (43⁰ C) water to the skin;

4. Trihoesthesia – is a sensation of touch of hair;

5. Hydroesthesia – is a sensation of humidity;

6. Sensation of electrical current;

7. Feeling of tickling.

 

Deep sensation

This includes joint and vibratory sense and pain from the deep-lying somatic structures, namely, muscle, ligaments, fascia, bone, and so on.

1. Joint sense – is a sense of position and passive movements

2. Vibration sense                               

3. Feeling of mass

4. Feeling of pressure

5. Kinesthesia

 

1. The joint sense (bathyanesthesia) – is a deep sense, which is based on the ability to distinguish position and passive movements in joints. Position sense or proprioception is tested by gently moving a terminal phalanx – in the lower extremities by vertical movements of the toes and in the upper extremities by similar movements of the thumbs and fingers. Examination of this feeling is always started from movements in joints of fingers, then – in a carporadial joint and further – in ulna etc. The loss of joint sense, which is called bathyanesthesia, results in disturbance of muscular coordination and is known as sensitive ataxia.

 

Sensitive ataxia is divided on:

 a) static

 b) dynamic

 

Static ataxia in legs may be investigated by means of Romberg’s test – patient is asked to stand directly with the extended forward arms and feet together. In case of ataxia difficulty of standing and instability occurs. That is magnified while eyes are closed.

Static ataxia in arms may be investigated by follows: we ask patient to extend forward arms and to place fingers separately. In case of ataxia consensually spontaneous (involuntary forced) movements (pseudoathetosis) in fingers of arms occurs.

 

Dynamic ataxia in arms may be examined by means of finger-nasal test, and in legs – heel-knee test.

 

2.   The vibration sense (pallesthesia) – may be tested by placing the base of the tuning fork over a bony prominence (it can be back of the hand, feet) during vibration and again when the fork is stopped (silent control application). We must control how many seconds the patient feels vibration of a tuning fork (to the moment when he feels only pressure). Normally in arms it is – 15-20 s, in legs – 10-15 s.

 

3.  The sensation of weight (baroesthesia) – is the ability to distinguish different weights, and it may be examined with the help of small weights, which are put in the patient’s palm. Normally the patient distinguishes a difference of weight about 15-20 grams. The loss of this ability is called barognosis.

 

 

4.    The sensation of pressure – is determined by simple pressing of finger or instrument baresthesiometer. The patient should feel pressure of different force and distinguish pressure from touch.

 

5.     Kinesthetic sense is a sensation of movement of dermal fold.

 

Complicated sensation (Integrative function of parietal cortex)

The role of the cortex in sensory appreciation is discriminative. Destruction of the parietal cortex does not produce anesthesia for any modality of sensation except as a transitory phenomenon. The basic sensation of pain, temperature, vibration, and touch are recognizable as such, but the ability to make fine sensory distinctions is impaired over the contra lateral side of the body – facial sensation being least affected for some reason.

 

1.       Stereognosis (Three-point distinction) is the ability to identify familiar object placed in the palm of the patient by palpation when the eyes are closed. It is complicated kind of sensation, which is based on the reception of separate properties of object (weight, form, surface, and sizes), synthesis and analysis of all these properties in the cerebral cortex and is particularly related to activity in the parietal lobes. For example, to identify by touch (with the closed eye) a pen, hammer etc.

 

2.       Graphism – is the ability to determine figures and numbers traced on the skin with the closed eyes. Graphesthesia – impaired graphism is very sensitive indicator of parietal lobe damage.

 

3.       Localization sense – is the ability to point an exact place of the stimuli.

 

4.       Discrimination sense (two-point discrimination) – tests the ability of the patient to differentiate one stimulus from two. It may be examined by Weber’s circus. After the patient closes his eyes the doctor puts stimuli by circus branches on either one side or both sides of skin of his body. At first pulling branches together, and then enlarging distance between them. He marks thus on what distance the patient feels two simultaneously put stimuli as two, and on what as one. The test leads are most sensitive of fingers, tough. The results of examine estimate under the special table.

 

5.       Baragnosis – is the impaired ability to distinguish different weights.

 

Anatomy of Superficial sensation pathways

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

The way which carries out pain, temperature and part of tactile sense has three neurons.

The first neuron is situated in unipolar cell bodies. The last are located in dorsal root ganglia of the spinal cord and homologous ganglia of the cranial nerves (ganglion intervertebral or ganglion spinals). Their dendrites are routed on peripherals within plexuses, peripheral nerves. There they are finished in various sensory skin receptors. The axons of these unipolar cells enter the spinal cord through the dorsal roots in a basis of dorsal horns, where they are finished.

The second neuron – the cells of the second neuron are situated in dorsal horns of the spinal cord. The axons create tractus spinothalamicus. The axons of these neurons cross the midline through the ventral commissura and go to the opposite lateral funiculus and then run in the lateral spinothalamic tracts. These tracts run upwards to the brain stem, where they pass through the oblong brain, the Varoliy’s pons, and peduncles of brain and are finished in nuclei of thalamus.

 

The features of spinothalamic tracts, which have diagnostic value

1.    The decussating in front of white soldering occurs not in a horizontal plane at a level of segment, but obliquely from below upwards during 1-2 segments. Therefore if we have lesion of lateral funiculus, the sensitive disturbance occurs on the opposite side 1-2 segments below than the level of a pathological focus.

2.    The caudal contributions to the spinothalamic tract are pushed laterally by the incoming contributions from higher up results in a lamination of the tract, with the fibers from the lowers segments of the spinal cord placed more dorsolaterally on each side. This explains the “sacral” sings and symptoms that result from more or less superficial involvement of the lateral funiculus even at the highest level of the cord. It is the Auerbah-Flatau’s law of eccentrically allocation of longer explorers.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Taking into account this fact it is possible to make the conclusion. In case  of extramedular pathological process (for example, the tumors squeezing a lateral fibber of lateral funiculus of spinal cord) disturbances of sensation will accrue from below upwards (at first on foot, then on leg, thigh, and the trunk, further in an arm (hand)), that is the ascending type of sensitive disturbance. In case of intramedular pathologic process (when first lesion of medial fibers is in lateral funiculus of spinal cord) sensitive disturbance will be distributed from above downwards, that is descending type of sensitive disturbance.

The third neuron is located in the nucleus of thalamus. The axons form thalamocortical tract and  pass through internal capsule, then within radiate crown, and are ended in post central gyrus and parietal lobes of brain hemisphere, and in upper parts of a gyrus – the sensation from lower extremities, on the average – from upper extremities, in lower – from the face and tongue are ended.

 

 

Anatomy of Deep sensation explorers

This pathway has also 3 neurons.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

The first neuron The unipolar cell bodies are located in the dorsal root ganglia of the spinal cord and homologous ganglia of the cranial nerves (ganglion intervertebral or ganglion spinals). The dendrites are routed on peripherals within plexuses, peripheral nerves, where they are ended in various sensory receptors in muscles, tendons and joints. The axons of these unipolar cells enter the spinal cord through the dorsal root and run in dorsal funiculus on one side of the spinal cord, where it divides into two paths – medial thin Holl’s pathway and lateral Burdach’s pathway. In Holl’s pathways fibers pass from segment Th₄ and below, and in Burdach’s pathway, from segment Th₄ and higher. That means the Holl’s path carries out deep sense from lower extremities and bottom of a trunk, and Burdach’s path – from upper extremities and top of a trunk.

This feature has topical and diagnostic value: at extramedular processes (for example, in cervical part of spinal cord) the disturbance of deep sense accrue for the descending type, and, on the contrary, at intramedular processes of spinal cord disturbance of deep sense occurs for the ascending type.

The second neuron is in Holl’s and Burdach’s nuclear of oblong brain. The axons of the second neuron create bulbothalamic tract. The fibers of this path are crossed on olives level of oblong brain, on the pons of brain stem they join fibers of spinothalamic tract lateral and create a medial closed loop. The medial closed loop (lemniscus medialis) consists of fibers of spinothalamic tract and bulbothalamic tract. The axons of the second neurons carry all sorts of sensation from opposite side of the body. The medial closed loop is ended in ventral nucleus of thalamus.

The third neuron – is in thalamus, from which cells thalamocortical tract starts. The axons of this path go through internal capsule, radiation crown and are ended in a postcentral gyrus, partially in the right central gyrus and in parietal lobes of a share. It is necessary to tell, that a part of fibers from the second neurons of deep sense are routed not to a thalamus, but to a cerebellum through lower legs of a cerebellum.

The part of impulses from muscles, tendons, joints, deep tissues run to a cerebellum (to its worm) after spinocerebral paths. For example, in dorsal horns of spinal cord there are cells, which axons borrow (occupy) lateral funiculus and rise to brain stem as spinoreticular, spinoolivar, spinovestibular, spinotectal pathways.

 

 

Sensation innervation of the face is carried out as follows

The first neuron of face, nasal sinuses, oral cavities and nose sensory conductors are situated in trigeminal (Gasser’s ganglion). Those for larynx mucose membrane, pharynx, radix of tongue – in ganglions of wandering and glossopharyngeal nerves (ganglion superior and inferior). Those for 2/3 front of tongue – in a geniculate ganglion (ganglion geniculi) of Facial nerve.

The axons of the first neurons as a part of sensitive roots of cranial nerves (V, VІІ, IX, Х a steam) are routed to a brain stem.

       nucleus tractus spinalis n. trigemini

               nuсleus terminalis

       nucleus alae cinerea

The second neurons are situated in the sensitive nuclei of the adequate cranial nerves. The axons of the second neuron make decussate and after that join medial closed loop, in which structure pass to ventral-lateral nuclei of a thalamus.

The third neuron is in thalamus. The axons form thalamocortical tract, pass through internal capsule, a radiate crown and are ended in lower parts of postcentral gyrus.             

 

 

Symptoms of sensory disturbances (sorts and types of sensory disturbances)

Depending on qualitative and quantitative changes of sensation in clinic we distinguish the following objective sorts of sensory disorders:

1. Anesthesia – complete loss of any sorts of sensation. For example:

Analgesia – loss of pain sense.

Thermoanesthesia – loss of a temperature sense

     Bathyanesthesia – loss of deep joint sense

     Astereognosia – loss of stereognostic sense

     Topanesthesia – loss of localization sense

     Pallanesthesia – loss of vibratory sense

2. Hypoesthesia – lowering of sensation.

3. Hyperesthesia – sensitization as result of lowering a threshold of energization in cortex of brain.

4. Dysesthesia – distortion of sensitivity, when instead of one stimulus the patient feels absolutely other. For example, warm touch one feels as cold.

5. Hyperpathia – results from rise of a threshold of energization, when there are strong, unpleasant, badly localized sensations of stimuli. Thus the mild stimuli are not received absolutely. In basis of hyperpathia the disturbance of the analytical function of cortex lays.

6. Synesthesia – sensation of stimuli not only in a place of its plotting, but also in the other place.

7. Polyesthesia – means sensation of one stimulus as several ones.

8. Alloheyria – sensation of stimuli in symmetrical sites on an opposite body part.

9. Alloesthesia – sensation of stimuli in the other place.

10. Dissociation of sense – phenomenon of fallout of some kind of sensitivity while saving others in the area of segment innervation.

 

Subjective sorts of sensory disturbances:

1. Paresthesia is a creeping sensation, cold, burning sensation, fever, numbness, itch, the pricking etc. Frequently paresthesia is the first sign of nervous system lesion.

2. Pain. The pain sensations can arise at stimuli by the pathological process of sensitive analyzers at any level (from receptors up to cortex). Pain is one of the most common complaints to be brought to the physician attention. The initial goal of the neurologist is to ascertain whether the pain represents disease of the nervous system as contrasted with visceral, ischemic, musculoskeletal, or psychosomatic causative factors. The most common pains of neurological origin, except headache, are those that originate from lesions of the peripheral nerves and the spinal roots. Of less frequency but of no less importance are those kinds of pains that reflect dysfunction of the sensory tracts of the central nervous system or thalamus.

 

Determine the following sorts of pain:

1. Local pain – is pain, for example, at palpation of the nervous trunk. That is pain, which coincides with the place of lesion.

2. Projectional pain – is a pain in zone of innervatioot only in place of stimuli, but also distally on a course of nerves or roots. To projection belongs the stump neuralgia – pain in absent segments of an extremity after its ablation. Or other pain example: during a trauma of a ulna nerve in the field of a ulna joint the pain gives back in V fingers of a paintbrush.

3. Irradiating pains – are pains, which are distributed from one nerve branch to another, not struck. For example, at neuralgia of the first branch of trigeminal nerve the pain is distributed to zone of innervation of the second or the third branches, in upper or lower jaw, in ears etc.

4. Displayed pains – are pains in zones Zacharyin-Hed’s at diseases of inner organs, when irradiation arises to certain zone on skin through cells of dorsal horns of spinal cord. For example, pain on ulnar territory of the left forearm and paintbrush at angina pectoris.

 

 

5. Causalgia (Greek causes – burning sensation, algos – pain). It is intensive thermalgia originating, for example, at traumas. It is pain without stimulation.

6. Reactive pains – are pains that originate at expansion of nerves. The pains can arise at palpation of pain points and at band spread of nervous trunks.

 

There is a set of pain points, for example, point of an exit of branches of trigeminal nerve, supraclavicular and subclavian point Herb’s for humeral plexus, scapular point Lasarev’s, junta spinal points, pain points at palpation of acanthus vertebra, interposes intervals, point Hara’s at pressing of transversal processes lumbar vertebras, point Raymist’s – point of lumbar-sacral concatenation, pain points Valle’s – on course Sciatic nerve, pain point of Femoral nerve at pressing of middle  of pupart sheaf. Signs of a tension the following: Laseque’s sign, Wassermann’s sign, Nery’s sign, Matskevich’s sign and many others. The pain points and tension signs will be shown to you on practical lesson during learning a special neurology.

 

 

 

 

Types of sensory disturbances

 

 

Determine the following types of sensory disturbances:

1.  Peripheral

2.  Segmental (sectional)

3.  Conductive

1.  The peripheral type occurs at lesion of dendrites of the first neuron of all sorts of sensation. The peripheral type is divided on:

   

a) Mononeuritic (or neural) pattern – is observed at lesion of one peripheral nerve and consists of disturbance of all sorts of sensation in innervative zone of this nerve. There is a pain in the field of nerve, sometimes hyperpathia, hyperalgesia, causalgia, tension signs of nerve, pain at palpation.

   

b) Polyneuritic pattern – is observed at multiple, frequently symmetric lesion of all peripheral nerves. Appears by sensory disturbance in distal parts of extremities as “socks” on legs and “gloves” on arms. The “stocking-glove” pattern of sensory loss is typical for peripheral neuropathy. But sometimes cerebral or spinal lesion may cause distal sensory loss, usually of a single extremity in the case of cerebral disease, and often in association with hyperreflexia and the Babinski sign in cases of either cerebral or spinal lesions.

    

c) Plexal pattern – occurs at lesion of dorsal root ganglia and appears by sensation disturbance in innervative zone of a plexus. In this case there are pains, tension signs of nerves going from a plexus, movement disturbance – peripheral paresis of muscles group, which innervated from this plexus.

    

d) “Saddle-area” pattern of sensory loss. This area is the “tail-end” of the body and is innervated by the sacral segments of the spinal cord and the sacral roots. A lesion producing saddle-area sensory loss will be found in the upper lumbar spinal level if it is due to a lesion of the cord (conus medullaris). The lesion will be at the middle of lower lumbar or upper sacral spinal level if it involved the cauda equina. Defective control of the urinary bladder and anal sphincter are regularly associated with this type of sensory deficit.

It is necessary to point, that at lesion of a peripheral nerve, many peripheral nerves and plexuses, in which near the sensitive fibers pass also movements pathway, simultaneously with sensitive disturbance there are the signs of flaccid paralysis or paresis.

 

 

2. The segmental (sectional) type disturbance of sensation is observed at lesion of sensitive fibers at segment level of spinal cord, and, means, at lesion of dorsal root ganglion, dorsal roots, dorsal horns of spinal cord, front white soldering.

 

Subtypes of a sectional type:

a) Segmental – radicular

b) Segmental – dissociated

  

a) Segmental – radicular pattern occurs at a lesion of dorsal root or simultaneous lesion of root and dorsal root sensitive ganglion. At lesion of dorsal root there is a loss of all sorts of sensation in its zone innervation according to the segmental type. The sensitive disturbance is appeared as transversal strip on a trunk and longitudinal strip on extremities (in human being there are 36 sensitive segments (31 spinal segments are on trunk and extremities and 5 segments at the expense of trigeminal nerve on the face).

(To show a segmental structure of the man body – table)

This type of disturbance of sensation arises at radicupathyes, at extramedular tumors. At lesion of dorsal root ganglion occurs herpes exanthema in a zone innervation of the struck segment (at a ganglionitis or ganglioneuritis) as bubbles (so-called herpes zoster), sharp pains and anesthesia in a segment.

  

b) Segmental – dissociated pattern. It is observed at lesion of dorsal horns of spinal cord and front grey soldering. Thus the disturbance of sensation appear as loss or lowering pain and thermoanesthesia and saving tactile and joint sense in given segment. Such disturbance are called dissociated and result from that in dorsal horns and front grey soldering pass explorers of superficial sensation, and from the explorers of deep feeling that do not go to a dorsal horn of spinal cord (recollect anatomy).

The dissociated type of disturbance of sensitivity more often arises at a myelosyringosis, when the sensitive disturbance are observed in certain dermatomes as “jacket” or “half jacket” at lesion of dorsal horns of spinal cord in thoracic segments, or “trousers” – at lesion of dorsal horns of spinal cord in lumbar segments.

It is necessary to remember, that lesion of dorsal roots or dorsal horaturally reduces or kills away reflexes, which are makes by the same dorsal root or dorsal horn.

 

3.    Conductive type.

 

 

The lesion of sensory explorers in spinothalamic tract, Holl’s and Burdach’s pathways,

bulbothalamic tract, medial closed loop and thalamocortical tract in limits spinal cord or brain cause conductive type of sensory loss. This type is divided on:

1. Spinal

2.  Cerebral

The sensory disturbance from the defined level of a lesion and downwards is typical for both subtypes.

1. Spinal pattern can be:

 

a) Complete transversal (is observed at a lesion that involves a diameter of a spinal cord, at which all sorts of sensation below that level of a lesion drop out,  pain and temperature sense drop out on 1-2 segments below than level of a lesion, and deep – from the same level. Usually, the deficits are in the lower trunk and legs, are bilateral and almost symmetric.

 

b) Half transversal or Brown-Sequard pattern – arises at a lesion of a lateral half diameter of a spinal cord, thus the deep feeling drops out on the side of a lesion, and pain and temperature sense- on the opposite side, since a level on 1-2 segments is lower.

 

c) Descending

 

d) Ascending, depending on extra- or intramedular lesion

 

e) Monotype

 

f) Hemitype

 

2. Cerebral pattern is divided on:

a) Brain stem pattern (alternating). At lesion of sensory fibbers in brain stem there is fallout of sensation on the face according to the segmental type on the side of lesion both fallout pain and thermoanaesthesia on trunk and extremities on opposite sides. Lesions in the pons and below in medulla and cord may result in dissociated sensory loss on one or both sides of the body because of different levels of crossing of the sensory pathways. A lesion of the lateral medulla (lateral medullar syndrome, called Wallenberg’s syndrome) will cause loss of pain sensation on the same side of the face and the opposite side of the body. In this situation, touch is preserved in areas where there is loss of pain perception.

 

b) The thalamic pattern (at a lesion of thalamus) is observed:

1. Hemihypoesthesia of all sorts of sensation on opposite side from the pathological focus.

2. Hyperpathia – the disturbance of deep feeling prevail

3. There are thalamic pains (burning, intolerable)

4. Hemiataxia – as result of lowering deep joint feeling.

 

c) Capsular pattern – in case of a lesion of sensory fibers in back leg of internal capsule arises hemi anesthesia of all sorts of sensation on opposite sides and hemiataxia owing to fallout of deep feeling.

 

d) Cortical pattern – arises at a lesion of a postcentral gyrus and upper parietal gyrus. Thus the sensation drops out on monotype in an arm either in a leg, or on the face depending on localization of a lesion in a postcentral gyrus.

 

The cerebral or thalamic disorders, when the lesions are above the pons, cause sensory disturbances that involve one entire side of the body. This pattern is also found in cases of hysteria, but then the line of demarcation usually is precisely in the midline, whereas in organic deficits demarcation is short of the midline. At stimuli of a postcentral gyrus cortical subtype paresthesia appears on the opposite side to the focus, on the face, in arm or in leg.  At lesion of parietal share combined and deep sorts of sensation suffer (develops astereognosis or fallout of joint feeling). The syndrome of disturbance of joint feeling can be shown as afferent paresis. This syndrome for the first time was described by Fester in 1936.  Appears – disturbance of movement functions owing to disturbance of joint sense. Such movement disturbances are characterized by disturbance of coordination of movements, awkwardness, and deceleration of movements. The syndrome of afferent paresis can be tag of a lesion of parietal share of a brain.

 

Examination of sensation.

 

The somatic examination of sensation is the most difficult and least reliable part of the investigation. It should be left to the end, at which time the examiner will know what specific questions to pose and what findings are realistic. The examiner must be wary of forming hasty conclusion and as open-minden as possible in evaluating responses, since the examination of sensation is so prone to bias and suggestion. On examination ask if the patient is aware of any abnormal sensation or loss of sensation. Paresthesia (tingling, numbness, burning, crawling, coldness, or dead feeling) are common symptoms of disorders of the sensory system at any level. Many people, unfortunately, sue the word “numbness” and “deadness” to refer to weakness or motor dysfunction. Try to determine just what the patient means. Transient paresthesias that appear after unusual posture or pressure on a limb are usually ignored but may be symptom of sub clinical neuropathy.

Although the patient should not watch the examination, when you are attempting to determine a zone or level of sensory loss, he should always first indicate the region where sensation is abnormal and where it becomes normal. He may be able to do this with as much accuracy as can result from examination.

If sensation is reduced in some region, start the examination in that region and advance to the normal zone by successive, identically applied pinprick stimuli at intervals of about 2 sm. Ask him to tell you when the pinprick sensation changes or when it becomes normal. The level of demarcation between abnormal and normal will be ill defined variable when sensory loss is not complete. Make notes or drawings of the levels determined, and if responses are inconsistent, repeat the test later. Elicitation of pain, touch, and temperature discrimination are all appropriate for determining a level or zone of denervation.

Since the majority of sensory deficits involve some loss of sensitivity to pain, test this modality first in the adult. Show the patient the common pin to be used and demonstrate on your hand how this stimulus will be applied. Hold the pin so that either your finger or the pinpoint touches the skin. You can thus deliver either a “sharp” or a “dull” stimulus. Do not use an intravenous needle.

Use the pin lightly but consistently, with just enough pressure to elicit a sensation of sharpness and pain.

  

 

     

 

Start on the upper chest, and then go to the hands and feet, comparing sensitivity on the two sides of the body, then distal to proximal areas, and finally upper to lower aspects of the trunk. If there differences, ask the patient to report where the sensation of pinprick is normal and where it seems dulled. Go back to the area of reference for reorientation. When sensory loss is partial, consistency will be less because of patchy and incomplete losses. A delayed, perverted, or unpleasant sensation after pinprick usually indicated root or nerve disease but is also found with thalamic lesions (thalamic hyperpathia). Devote the most attention to the hands and feet since differences and deficits will be most intense and easily detected there. The sole of foot, however, is not a good area to estimate pain loss because of its unusual sensitivity. When pinprick is not felt on the sole, either the part is denervated or the patient has hysteria of some fortitude.

Pain and temperature sense are closely associated in the nervous system. Reduction in or loss of either modality has the same meaning, and a deficit in one will usually be accompanied by a deficit in the other.

 

Test for temperature discrimination is done most commonly in cases of suspected thalamic or cord lesion when pain loss is equivocal. At times, pinprick stimulus will elicit dysesthesia, to the conclusion of patient and examiner. When this happens, turn to test of temperature discrimination.

The test is difficult to implement because of the difficulty of maintaining constant temperatures in the test tubes. Obviously the test can be made more sensitive by reducing the difference between the temperatures of the two tubes. Set up the test by putting crushed ice and water in one tube and hot tap water in the other, keeping the outside of the tubes dry. Change the water when it approaches room temperature.

Apply the cold and hot tubes in irregular alternation, letting each dwell on the skin long enough to register cold and heat. Start with a normal area of reference and frequently check the ability to sense hot or cold there. Ask the patient to report the sensation. Normally, the patient’s reports will show quick discrimination and few mistakes. Compare the two sides and various areas, as indicated, for the ability to discriminate cold from hot, much as one test for pain. Rough levels or zones of loss should be estimated.

 

 

 

 

 

Vibratory sense and position sense are closely allied functions and are diminished or lost when the posterior columns of the cord are diseased, in cases of peripheral neuropathy and lesions of the brain stem and cerebrum. Fibers conducting these modalities do not synapse or cross until they reach the medulla.

Always test first for loss of vibratory sense in the hands and feet and then more proximally when peripheral losses are found. Use a 256-HZ tuning fork. Strike it on some firm but not hard surface and apply the end of the fork firmly to the dorsum of the great toe or to a distal knuckle of a finger. Ask the patient what he feels. Be sure he feels vibration. The fork may be applied to the forehead or sternum if he does not understand what is meant by vibration. Always surreptitiously stop the vibration at some time in the examination to be sure the patient is not reporting only the sensation of pressure. In people over 60, vibratory sensation so tested is often absent in the toes but is never absent on the shin or in the fingers of the healthy person.

 

 

To test for position sense, hold the sides of the patient’s great toe. Have the patient watch while you demonstrate up and down movement. Then ask him to call out “up” or “down” with eyes closed as you move the toe. Normally a few degrees of movement will be sensed and the direction identified. The normal limits are quickly learned. If the initial two or three responses are correct, do not stop here and accept this as evidence of normal position sense. A patient who guessing will be correct 50% of the time and may well call two or three consecutive movements correctly. Give the patient at least six trials before concluding that position sense is intact. Position sense in the thumb may be tested in a comparable manner.

 

 

 

 

 

 

 

Always check pallesthesia and position sense carefully when the patient complains of clumsiness of the hands or difficulty in balance or if he demonstrates loss of manual dexterity, unsteady gait, or poor performance on heel-to-knee test or on tandem walking. The differential diagnosis of cerebellar vs. spinal cord, root, and peripheral nerve disease may rest largely on the demonstration of the presence or absence of disturbed pallesthesia and position sense and their respective distributions.

 

Testing for touch is done in a manner comparable to testing for pain. A cotton ball is used, with a small piece pulled out to reduce the area of contact. Apply this to a reference area to acquaint the patient with the sensation. The normal person of any age will be able to sense a wisp of cotton pulled a short distance over the skin anywhere the skin is not calloused. Ask him to close his eyes and say “yes” each time he feels the cotton. Check as before for the patterns of loss that are most common.

Compare the regularity of response on the right with that on the left side and the distal with that on the proximal aspects of the extremities. Then ask the patient if he believes there is any difference in the contrasted areas. Avoid applying the test stimulus with a predictable rhythm lest the patient anticipate that rhythm and respond accordingly. The sensation of touch is relatively enduring, and other losses are apt to be manifested before touch is lost.

 

Testing the ability to identify small objects in the hands without visualization is an important part of the sensory examination. Use coins of several denominations, a paper clip, rubber band, small bar of soap, cotton ball, pencil, key, and so on. The normal person will hold the object with the fingertips, turn it around, follow its contours, rub and manipulate it in a knowing way, and usually give a correct answer. If the object is handled knowledgeably but not identified or bizarrely misidentified, the integrity of the patient is in question. An exception is the aphasic patient who may not be able to summon the proper name of the object or the patient in whom a lesion has effectively “disconnected” the parietal association areas in the dominant hemisphere with the rest of the brain. The patient with astereognosia does not handle the object well, fumbling it in the palm, trying but failing to grasp it securely with the fingertips, even dropping it. If the patient cannot identify some or all of the objects, the presence of posterior-column disease should be suspected, or, if the patient’s difficulty is unilateral and accompanied by little or no other sensory loss, the existence of Parietal lobe disorder is probable.

 

Graphesthesia refers to the ability to recognize letters or numbers by feeling them being traced on the skin. Generally this is done on the palm. Make the shape of the numbers as well defined as possible. Before testing with the patient’s eyes closed, draw several numbers while his eyes are open to make sure that he understands the test.

 

 

 

 

Two-point discrimination is commonly determined on fingertips and shins. For the fingertips, hold two pins. Do not stick, but touch simultaneously with the sides of the points. Apply one pin, then two held at a certain distance apart, in irregular alternation and ask the patient to report “one” or “two”. Normally a distance greater than 5 mm is all that is necessary for the patient to detect that there are two points instead of one. If distances appreciably greater are needed, a sensory defect is suggested. The examiner should measure the distance at which two points can be discriminated from one and thus decide whether normal limits are exceeded. Experience will yield a baseline for future comparison.

 

 

 

     

 

A comparable test can be done on the shin using fingers. Two fingers should be sensed if they are over 40 mm apart. Reduction in two-point discrimination is usually accompanied by loss of normal stereognosis and may be based on either central or peripheral sensory loss. When this function is disturbed in the face of relatively preserved superficial and deep sensation, a parietal lobe lesion should be suspected.

The techniques of examination of superficial, deep and complicated sensation are demonstrated on practical lesson.

 

 

Syndromes of lesion of sensory explorers at different levels

 

 

 

1. The lesion of peripheral nerve – appears by fallout of all sorts of sensation in the field of a nerve, pains, paresthesia.

The pain and paresthesia produced by lesions of the peripheral dermal nerves are usually limited to the region supplied by the affected nerve or nerves.  There is often burning or prickling in quality, sometimes described as “sharp”. The location of the pain complained of may be compared with the area of skin supplied by the dermal nerves, although the clinical description by the patient may not conform exactly to the graphic region depicted.

In lesion of nerves composed of both somatic motor and sensory fibers, corroboration in diagnosis may be afforded by the detection of weakness, wasting, decrease in the muscle stretch reflex, and electromyography findings of the denervation in the muscles supplied by the affected nerve peripheral to the site of the lesion.

Signs of autonomic fiber involvement may include alteration in sweating, skin hue, texture, temperature, and distribution of hair.

In peripheral neuropathy, the subjective disturbances are the same as in dermal neuropathy but are confined to the distal portion of the extremities, usually most prominent in the lower limbs. In mononeuritis multiplex, the lesions are disseminated; the several nerves are involved at random.

 

 

2. The lesion of plexus – appears by fallout of all sorts of sensation on one extremity, pains, paresthesia, and vegetative disturbances. Diseases of the brachial or lumbar-sacral plexus are usually associated with pain which may be maximal in the proximal limb with variable extension diffusely or to a portion of the involved extremity.

 

3. Lesion of sensory (dorsal) nerve root – loss of all sorts of sensation for the sectional type in zone of innervation of the certain segment, and also pain, lowering of reflexes.

 

 

 

Spinal lesions should be given diagnostic characteristics as follows:

a) the first of these characteristics is localization of the pain in the dermatomes supplied by the affected nerve root. The pain, although often widely distributed throughout the dermatome, occasionally is limited to a small area within it. It is important to remember this point, since it frequently accounts for failure in diagnosis. The charts depicting dermatomes serve an important function in determining whether the pain under consideration is of radicular origin. Although dermatome in distribution, nerve roots pain in the limbs seldom extends beyond the wrist or ankle. Furthermore, in most instances, pain in the spinal column which is temporally associated with pain in a limb, with paresthesia, or with both, is present.

As a rule, the pain extends to regions that approximate the dermatome distribution of the nerve root supplying the irritated viscous or deep somatic structures.

The most reliable features of root pain are aggravation by the chin-chest maneuver, intensification after several hours in a horizontal position, and amelioration soon after assuming an upright position.

 

b) root pain is frequently produced or, when present, is aggravated by coughing, sneezing, straining, as in defecation, or any other measures that suddenly increase intra-thoracic and intra-abdominal pressure.

 

c) root pain may be awaken in the patient at night after several hours of sleep and may be relieved approximately 15 to 30 minutes after the upright position is assumed.

 

d) root pain often results from, or is intensified by, other maneuvers that stretch the involved roots.

 

Lower lumbar and sacral roots may be stretched from the periphery by the straight-leg raising test (Laseque’s sign) or by bending forward, as in an attempt to touch the floor without bending the knees.

 

Cervical roots may be stretched by downward or downward and outward, displacement of the shoulder girdle.

 

The chin-test maneuver of passively flexing the neck so that the chin rests on the chest induces ascension of the spinal cord within the spinals canal. Thus, the nerve roots, particularly those of the lower thoracic, lumbar, and sacral segments, are placed under tension, with consequent production of pain from any one of them which may be diseased.

 

e) root pain may be aggravated by those spinal motions that narrow the intervertebral foramen thought which the diseased nerve root passed. In cervical root disease, simultaneous extension and lateral flexion of the neck to the affected side alone or after a blow to the vertex of the head (Spurling’s sign) may result in sudden aggravation of the neck and dermatome arm pain, paresthesia, or both.

In the lumbar region, lateral flexion of the spinal column toward the affected side further narrows the neutral foramen and may result not only in aggravation of the spinal pain but also in dermatome limb pain and paresthesia.

 

4. Lesion of a sensory (dorsal) root and ganglion – same manifestations + herpes zoster.

 

5. The lesion of a sensory (dorsal) horn of a spinal cord cause the same manifestations, as well as at lesions of sensory (dorsal) root, dissociated disorders of sensation only are observed.

 

6. The lesion of front grey soldering cause sectional type –  dissociated disorders of sensation symmetric on both sides as “butterfly”.

 

7. The lesion of dorsal funiculus of spinal cord – deep feeling drops out on one side according to the conductive type

 

8. The lesions of lateral funiculus of spinal cord – pain and temperature sense drops out on the opposite side according to the conductive type.

 

9. The lesion of half of diameter of a spinal cord, Brown-Sequard sign – on the side of the focus deep sense drops out according to the conductive type from level of lesion. Paresis of an extremity, the zone of an anesthesia at level of lesion and radicular pain, is observed on opposite side – drops out pain and temperature sense 2 segments lower than level of focus.

 

10. Lesion of diameter of a spinal cord – there is anesthesia of all sorts of sensation according to the conductive type is lower than a level of focus: deep sense from a level of focus, superficial sense – 2-3 segments lower. Central paralysis. Defective control of the urinary bladder and anal sphincter according to the central type. Trophic disorders.

 

11. Lesion of a medial closed loop – hemianestesia,

                                                              sensitive hemiataxia

 

12. Lesion of thalamus –    hemianestesia,

                                              sensitive hemiataxia, 

                                              hemianopsia,

                                              hemialgia.

 

Since the thalamus is concerned with sensory impulses from the opposite side of the body, the pain resulting from lesions within it is confined to the opposite side of the body. In large lesions the entire opposite half of the body, including the head, may exhibit hyperpathia discomfort. In less extensive lesions the pain may be limited to large contiguous portions of the body, such as the whole lower extremity and lower part of the trunk or the side of the head, upper extremity, and chest.

Characteristically, thalamic pains appear as the patient is recovering from a thalamic infarct. These pains are persistent and are greatly aggravated by emotional stress and fatigue. They are usually described as burning, drawing, and feeling of pulling, swelling, and tenseness, above all they have a peculiar, highly distressing quality.

 

13. Lesions of sensory pathways in internal capsule – hemianesthesia

                                                                                      hemianopsia

                                                                                      hemiplegia

 

14. Lesions of postcentral gyrus – monoanesthesia on the opposite side.

 

15. Stimulations of postcentral gyrus – sensory “Jackson“.

 

Students’ practical Study Program

 

Step I.  Aim: To determine presence or absence any type of sensory disturbances on the patients. For this purpose it is necessary to hold examination.

 

Step II. Aim: To determine type of sensory disturbance in patients. For this purpose it is necessary to hold examination.

 

Step III. Aim: To find level of lesion of sensory explorers.