Theme: Introduction on Neurology

Theme: Introduction on Neurology.

General principles of nervous function. Active movement and their disorders. Pyramidal system. Central and peripheral paralysis. Extrapyramidal system and syndromes of lesion. Cerebellum, syndromes of lesion. Sensitivity and syndromes of sensory disorders.  Sorts and types of sensory disorders. Pathology of smell and visual analysers. Syndromes of oculomotor nerves disorders.  Localization of Cortex functions. Syndromes of lesion. Cerebral spinal fluid, meningeal syndrome.

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

1. central

2. periph

 

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

The first (central) neuron is called tractus corticospinalis.

The second (peripheral) neuron is called tractus spinomuscularis.

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

in upper part the muscles of lower extremities are presented;

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

in lower part – the face muscles are presented.

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

 

 

 

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

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

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

 

The second neuron – peripheral – tractus spinomuscularis.

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

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

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

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

3.     ramus meningeus

4.     ramus comunicante albi.

 

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

That’s the reason to make following conclusions:

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

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

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Face, tongue and pharynx muscles innervation.

 

This way is called tractus cervicomuscularis.

The first central neuron is called tractus corticonuclearis.

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

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

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

 

Thus we can make the following conclusions:

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

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

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

 

Movements disturbances.

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

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

 

Paralysis is divided into

 Central ( spastic )

 Peripheral ( flaccid )

 

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

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

 

main features of central or spastic paralysis are:

1. It is a diffuse paralysis.

2. There is spastic hypertonus of muscles

That means

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

 “ clasp – knife “ symptom

 in course of evaluation tonus decreases

3. Hyperreflexion of stretch and periostal reflexes.

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

 

 

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

To flexing ones belong Rossolimo (pic)

 

 

 

Jukovski (pic)

 

 

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

 

 

 

To extensing reflexes belong Babinski (pic)

 

 

Oppenheim’s (pic)

 

Gordon’s (pic)

 

 

Shtrumpel, Grossman, Sheffer (pic)

 

 

 

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

 

There are following pathologic reflexes on upper extremities:

 

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

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

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

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

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

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

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

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

6. Pathologic synkinesis

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

 Global

 Coordinatory

 Imitating

 

 

Peripheral ( flaccid, atonic ) paralysis.

 

It occurs at lesion of tractus spinomuscularis or tractus nucleomuscularis.

The main features of peripheral paralysis are :

 

1. Areflexion or hyporeflexion

2. Atonia or hypotonia

3. Muscular atrophy

4. Fasciculation of muscles

5. It is limited paralysis

6. There is reaction of degeneration.

 

 

 

The Basic Neurological Examination of Movements

 

Gate

Volume of active movement and Muscular weakness

Muscular tone

Muscular stretch

Reflexes

 

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

 

 

 

  

                                                                                           Extrapyramidal

Motor dysfunction can be caused by lesions of muscles, neuromuscular junction, peripheral nerve or central nervous system.

 

The pyramidal system, extrapyramidal system and cerebellum are the main components of central nervous system which are involved in motor function coordination.

Extrapyramidal system consists of:  

·        cortical areas  4, 6, 8

·        the basal ganglia: n. caudatus, n.lenticularis (putamen, globus palidus)

·        the nuclei of brain stem (black substance, red nucleus, vestibular nuclei, reticular nuclei, nucleus of Darkshevych, Lues’ body, lower olives)

·        spinal cord: g-motor neurons and a-small motor neurons, which are located in anterior horns of the spinal cord

There are two parts of Extrapyramidal system:

·        pallidum (globus palidus, black substance, red nuclei, vestibular nuclei, nucleus of Darkshevych, lower olives, Lues body)

·        striatum (cortical areas  4,6,8, n. caudatus, putamen)

Pallidum is phylogenetically older then striatum. That’s why iewborn babies pallidum

dominates. And only at the age of 4 – 5 months old striatum starts to influence on motor functions.

 

The main connections between different parts of Extrapyramidal system:

Pallidum and striatum are closely connected with each other by means of such pathways:

·        nigrostriatal (dopaminergic) – black substance – nucleus caudated – it inhibits the neurons of striatum

·        strionigral (GABA-ergic)- nucleus caudated (GABA) – black substance – it controls production of dopamine.

That means inhibition of inhibition. Normally there is a balance between GABA and

dopamine.

Extrapyramidal system receives impulse from thalamus by means of such pathways:

·        T – EPNS – T

·        T – cortex – EPNS – T

·        T – cortex  – pons – cerebellum – thalamus

To the efferent pathways of extrapyramidal system belong:

·        Tr. olivospinalis

·        Tr. rubrospinalis

·        Tr. vestibulospinalis

·        Tr. tectospinalis

·        Tr. reticulospinalis

 

The main functions of Extrapyramidal system are:

1.   It prepares muscles to smooth economical movements

2.   It determines the posture

3.   It makes automatical involuntary regulation of conscious movements

4.   It provides automatical stereotyped movements and reflector protective movements

5.   It provides motor manifestation of emotions.

 

Normal function in the basal ganglia appears to depend on a homeostatic relationship between various neurotransmitter agents – DA and GABA. Neurophysiologically this balance may be viewed as existing between those action is inhibitory iature (DA and GABA) versus those with excitatory properties (ACH). Disturbances of their homeostasis result in one or another of the symptoms which are generally attributed to this area of the brain. In general, dopamine deficiency allows for cholinergic hyperactivity and can be correlated with the akinetic-rigid disorders such as Parkinsonism. Dopamine hyperactivity and/or cholinergic hypoactivity result in the hyperkinetic phenomena encountered in Huntington’s chorea.

 Considerable extent disorders are directed to a better understanding of role and reestablishing balance of these neurotransmitter agents. 

There are two main syndromes of the Extrapyramidal system’s lesion: Parkinson’s syndrome and syndrome of involuntary movements.

In 1817 James Parkinson was the first who described the major manifestation of this syndrome.

In 1874 this disease was called after James Parkinson – Parkinson’s disease.

In 1920 Tretiakov was the first who noticed that the greater cell loss in the substantia nigra, the lower concentration of dopamine is in striatum and more severe the degree of clinical Parkinsonism. The exact mechanism, however, by which selective damage to substantia nigra occurs, is unknowowadays exactly. But according to the modern investigation it is considered that in base of this disease is inborn deficiency of tyrosinetransferase enzyme which provides transformation of tyrosine in dopamine. 

In the light of these findings Parkinsonism may be defined in biochemical terms as an inborn dopamine deficiency state.

The physiologic role of this system appears to be one of inhibitory modulation of striatum which is produced by counterbalancing of excitatory cholinergic activity in this region. Acetylcholine, the neurotransmitter of this latter system, is in abundant supply in striatum and its concentration has been shown to be unaltered in Parkinsonism. Normally, there is a balance between the effects of acetylcholine and dopamine.

About 60 – 187 persons per 100 000 population suffer from this disease all over the world. In Ukraine about 133 people per 100 000 population have Parkinson’s disease. An average age of manifestation is 45 – 52 years old.

There are three basic symptoms of Parkinson’s syndrome:

1.   Hypokinesia (Akinesia)

2.   Rigidity

3.   Tremor

The main pathogenetic mechanisms are:

1.   Great cell loss in the substantia nigra, low concentration of dopamine in striatum, the influence of striatum on pallidum. As a result akinesia occurs.

2.   The main cause of rigidity is increasing of tonic reflex on muscles tension.

3.   The main source of tremor is thalamus (its nucleus ventrolateralis).

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Hypokinesia (Akinesia).

·        The gait and posture are constantly affected as to produce a stereotyped picture: a lack of mobility of facial expression with infrequent blinking of the eyelids, the head and the shoulders are stooped forward, the arms are slightly abducted, the forearms are party flexed, and the phalangeal joints are extended at the interphalangeal joints.

·        Poverty of movement which result from the bradykinetic and akinetic state.

·        The gait is shuffling and the steps are slight.

·        Parallel footprints.

·         The loss of associated swinging of the arm or arms when walking – (acheirokynesis).

·        A lack of mobility of facial expression (Bechterev’s symptome)

·        Infrequent blinking of the eyelids (Mary’ s symptome)

·        Fixed look.

·        Inertia of rest (that means it is very difficult for patient to start moving).

·        Inertia of movement (As the patient starts to walk, the movements of lower extremities may be quite slow. As though in an effort to «get going» he may lean forward, causing him to hurry his steps. This results in a shuffling of the feet which may increase in rapidity until the patient is almost running, the so-called propulsive gait. Similarly, a deviation of the center of gravity to one side or backward produce lateropusion or retropulsion)

·        Micrography – handwriting is too small.

·        Speach is quite and inexpressive (bradylalia).

·        Pardoxical kynesia is possible after strong impression or great emotions.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Rigidity (plastic type of increased muscle tone):

·        Cogged-wheel symptom

·        Tonus increases in course of evaluation of nervous system state

·        Tonus is expressed in the same manner in the group of flexors and extensors.

 

Tremor:

·        Are much more expressed in distal parts of extremities, sometimes tremor of lips or lower jaw can occur

·        It looks like coins counting

 

·        It is much more expressed while resting. It disappears or decreases while moving

·        Its frequency is 3 – 6 times per second.

 

Besides these basic features of Parkinson’s disease sometimes can occur:

·        Bradyphrenia (thoughts are too slow)

·        Bradymnenia (recollection is slow too)

·        While speaking such patients are boring (akairia  – Astwatsaturov symptome)

·        Usually they are in a bad mood. Depression is very typical for the patients with Parkinson disease.

·        Sometimes they have autonomic disorders. Parasympathetic nervous system dominates in such patients – they have running saliva (aeriel symptome), hyperhydrosis, fatty skin and type of hair, bradicardia and arterial hypotension.

At early stages of Parkinson disease following tests can be used:

1.   The symptom of air pillow or Vartenberg symptom – The patient is lying down. One props up his head a little bit and then quickly takes his hand out. Normally the head is falling down. But in patients with Parkinson disease the head stays in the same position for a while.

2.   The symptom of Noica–Haneva – While evaluations of muscle tone one asks the patient to raise his opposite extremity. In patients with Parkinson disease the tonus suddenly increases.

3.   Westfahl’s phenomena of paradoxical muscle constriction – While foot extension it stays in the same position for a while.

4.   Hand extension test.

5.   Test of knee flexion – The patient is lying on his abdomen; his lower extremities are bended in knees. In patients with Parkinson disease the legs are fixed in this position for several minutes.

 

 

According to the prevalence of this or that symptom there are different clinical forms of Parkinson disease:

1.   Rigid (hypokynesia dominates)

2.   Trembling

3.   Mixed : rigid – trembling or trembling – rigid

 

The degree of severity of clinical Parkinsonism (according to Petelin):

The first degree – expressed one or two main symptoms. The patient preserves professional and home activity.

The second degree – The patient is disabled professionally.

The third degree – The patient cannot take care of himself.

 

Besides Parkinson disease (or idiopathic Parkinsonis) there is symptomatic one. It is caused by:

1.   Craniocerebral trauma ( Muhammad Ally)

2.   CO, Mn intoxication.

3.   Brain tumor.

4.   Encephalitis (Economo)

5.   Strokes.

6.   Cerebral atherosclerosis.

7.   Medicinal parkinsonism (reserpinum, neuroleptics)

 

Another syndrome, which usually develops at striatum lesion, is hyperkynetic–hypotonic

The main clinical signs of this syndrome are:

1.   Muscular hypotonia

2.   Involuntary movements – hyperkynesis.

 

All involuntary movements are characterized by:

n the amplitude of the movement;

n location of muscle involved:

n the rate;

n the duration of contraction and the relaxation.

The same kind of the involuntary movement might result from organic disease in one patient and from an emotional disturbance in another.

1.   Chorea

·        spontaneous, irregular, purposeless and asymmetric movements

·        they are present at rest and subside during sleep

·        there are some symptoms , which are very typical for chorea:

eyes and tongue symptom ( or Hersonsky’s symptom ) – the patients are unable to maintain tongue protrusion for more than a few seconds; Hordon’s II symptom – while checking knee – reflex crus stays in the position of extension for a while  and then slowly goes down; Cherni symptom  – pathologic sudden abdomen at breath.

·        The most common diseases with chorea syndrome are Huntington’s chorea (inherited disease), rheumatic subcortical encephalitis or chorea Sydenhams (juvenile disease), atherosclerotic chorea, chorea gravidarum, electric chorea.

 

2.   Athetosis

 

·        Movements are slower and more sustained than choreiform movements

·        they affect primarily the distal portion of extremities

·        snakelike movement of any combination of flexion, extension, adduction and abduction in varying degrees

·        They are regularly associated with increased muscular tone

·        It is supposed that athetosis is the result of nucleus caudated lesion.

 

·          

 

3.   Choreoathetosis

·        is a term selected to describe movements that are intermediate between chorea and athetosis.

 

4.   Ballism and hemiballism

·        Its the more or less continues gross abrupt contractions of axial  and proximal muscles of the extremities;

·        In the most cases this movement disorder is confined to one side of the body (hemiballism)

·        It may be associated with hypotonia.

 

5.   Myoclonus

·        is a jerking movement of one or more muscle groups (for example palatine, tongue, pharynx, larynx, diaphragm and skeletal muscles)

·        usually only one muscle group is involved

·        They are synchronous in most of cases and sometimes they are asynchronous

·        Their frequency is about 15 – 18 per minute

·        They may be induced by visual, tactile, or auditory stimuli (stimulus-sensitive myoclonus) or by the initiation of the voluntary movement (intention myoclonus).

·        Myoclonus – epilepsy is typical for chronic form of forest spring form encephalitis

 

6.   Torsion spasm

·        Twisting or turning movements

·        The muscles of trunk and neck are involved.

·        Sometimes torticollis can occur.

·        Usually it is the result of putamen lesion.

 

7.   Tics

·        are an involuntary compulsive stereotyped movements

·        they may be simple or complex

·        tics may involve any portion of the body ( they are most common about the face  where they are manifest as blinking, grinning, smirking, lip licking, nose wrinkling)

 

8. Facial cramp

·        is tonic seizure in facial muscles

9. Tremor

·        Is rhythmical jerking of arms, legs or head

·        Its frequency is about 4 – 6 per second

 

Students’ Practical Study Program

Step I. Aim: Find out the symptoms of extrapyramidal system’s lesion. To do it it’s necessary to examine the patient, paying attention to hypokinetic, rigidity, tremor, hyperkinesis, vegetative defects, changes of muscular tone and define the conclusion for the presence or absence of lesion.

 

1. Hypokinesis (Akinesis). The terms bradykinesis, hypokinesia and akinesis aptly describe the degrees of impaired movement which occur without any disturbance in muscle power, coordination or presence of rigidity. In all the acts of daily living the patient is conscious of delay in execution which at times may reach a total standstill. The gait and posture are constantly affected and produce a stereotyped picture: a lack of mobility of facial expression with infrequent blinking of the eyelids, the head and the shoulders are stooped forward, the arms slightly abducted, the forearms party flexed, and the phalange joints and extended at the interphalange joints.  As the patient start to walk, the movement of the lower extremities may be quite slow. As though in an effort to «get going» he may lean forward, causing him to hurry his steps. This results in a shuffling of the feet which may increase in rapidity until the patient is almost running, the so-called propulsive gait. Similarly, a deviation of the center of gravity to one side or backward produce lateropusion or retropulsion. In less advanced stages of the illness the gait may be almost normal and the condition may be revealed only by a slight forward stoop and loss associated swinging of the affected arm or arms when walking.

 

2.  Rigidity – is a form of increased muscle tone.

n Its often terms «cogwheel»,

n in that when the extremity is passively moved, rhythmic «give» in the resistance is detected, possibly related to an underlying tremor;

n flexor and extensor steadily contract leading to increased resistance to passive movement.

n In its early stages it can be induced by having the patient carry out active synkinesis movement of the opposite limb.

 

3. Tremor. The tremor has often been described as having distinctive characteristics. Parkinson tremor:

n designate the common pill-rolling type,

n  its occurs in an attitude of repose (at rest) usually lessens with  movement.

n the involvement is greater  distally,

n  Its rate is from 3 to 6 per second

 

4.  Involuntary movements.

All involuntary movements are characterized by: the amplitude of the movement; location of muscle involved: the rate; the duration of contraction and the relaxation.

Even the description of abnormal movements is difficult. No matter how carefully various movement disorders are defined, and how carefully we observe them in practice, we still find patients whose movements cross these arbitrary boundaries. In going about the task it is helpful to do so in steps, observing the presence or absence of certain qualities that will aid in description and classification. The amplitude of movement, amount and location of muscle involved, speed of onset, and duration of contraction and relaxation should be noted. The rhythm or lack of it the uniformity or variability of movement pattern are worthy of note. 

1. Finally, it may be possible to observe during the examination or to ask the patient directly about the influence of the following factors: voluntary movement, emotional stress, posture, rest, exercise, diversion of attention, and the sleep. Involuntary movements, regardless of cause, are nearly always intensified by emotional stress, and mostly subside during sleep. Consequently, observations of the effect of emotion and sleep on the abnormal movements are of little help in deciding whether it is organic or functional origin. Pay attention, cheeking a movement disorder when one fails to recognize a unique organic pattern, often a psychoneurotic diagnosis is putting on. The pitfall can be avoided if the physician looks for associated evidence of functional or of organic disease of the nervous system before making conclusions. Obviously, with greater experience these errors in diagnosis are less likely.

1.   Athetosis.

n Movements are slower and more sustained than choreiform movements;

n they affect primarily the distal portion of extremities;

n  snakelike movement of any combination of flexion, extension, adduction and abduction in varying degrees.

2. Ballism.

n Its the more or less continues gross abrupt contractions of axial  and proximal muscles of the extremities;

n  In the most cases this movement disorder in confined to one side of the body (hemiballism)

n It may be associated with hypotonia

n It may be result from lesion in or near the subthalamic nucleus.

3. Dystonia implies any disturbance in tone; its use generally is restricted to the mobile spasm of axial and proximal muscles of the extremities.

    Dystonic movements are included:

a)  torsion spasm – in which the spasm result in twisting or turning movement

b)  spasmodic torticollis – is the most commonly observed torsion spasm.

 Dystonic movements thus tend to involve large portions of the body and have undulant sinuous quality which, when severe, gives rise to grotesque posturing and bizarre writhing motions. Writer’s cramp may be a form of focal dystonia

4.  Myoclonus.

a) is a jerking movement of one or more muscle groups

b) its usually arrhythmic

c) they may be spontaneous or they may be induced by visual, tactile or auditory stimuli.

5.  Tics.

a) is an involuntary compulsive stereotyped movement;

b) they may be simple or complex; tics may involved any portion of the body ( they are most common about the face  where they are manifest as blinking, grinning, smirking, lip licking, nose wrinkling);

 

Step II.  To find out of the extrapyramidal system leading.

 

 

Make the conclusion for the presence of extrapyramidal system’s lesions.

 

Step III. Aim: To localize processes within the separate anatomic structures of extrapyramidal system.

      It’s necessary to use algorithm of differential diagnosis, which is in methodological indication for students.

 

Step IV. Aim: To put topical diagnosis and explain it. To show in topical diagnosis the leading syndromes and the section of lesion of extrapyramidal system. (For ex., Parkinson syndrome, akinetic form – the pallidum lesion. Chorea – striatum lesion).

 

Cerebellum

 

Cerebellum is located in the posterior cranial fossa. It contains two large lateral hemispheres, flocculo-nodular lobe and three pairs of peduncles. Cerebellum is a reflexional organ of coordination of movements, equilibrium and muscular tone.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

The gray matter of cerebellum is presented by the cortex of hemispheres and nuclei of cerebellum.

·        Nucleus fastigii – phylogenetically the oldest one, which is closely connected with vestibular nuclei.

·        Nucleus globosus, nucleus emboliformis.

·        Nucleus dentatus – this one is considered to be phylogenetically young structure.

There are next layers in the cortex of the cerebellum:

1.   Granular one – it consists of small cells with short dendrites and long axons.

2.   Ganglionar one – it consists of Purkinie cells

3.   Molecular one – it consists of basket cells.

 

The white substance of cerebellum is presented by:

1.   Associative fibers, which connect gyres with each other.

2.   Commissural fibers, which provide connection between the hemispheres of cerebellum.

3.   Projection fibers that provide connection of cerebellum with other structures.

 

Cerebellum is connected with all the other parts of CNS by means of its peduncles:

The lower peduncles (corpora restiformia) provide connection with oblong brain and spinal cord:

·        Tr. spinocerebellaris dorsalis (Flexig’s)

·        Tr. vestibulocohlearis (from nuclei vestibularis to nucleus fastigii)

·        Tr. olivocerebelaris (from lower olives to nucleus dentatus)

·        Fibre arcuate externe (from nuclei Holl and Burdach to hemispheres and vermis)

The middle peduncles (pedunculum cerebellaris medii) provide connection with pons. They are presented by fibers of tr. pontocerebellaris. They connect nuclei of pons with the opposite hemisphere of cerebellum.

The upper peduncles of cerebellum (pedunculi cerebellaris superior) connect cerebellum with middle brain. They include two systems:

·        Afferent  one – from spinal cord to cerebellum – tr. spinocerebellaris ventralis (Hover’s)

·        Efferent one – from cerebellum to the structures of extrapyramidal nervous system – tr. cerebellotegmentalis et tr. dentorubralis.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

A special attention we should pay to the way of cerebellum correction. It consists of six neurons. The impulse runs from motor area of brain cortex to the pons, then some of impulses go to the spinal cord and the others go to the cerebellum in order to confirm information about coordination of movements. Then it runs to the anterior horn.

The first neuron – tr. fronto-temporo – occipito- pontinus

The second neuron – tr. pontocerebellaris (pontino- cerebellaris decussation)

The third neuron – tr. cerebello – dentatus

The forth neuron – tr. dentorubralis (Vernekink’s decussation)

The fifth neuron – tr. rubrospinalis (Forel’s decussation)

The sixth neuron – tr. spinomuscularis

Thus brain cortex and nuclei rubri are connected with opposite hemispheres of cerebellum. And the segments of spinal cord have homolateral connection.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

The main functions of cerebellum are:

n body equilibrium

n regulation of muscle tone

n coordination of movements

n synergy

Equilibrium and regulation of muscle tone are the functions of flocculo-nodular lobe. Coordination of the movement and synergy are the functions of the cerebellum hemispheres.

Cerebellum lesion produces cerebellar ataxia. There are two kind of ataxia:

1.   static one (it develops at lesion of vermix)

2.   dynamic (it develops at lesion of hemispheres)

 

Static ataxia means standing and walking disorders. Usually it is checked by means Romberg test. The Romberg test is called positive when unsteadiness is increased by closure of the eyes. As a rule, it is present at such diseases as tabes dorsalis, combined degeneration, or polyneuritis with a loss of proprioceptive sensation in the muscle of lower extremities. As a matter of fact, on average person does not stand so steadily with the eyes closed as with opened ones, and the unsteadiness of station associated with cerebellar disease or even with loss of vestibular function is aggravated perceptibly by closing the eyes. Hence, the Romberg test, when positive, requires careful neurological examination of the various systems concerned with balance before a final decision can be made. Sometimes the test is worth performing in hysterical patients. They may sway dramatically and even give the impression that they will fall over in tin-soldier fashion. This may be minimized by instructing the patient «don’t sway» or by distracting the attention to a second task at the same time, such as «stick out your tongue and wiggle it from side to side».

 

  

 

Dynamic ataxia can be observed while moving. Its main features are:      

1.   Nystagmus originating in the central nervous system may be horizontal, vertical, vertical rotary, or dissociated (different in each eye). It is rhythmic, having a quick and a slow phase, and the direction of the quick and slow movements depend on the position of eyes. It has long duration, lasting for months or years.

2.   Scanning speech

3.   Intention tremor (Nose-Finger-Nose Test, Heel-to-Knee Test, Toe-Finger Test, Finger-Nose Test)

 

Test Finger to-nose

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

eel-to-Knee Test

 

 

 

 

4. Macrographia

5. Missing while coordinatory tests checking

6. Dysmetria (disturbed ability to gauge distances)

  

 

 

 

 

7.   Muscular hypotonia

8.   Adiadochokinesia (disturbed ability to perform rapid alternating movements)

9.   Asynergia

 

Cerebellar lower peduncles lesion can cause:

·        Cerebellar ataxia

·        Bulbar syndrome

·        Sometimes pathology of Holl’s and Burdach’s nuclei is associated with this lesion. Then ataxia is complex and is called cerebellar – sensitive ataxia.

 

Cerebellar upper peduncles lesion can cause:

·        Cerebellar ataxia at the side of lesion

·        Trochlear Nerve lesion

·        Midbrain lesion symptoms

 

Nucleus ruber lesion can cause:

·        Cerebellar ataxia in the opposite extremities

·        Resting tremor

·        Webber’s syndrome or paresis of convergence may occur

 

Pontino – cerebellar angle lesion manifests as:

·        Cerebellar disorders and pathology of VII, VIII, V, VI pairs of CNs at the side of lesion

·        Pyramidal and sensory hemisyndrome on the opposite side.

 

Kinds of ataxias

1.   Cerebellar

2.   Frontal

3.   Sensitive

4.   Vestibular

5.   Hysterical

6.   Mixed

 

 

 

 

 

Students’ practical Study Program

 

Step I.  Aim: To determine the presence of signs of cerebellum lesion. For this purpose it is necessary:

1.   To gather an anamnesis and to examine patient’ status.

2.   In course of analysis of the complaints of the patient to find out presence of attributes of a lesion of a cerebellum (giddiness, instability at standing and walking, clumsy discrepancy of purposeful movements, tremor of extremities at execution of exact movements, deterioration of vision, change of speech etc.

3.    To carry out tests on synergy and coordination, change of speech, letter, muscles tone.

4.   To pay attention to the appearance of the patient.

5.   To formulate a conclusion about presence or absence of a disturbance of coordination.

 

Step II. Aim: To determine the character of cerebellum lesion. For this purpose it is necessary:

To analyse the patient’s neurological status using the following criteria:

1.   Disturbance of body equilibrium – there are complains on instability during walking, difficulty in standing and sitting.

Objective: instability in Romberg posture, in standing position there is tendency to fall back or forward, difficulty in walking, ataxia during walking, with the widely placed legs and balance with arms. Difficulty at turning, flank walking.

2.  Disturbance of regulation of muscular tone – there are complains on muscular hypotonia and flaccidity of muscles.  Objective: muscular hypotonia, excessive mobility in joints.

3. Disturbance of coordination of movements – there are complains on awkward movements, tremor during fulfillment of coordination movements, disturbance of speech and handwriting. Objective: (+) signs on adiadochokinesis (delay in turning wrists), ”parsleys”, on hypermetric of movements, intention tremor in performance of finger-nose and heel-knee tests, (+) assay on bond of lines, change of handwriting. Scanning speech, nystagmus.

4. Disturbance of synergy of movements. Objective:  (+) Babinski test on an asynergia of a trunk, (+) a sign of absence of a return jerk Stuart-Holmes’s.

5. Make a conclusion about presence of pathology of cerebellar function.

 

Step III. Aim: To determine level of a lesion of the cerebellum. For this purpose it is necessary to use the following criteria:

 

Lesion of the worm. Static ataxia, trunk ataxia, “drunken gait “, hypotonia in extremities. At the given stage it is important to be able to differ such kinds of ataxia as:

– cerebellar: a) static; b) dynamic

– frontal

– vestibular

– sensitive

– hysterical

– mixed

 

Lesion of hemispheres of a cerebellum. Objectively: (+) of finger-nose and heel-knee tests , test on a adiadochokinesis, index test, test “parsleys”, Ojyhovski test, (+) Babinski test on an asynergia of a trunk, (+) test on hypermetric of movements, (+) a manual Doynikov’s phenomenon.

 

Lesion of a frontal lobe, cortex of a brain. All cerebellar disturbances will be on the opposite party: an astasia, abasia, the cerebellar ataxia will be on the opposite part.

 

Lesion in the Pons Varoliy’s. The cerebellar ataxia will be on the same party.

 

5. Make a conclusion about a level of lesion of cerebellar pathways.

 

Step IV. Aim: Make a differential diagnostics of pathological focus level with the help of

“Algorithm of differential diagnosis of cerebellar disturbances” or using “the Methodical indications on theme: “A Cerebellum. The anatomic-physiological data”

 

 

Sensation. Signs of sensation disturbances

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.

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.

 

 

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.