ALBERT SZENT-GYÖRGYI MEDICAL UNIVERSITY

PHYSICAL EXAMINATION AND

PRACTICAL NEUROLOGY

Edited by

LÁSZLÓ VÉCSEI MD

Szeged

1995

sity

•.

. ..

1. PHYSICAL EXAMINATION

Skull

Meningeal irritation

TABLE OF CONTENTS

Spine, olfaction, vision, visual field

Pupils, fundus

Eye movements

Trigeminal nerve, corneal reflex

Hearing, vertigo

Pharyngeal and soft-palate reflex, tongue movements

Muscular system

Reflexes

Sensorium

Cerebellar tests

Vegetative functions

Speech, cognitive functions

Examination of unconscious patient

II. PRACTICAL NEUROLOGY

Cranial nerves

Musculature

Reflexes

Sensorium

Coordination

Extrapyramidal system

Vegetative system

Speech, cognitive functions , psychic state

References

Supplement

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lntroduction

This coursebook aims to summarize the basic knowledge which is necessary for the

neurological examination of patients. There are two important considerations in the

evaluation of neurological symptoms: one is to localize the pathologic condition and the

other is to determine its nature (frequent patho\ogic processes inc\ude infarcts,

haemorrhages, tumours, inflammations and degenerative lesions).

The rapid development of neuroradiology (CT , MR\, DSA, SPECT, TCD, PET , etc.) and

electrophysio\ogy (EEG, VEP, AEP, SSEP, ~MG, ENG, etc.) no doubt helps the work of

the neurologist considerably. Careful history-taking and thorough neurological

examination, however, have not become any less important. - On the contrary, they still

require a solid grasp of anatomy and physiology. Only on the basis of a correct history

and foci identified through examination can we ask further questions correctly from the

patient. Otherwise, it can occur that the patient will und ergo unnecessary or inappropriate

diagnostic tests.

Experimental neurology has c;jeveloped considerably in the past and this has enabled us

to treat diseases of the centra\ nervous system in ever increasing numbers ("control\ed

release" products, the use of novel antiepileptics; feta\ brain transplantation, excitotoxin

antagonists, compounds influencing nitrogen-oxide metabolism, gene therapy,

neuropeptides, growth factors , etc.). Being able to choose neuro\ogical therapies out of

those presently available and to be introduced in the future requires up-to-date

knowle~ge of pharmacology, pathophysiology and biochemistry.

•.

·\Mlat are the tasks of the neurologist attending to the patient? He should know how to

t~~e history by asking the right questions; having examined the patient, he should be able

to localize the pathologic changes, ;md on the basis of history and the ·results of the

physical examination, order the necessary tests in order to set up a diagnosis (d ifferential

diagnosis) . Decidi1ng on the appropriate diagnostic steps is a crucial part of the

neurologist's work, as the right path has to be found between unnecessary and

expensive tests and those which are strictly required . Furthermore, his tasks include

analyzing the test results thus obtained, establishing a diagnosis and embarking upon a

therapy. This coursebook aims to help with the first set of these complex tasks.

The ftrst chapter deals with the examination of patients and the second summarizes the

most important areas of practical neurology. Before reading it, it is recommended to

revise the relevant chapters of functional anatomy. Atlases of the human body, diagrams

and summaries might be of help while studying it. \Mlat is most important, however, is to

actively participate in clinical neurological practices.

Professor László Vécsei

Head of Clinical Neurology

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1. PHYSICAL EXAMINA TION

1. Thc skull is intact, there is no sign of trauma, no tenderness is indicated on percussion.

lnsped the size of the skull a11d i11 ·' case of morpholog_ical cha11ge (microcephalia,

n at:rocephalia), precisely measure its circ~mfere11ce. Exami11e the scalp carefully, looking for

»i •ns of trauma and other changes 011 the ski11. If there is any sign of trauma, describe its cxact

ll lzc and character. Following this, with fingertips ·carefully palpate the scalp (impressio11,

lu mp, scar). Percussing the skull, look for tender, painful areas and with the help of a phoncndoscope, !isten for larger vascular malformations (systolic sy11chro11ic murmur). ln all

·ascs, check the pressure se11sitivity of the trigemi11al and occipital nerve exit points and

·nrcfully auscultate above the carotids a11d the supraclavicular depressio11.

2. Frce ncck, without signs of meningcal irritation. Lasegue's negative.

Thc examination of neck stiffness is of primary importa11ce: i11 case of positive findings,

i111 111ediatc diagnostic activity has to be decided (meni11gitis, subarachnoid haemorrhage, and thc

hi;rn iation of cerebellar tonsils into the foramcn mag11urn) . Neck stiffness can be causcd,

howcvcr, by CSF hypoto11ia, meningism (partial symptom of an infectious disease, without

significant multiplication of cells), and cervical turnour as well.

Brudz_inski's siin: Put your hand on the nape of the paticnt, who is lying flat on his back and

move his head gradually forward. As a response (in a positive casc), observe ílexion in the

joints of the lower limbs (hip, knce).

Kcrnig's sign: ' 1. Lift by the ankles the lowcr limb(s) of the pa_tient, who is lyi11g flat 011 his

back. ln a positive case, the k11ee is ?y11t. 2. The ~atient is lyi11g with his Iegs bent at the hip and

in the knee. Immobilizi11g his thighs, lift his leg(s). During the extension of the knee, reflex

guarding occurs.

The basis of the Laseguc's sig11 is that the traction of the roots in a pathological state ca11

produce sevcre pain. ln a positive case, if the extended lower limb is lirted by the ankle a[ld a

ccrtain angle is reached, the patient experie11ces strong pain, wh.ich radiates ·into_ the lower limb.

Pcrform the examinatio11 011 both lower limbs alld record the a11gle; the radiation a11d the

localizatio11 of the pai11. (Valleix's poi11ts: te11derness is founq at palpation along the sciatic

nervc). Always ask the patie11t about problems i11 co11nectio11 wifh passi11g urinatio11 or

dcfecation, carefully ~heck for possible muscle atrophy a11d also ex~1i11e the tonc of

paravertebral musculature. „... ' ·

2

3. Spine is morphologically intact, thcrc is no pain on pcrcussion.

Examine whcther the cervical lordosis, thoracic kyphosis and lumbar lordosis exceed the

physiological rate (kyphosis, scoliosis, gibbus). Pay special attention to the examination of the

neck (cxtcnded scalp + short neck: Klippcl-Fcil formation), as well as to the examination of thc

skin abovc the spinc (Mongolian spot, hypertrichosis, haemangioma). Check for tenderness by

percussing thc spinous processcs with fingcrtips or a rubbcr hammer.

4. Olfaction is rctaincd on both sidcs. Vision is intact. With a confrontational mcthod, the

visual tieid is complcte on both sides. (n. 1„ n. II.)

For the cxamination olfaction, a well-known, strong-smelling substance, kcpt in a closed

container, is ·appropri áte. (Do not use any substance that stimulates the sensory nerve endings of

n. V.) During the cxamination, with onc nostril covered, the patient, with closed cyes, identifics

the test matcrial and the same proccdure is repeated on the other side. In casc of dysosmia, we

check the integrity of the nasal mucosa. The dysosmia thus identified can be: anosmia,

hyposmia or parosmia.

Its causes are:

(1) rhinogenous (mucous membrane disease),

(2) damage to the olfactory ncrvc (injury, olfactory nerve mcningioma),

(3) introductory phase of temporal epilepsy (uncinate attack, olfactory hallucination).

During the examination of vision, the paticnt covers one eyc, and from approximately 5 meters

we check his ability to count fingers. The result is given in the. number of meters at which

fingers could be counted. The _precise examination rcquires the recognition of Blaskovics

nurnbers and letters. If the patient cannot count fingers, he can only sce objects and light.

When the visual field is examined we wish to establish its extent and also to look for

-- insular loss: scotomas

-- hemilatcral visual loss: hemianopsia

-- loss of quadrant: quadrantanopsia

-- concentric narrowing of the visual field.

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Mci~eover there can be ipsilateral homonymous or bilateral heteronymous anopsia.

The scotoma can be negative (neurological in origin, without the patient being aware of it),

positive (in front of the retina), and colour scotoma. During the examination of the visual ficld,

tbc patient covers one eye and focuses with thc other eye on the middle of the examiner's

,forehead. Move your fingers along the planes of an imaginary perimeter, in a circle of

approximately 40 cm i11 radius in front 9f the open eye. (Oculopalpebral reflex: with a quick

movement, place your ha11d into the visual field: the response Ís shutiing the cyes.)

5. Round, ccntral pupils of equal size and mcdium width with thcir ed,ges intact, which

rcact well to light, to accomodiation, and to convcrgencc. Thc fundus on both sides is

intact. (~. II„ n. ID.)

(Pupil reflex: Pathway: retina- optic 11erve- lateral geniculate body- veg~tative 11ucleus of 11. III.)

ln physiological co11ditions the pupils are of medium widtb aod eqi.!al i11 size. If a differencc i11

width is obscrved, it is calleci a11isocoria. (Mydriasis: wide, miosis: narrow pupil).

The exami11ation of the response to light:

a. Direct response to light: The paticnt focuses 011 a poi11t i11 the distance. Alternately, cover. one

eye and shi11es light the other. As a physiological respo11se to light, constriction of the pupil

ocwrs immediately.

b. lndirect or consensual response to light: Thc. patient focuses on a -point in the distance. His

visual field is divided at nose levei with our palm or perhaps with an opaque object. Shine light

into one eye, while examining the respo11se of the other. Then reverse the procedure.

e. The examination of convergence and accomodation: ln both cases the standard respons.e is

that the pupils constrict, the bulbs converge and the convexity of the lenses become more

marked. For the evaluation of convergence, the patient looks ahead in t)1e distance. Put your

index finger in front of the eyes (within the near point) and ask him to focus on it. When

accomodation is. examined, put your index fi11ger 80-100 cm far from the patient's eyes and ask

to focus.

d. The examination of fundus: The fundus : is examined with an ophthalmoscope.

Physiologically on both sides yellowish-white optic discs can be found, which are of normal

colour and have sharp edges. Any sign of prominence, temporal .discoloration, atrophy or

bleeding are pathológic.

6. Thc cyc movcmcnts arc f'rcc, conjugatcd, without nystagmus or doublc vision.

(n. ID., IV., VI.)

Eye movements are categorized as follows:

4

a. Searching eye movements: during informal conversation, ·e.g. while taking a history, watch

the movements of the patient's eyes.

b. Ordcred eye movement: ask thc patient to look in a Fertain direction.

e. Guided eyc movemcnt: ask the patient to follow in all directions the movement of your

fingcrs.

d. Reflex eye movement: the movement of thc head or cyes as a response to sudclen light or

sound. Ask the patient about doublc visio~ and observe the conjugated movcment of the bulbs.

Distinguish betwcen the following types of nystagmus:

a. optokinetic nystagmus: the patient's eycs follow an objcct, which movcs quickly in front of

him (slow component of nystagmus), then thc eycs rapidly movc back to ccntral position (fast

component). Optokinetic nystagmus might be absent in case of diseasc proccsses in the

temporal and o~cipital lobe, though the visual field might be still intact and thc glancing

movenients might be present (its examination: turning a black-and-white striped cylinder in

front of the paticnt's cyes).

b. congcnital nystagmus: it appears or increases when thc gaze is fixed. lts direction can be

differcht. Acquired nystagmus is inhibitcd by fixation.

e. labyrinthine nystagmus: gcncrally it has a horizontal, more rarely a rotatory and vcrtical

component. lts direction is permanent, indcpcndent of the direction of the glancc. lt is

accompanied by dizziness, which disappears spontaneously after a while.

d. rotatory nystagmus: it is indicative of brainstem lesion.

e. gazc weakness nystagmus: its direction ·is thc same as that of the gaze. Physiologically a

small amplitude nystagmus can be observcd when the patient looks to the side. (It can: be

observed with a large amplitude in case of multiple sclerosis, or barbiturate intoxication) .

f. dissociated nystagmus: it is a nystagmus of the two eyes with different amplitudcs. It occurs

primarily as a result of injury to thc fasciculus longtudinalis medialis (FLM). It appears in cases

similar to large amplitude gaze weakness nystagmus (multiple sclerosis, barbiturate

intoxication).

g. retraction nystagmus: rhythmical movcmcnt of thc cyes backwards (lesion

mesencephalon).

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h. pendular nystagmus: while in one eye the direction of the nystagmus is caudal, on thc other it

is cranial. Generally a· rotatory component can be observed. lt occurs in case of rostra! damage

to the brainstem and diencephalon.

i. positional nystagmus: ccntral positional nystagmus is thc conscquence of a disturbance in the

vcrtebrobasilar circulation. Pcripheral positional . nystagmus, on the other hand, is related to

labyrinth dysfunction.

From a practical point of view, it is very important to distinguish between central and pcripheral

nystagmus.

!f the origin of the nystagmus is peripheral:

- it increascs whcn the cyes arc shut,

- and often there is a rotatory component.

- If thc position of the head changes, the nystagmus appears

with a ccrtain latency,

- and it is syntropic.

If thc origin of the nystagmus is ccntral :

- it dccreases whcn thc eyes arc shut.

- As far as its direction is concerned, most frequently it is

horizontal and vertical ,

- and a glazc weakness can also occur, as well as dissociated

nystagmus.

- After the position of thc head changes, it appears without

latency.

ln case of pcriphcral nystagmus, caloric vestibular irritability decreases, while in case of a

ccntral one, oftcn vestibular hypcraesthesia or norma! caloric vestibular irritability cán be

observcd.

7. Thc trigeminal ncrvc is well and thcre is a lack of f'acial asymmctry. Corncal reflex is

cqually activc on both sidcs. (n. V., n. VII.).

Whilc the tecth arc clcnched, palpate the masscters and tcmporal muscles. Ask thc patient to

opcn his mouth and watch the position of the tip of the chin for possiblc dcviation

(in casc of paresis, it. moves to thc weak pterygoid muscle side; it is the function of n.V.). •.. Whcn thc motor function of n. VII. is cxamined, ask thc patient to wrinkle his forehead

strongly, shut his eycs resolutely and puli his lips to the sidt; as far as he can, showing his teeth .

6

If asymmctry is suspccted, ask him to blow up his checks (scparatcly on each side, thcn both

together). During the examination of the corncal reílex (affcrcnt n. V. ophthalmic branch - pons

- efferent n. VII.), ask the patient to look supcrolaterally, thcn in thc oppositc eye, with a piece

of cottonwool, touch the cornea on the bordcr with thc sclcra. Thc paticnt rcsponds by blinking.

The patient has to be asked whether the sensitivity of thc cornea is the same on both sidcs.

Testing tastc is done by giving the patient a board with the four basic tastcs (swect, salty, sour,

and bitter) written on it. Wrap somc cottonwool around a woodcn stick and, having dipped it

into the appropriate liquid, touch the patient's tongue with it. Following this, the paticnt points -

to the appropriate word and rinscs his mouth thoroughly several times. Then examinc thc two

halvcs of the tongue symmetrically. (N . IX. inncrvates thc posterior onc-third of the tongue.)

8. Hcaring is norma! on both sidcs. Paticnt docs not mention vcrtigo. (n. VID.)

The patient inscrts his finger into the extcrnal mcatus of one car. The observer stands cc. 5-6

mctcrs behind him and utters some words with diffcrent intcnsity (loud, conversational,

whispcrcd voice). The paticnt rcpeats thc won.ls. Weber and Rinne hearing tcsts arc uscd to

diffcrentiatc the conductive and sensorineural hearing impairmcnts.

Weber test consists of placing the tuning fork on the vertex and asking the paticnt in which ear

the sound is bettcr heard. Normally the sound is hcard equally on both sides. Latcralization is a

phenomenon when the patient can hear the sound better on one side (in the diseasc of the

middle car the paticnt latcralizcs to the pathologic ear, and in the disturbancc of the internal ear

he latcralizes to the healthy ear).

Rinnc test: the tuning fork is placed on the mastoid bone (bonc conduction). If the patient

cannot hear the sound, the tuning fork is held besidc the ear (air conduction). As air conduction

is bctter than bonc conduction, the patient slill should be able to hear the sound physiologicalty.

In case of conductive hearing disorder the paticnt has disturbances in hearing deep voices, whilc

in neurogenic hearing damage he has a problcm with high voices.

The vcstibular cxamination consists of:

(1) rotation test, (2) caloric test, (3) galvanic test.

On rotation the direction of nystagmus is the same as that of rotation (optokinetic nystagmus).

If rotation is brought to a sudden stop, post-rotatory nystagmus in oppositc direction can be

noticed. Deviation and past pointing arc in thc direction of the slow component of thc

nystagmus .

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'1 oric nystagmus is examincd by injccting watcr - colder or hotter than the body temperature -

nl > thc cxternal auditory canal. Stimulation wíth hot water induces nystagmus to the same side

·old water causes the opposite).

Ir thc stimuli mentioned above cannot be applíed (unconscious patient, perforated car drum),

lhc vestibular apparatus can be stimulated by galvanic current. The direction of nystagmus is

thc samc as thc dírcction of thc current (this is not a sp;ecific stimulating method).

1) ·tailcd examination of hearing and exact control of the vestibular nerve fünction should be

dom: ín cooperation with an otorhinolaryngologist.

(Normai detailed description of n. VIII.: hearing is norma! on both sides, Rinne test is positive

~ 11 both sides, Weber test is not lateralised, no vertigo experienced.)

9. l'haryngeal and soft palate reflexes ean be clicitcd. Shrugging of shoulders is norma! on

hoth sidcs. No difficultics in tonguc movcmcnt<>, tongue apcx is in midline. (n. IX., X., XI.,

XII.)

The palatal arch rises ifit is tickled with a tongue depressor and the uvula deviates to the side

(so ft palate reflex). If the posterior portion of the pharynx is irritated with the depressor, it

dcvi ates upwards and to the side, causing regurgitation (pharyngeal reflex). There is a loss of

soft palate and pharyngeal reflex in case of the n. IX. lesíc:n. lpsilateral to the lesion, on the

posterior third of the tongue disturbances of taste could be found (with detailed examinations

sensational disturbances can be noticed). Lesion in the motor fibres of the n. X. causes

di sturbances in pharyngeal and laryngeal muscle movements. As a consequence of phonetíc

paralysis, hoarsencss is present. ln more severe cases aphonia occurs. (Detaíled examinatíon of

vocal cords is the duty of an otorhinolaryngologist). Lesion of the n. IX. causes difficulty in

swallowing solids, while lesion of the n. X. causes difficulty in swallowíng liquids.

The function of the n. XI. could be tested by bending of the head and shrugging the shoulders.

Duc to lesion, atrophy occurs on the same side in the sternocleídomastoíd and ín the upper thírd

of the trapezius muscles.

•..

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On examining thc n. XII., the patient is asked:

to protrude his tongue, to move it írom side to side, to raise it, and to touch the soft palate with

the tip of it.

If the patient is unable to move his tongue, bilateral lesion of the XIIth nervc is apt to be

prcsent. The patient cannot swallow or speak. Lesion can be due to pseudobulbar palsv

(bilateral lesion of supranuclear fibres) or bulbar palsy (nuclear lesion).

When there is a peripherial lesion of the XIIth ncrvc, thc tonguc deviatcs to the paralysed side.

Within one or two wceks atrophy occurs at the same placc and fasciculation can írequently be

obscrvcd.

(Normai detailed description of IXth. Xth. XIth and Xllth nerves: articulation, phonation,

swallowing are norma!. Pharyngeal arches arc symmetrical, uvula is in midposition. Pharyngeal

and soft palate reflexes are elicitable symmctrically on both sides. Therc is no hoarseness or

torticollis. Bcnding of hcad and shrugging of shoulders are symmetrical. Protruded tongue is in

midline. Both sides of the tongue arc massy; atrophy and fasciculation cannot be noticed.)

10. NQrmotrophic, normotonic muscular systcm, sustaincd musclc strcngth .

Muscle trophy (atrophy, hypertrophy, pseudohypertrophy) is examined by observation,

symrnctrical palpation on both sides.

ln casc of asymrnctry mcasure circumfercncc (7, 14, 21 cm írom thc joint, comparing both

sidcs).

Muscle tone (hypotony, atony, hypcrtony) can be cxamincd by passivc, symmetric rnovements

of thc limbs on hoth sidcs.

Due to rigid tonc-increasc, both the agonistic and thc antagonistic muscle toncs are incrcased .

Therefore resistancc is cxperienccd against passive movements in both dircctions

(Parkinsonism).

ln casc of spastic tone-increasc (Wcrnickc-Mann type prcdilcction of tone distribution) ílexor

tonc-increase can be found in uppcr limbs and cxtcnsor tonc-increasc in Iower lirnbs (ccntral

paralysis).

Deccrebration rigidity oc.:curs if thcrc is a brainstem lesion. U ndcr such c.:ircumstanccs extcnsor

tone-increase arises in cac.:h limb.

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Whc11 muscle strength is tested, bilateral comparative examination should · be done as

mcntioned carlier.

Thc patient is asked lo pcrform movemenls against resistance. Or onc of thc paticnt's limbs is

f'ix..:d and he is asked to pcrform some movcments undcr such circumstanccs.)

lkcrease in muscle strenglh is callcd paresis, it can be mono- (one limb), hemi- (both limbs on

)ll <.: side), para- (both lowcr limbs), tctraparesis (cach limb). If no muscle strength can be

111..:asured, the patient has plcgia.

Thc gait of the paticnt rising from a squat to standing position, rising on loes . or standing on

h..:cls can give us essential information about the statu_s of certain musclc groups. Frequently

mild parcsis can be observed by "latent paresis examination". The palient sitting or being in a

n.:cumbent position is asked to cxtend his arms in front of him with his palms supinated. Duc to

latcnt paresis thc arms descend, pronation can be ob_scrvcd. The same examination of the lower

Jimb is the following: thc patient in recumbent position has to mise his hip with flexion of both

km:es (or Icgs cxtcnded). One of lhe limbs or both desccnd in casc of latent parcsis.

ln many cases the clinical obscrvations provide cvidence to set up the diagnosis.

l) ue to disordcr of lhe mcdian nerve, the thumb is in thc same planc as thc other fingcrs. This

phenomenon is called "monkey paw" (thc thenar is atrophic, thc movemcnts of lhe lhumb arc

w..:ak).

"Clawhand" develops due lo_lesion of the ulnar ncrve. This phenomenon is caused by a llcxion

contraction developed in the interphalangeal joint" of the 4th-5th (rarely in lhe 2nd-3rd) fingers .

l .csion of the radial ncrvc resulls in wrist drop (most frcquently caused by longcr prcssurn

loading, c.g.: it develops in alcoholic state when the person sleeps for long with his head on 011e

of his arms).

()uc to a lesion of the peroneal nerve, thc paticnt walks raising his legs higher for the extcrnal

l'ootcdge is weaker (footdrop. "steppage gait").

(Normai dctailcd description of the muscular system: muscle trophy is symmctrical; alrophy,

hypertrophy, pseudotrophy cannot be fou11d. Muscle tone is sustained in cach muscle group.

Ha11ds' gripping slrenglh is norma!; the palicnt can s~and 011 hecls, rise 011 loes; he ca11 squal and

rise to standing position. ·Lak11t paresis, hyperki11esis, fasciculation ca1111ot be observed.) •..

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11. Relativcly brisk deep reflexes. Abdominal skin reflex can normally be elicited. No

pathologic reflex.

Deep reflexes should be elicited in lying position, joints in central position, compare the two

sides. Reflexes ean be sluggish, relatively brisk, brisk (signifieant muscle reaction), or unduly

brisk when thcrc is an extcnded reflexogenic zone.

Jendrassik manoeuvre can be applicd if the reflex is difficult to obtain. The patient is asked to

grip his own hands and puli them in opposite directions (but not to Jose their hold). During the

cxertion we try to elicit reflexes on the lower Iimbs. Decp reflexes most often examined in

clinical practice arc the following: biceps (C5-C6), triceps (C6-C7), radius (C5-C6), ulnar (C7-

C8), knec jerk (L4 ), Achilles (S 1 ).

The reflex of the masseter muscle (innervated by the Vth nervc) can be elicitcd by striking the

mental point (lower jaw hangs a Iittle) with a finger. (lt results in rising of the jaw.)

Superficial reflexes arc observcd by mechanical stimulation of the receptors in the skin and in

the mucous mcmbranes. On scratching the abdominal wall the abdominal muscle contracts

(abdominal skin reflex) (dermatomes: Th 7-8,Th 9-10, Th 11-12), the umbilicus deviates to the

stimulated side.

(Corneal reflex is mentioned here: when the cornea is touched with a wisp of cotton, the patient

winks (afferent: Vth nerve, efferent: Vllth nerve).

Cremaster reflex: the proximal and the medial surface of the thigh is slightly scratched, the

testiele on the same sidc elevates (Ll-2).

Anal reflex: on touching the anus there is a contraction of the e;xternal anal sphincter (S4-S5).

(The pharyngeal and soft palatal reflexes have been mentioned previously. Briefly: if the soft

palate is irritated there is a contraction, the uvula deviates to the irritated side. On examining the -

pharyngeal reflex the posterior portion of the pharynx is touched, the pharyngeal muscle

contracts and regurgitation may occur.)

Pathological reflexes cannot be elicited in physiological circumstances. They arc caused by

lesion of the supranuclear neuron-system (lesion of the central motor area and pyramidal tract).

On the upper limbs usually two pyramidal signs could be observed, Trömner and Hoffmann

signs. Trömner sign: quick and short lenn opposition and flexion of the thumb on snapping thc

fingertips of the flexed fingers. Hoffmann sign: suddenly the flexcd termi na! phalanx of the ring

finger is released, the result is the same as that described in Trömner's sign. These two

'1

1 ~

1

11

f 11

111

l i

11

111

th

pi

1

11

llt

11

'1 di

111

' 1 i

10

:Iicitcd. No

are the two

, or unduly

is askcd to

During the

xamined in

. ulnar (C7-

striking the

. kin and in

: contracts

atcs to the

the paticnt

atched, thc

~r (S4-S5).

if the soft

mining the ·

~a! muscle

caused by

1idal tract).

Hoffmann

apping lhc

of the ring

11

1 11ninations are done together. Their bilateral occurence is not necessarily pathologic, but

1111il atcral occurence refers to lesion of the pyramidal tract.

J nwcr limb pyramidal signs are the following:

1. Babinski group: Babinski sign must be known by all practising doctors. It is elicited by

·11imulating (scratching) the lateral side of the sole of the foot and results in isolated, slow and

l<Jnic dorsiílexion of the big toe. (There can also be fanning: plantar flexion of the lesser toes

111H.l Babinski.)

' l\ 1nic dorsal flexion can also be elicited by pinching the Achilles tendon (Schaefer sign),

~ trok ing around the lateral malleolus (Chaddock sign), stroking downward the median side of

lhc tibia (Oppenheim sign), and compression of the calf muscle (Gordon sign).

2. Mendel-Bechterew sign. Striking the outer part of the dorsum of the foot (cuboideal bone of

ihc 4th and 5th metatarsal bone) results in plantar flexion of the toes (tarsophalengeal reflex,

phys iological dorsiflexion of the toes) .

,l. Rossolimo sign. ln the supine position the undersurface of the patient's toes are tapped by

l'ingcrs, the sole is slightly stroked. Positive Rossolimo results in plantar flexion or retraction of

1hc toes.

4. Patellar and ankle clonus may also indicate a lesion of the pyramidal tract. (A quick distal

prcssure on the patclla and a sudden dorsal pressure on the foot result in rhythmic jerks in the

quadriceps of the thigh and in the triceps of the calf, respectively. If jerking continues

(incxhaustible) as long as the prcssure is on, it is considered to be a pyramidal sign.)

Rcílexcs showing lesion of the premotor region:

Thc supporting reaction is positivc if thcre is an increase in the extensor tone in the proximal

muscles of thc limb on passive dorsiflexion (if thcre is flexion the supporting reaction is

ncgative). lt results from lesion of the forehead, temporal lobe or cercbellum.

Thc forearm sign of Léri: the elbow is slightly bent; the supinatecl upper .Jimb is in loose support

thcn the hand and wrist are firmly flexcd . The physiological answer is ten~ion of the biceps

muscle, Jlexion of the forearm. Its absence refers to lesion of the pyramidal tract, and the sign is

increased in lesion of the premotor region.

Mayer's reflex normally consists of adduction of the thumb on downward pressure of the index

or ring finger. Lesion of the related pyramidal tracts and adequate segments (C6-Th 1) results in

pathologic reduc4on or absence of the reflex. Increased reflex occurs (forearm muscles

contract) if there is a lesion in the premotor cortex region (Br. 6) of the opposite side.

12

Grasp reflex is an involuntary closure of the hand, which can be eliciteci by tapping thc radial or

ulnar side of the hand (it is positive in lesions of Br.6). When analysing the reflex it is

important to know that it can be elicitcd only in casc of adequatc ccntral motor inncrvation.

Sucking reflex is a similar phenomenon, the lips deviate to the dircction of the irritation.

Touching thc teeth with a hard object results in strong occlusion (Bulldog reflex). Greedy reflex

is bulldog reflex accompanied by inastication and deglutition.

Reflexes showing frontal lesion:

Frontal lesion is charactcrised by akinesia, poor initiation and catalepsy (upholding thc passive

position of limbs).

Midline reflexes arc obscrved in lesion of this arca.

Glabella reflex: thc glabella or thc nasal radix is slightly tappcd and thc result is blinking.

Medio-pubic reflex: the pubic symphysis is tapped, the abdorninal muscles and the thigh

adductor contract. lf the hip flexor or thc major pectoralis muscle react the reflex is incrcased.

Reflexes showing lesion of the brainstem:

Oculocephalic reflex: is an important test to decide about the lesion of the brainstern. The test is

donc by rotating the head slowly, and passi vcly to one s ide, and thc bulbs move to the other

direction as a reflex. This reflex might be damagcd if there is a lesion of thc brainstcrn.

Tonic ncck reflex: the head of thc supine patient is rotated to one side. The flexion tone is

increased in the limbs on thc same side. On the opposite sidc the flexion tonc is decreascd

resulting in excess weight in the 11exors (positive test). lt is most frcquent in scverc lesion of the

brainstem, or possibly in lesion of the parietal lobe.

12. No complaints of scnsory disturbance.

During scnsory examination the patient answcrs thc questions, whilc lying on a bed with his

eycs closed. Always comparc syrnmetrical parts, starting from the injured area to the healthy

region, and the examination is also repcated in the other dircction. U sually, start from the

proximal towards the <lista! parts.

13

, 1 ~ xa mi nation of thc spinothalamic scnsations

1. Scnsc of tc mperature (it is tested with a test tuhc with icc watcr or hot water; pathologic

1y1 ·s: lhcrmhypcsthcsia, thcrmanasthcsia, thcrmhypcrcsthcsia)

1, Scnsc of pain (cxamincd by pinprick; pathologic typcs : analgcsia, hypalgcsia, hypcralgcsia)

l Tacl ilc scnsation (cxamincd by a wisp o f cotton or brush: pathologic typcs: tactile

1l 1pcsthcsia, anesthcsia, hypcrcsthesia)

1\ , l ·'. xamin ations o f Goll-Burdach scnsation lypcs

L .lo int movemcnt (passive joint movcmcnts; absencc of it: kinanesthesia)

' · Scnsc of joint Jocatio n (o n eme side the limh is mov_cd pass ivc ly and thc paticnt imitates thc

~umc movcments on thc othcr sidc, or he dcscribcs the locatio n of thc movcd jo int; dccrcase of

it : hathypcsthcsia)

1. Graphcsthcsia (draw diffcrent figures or shapes - circlc, cross - o n thc skin of thc paticnt

whnsc cycs arc closcd)

1. Vihratory scnsation (a vibrating tuning fark is put on to bony promincnccs; dccrcasc:

pul lcsthcsia)

~. Scnsc of two-point discrimination (differentiating simultaneous stimuli of thc skin : c.g.

prcss ing cvenly with two ncedles)

(1 , Rccognition of wcight and strength: dcpcnds on sustaincd deep sensation.

Scnsory disturbanccs arc presentcd in a scnsory schemc. Vario us sensations arc indicatcd

liffcrcntly. Prcsent thc rcgio n of ci thcr thc scgmcntal or thc pcriphcrial ncrvcs in the schcmc.

(Normai dctailed dcscription of scnsory circlc: tempcraturc, pain, tactilc, dccp scnsation,

vibratory scnsation, double s imultancous sc nsat ion on thc l'acc, trunk and limbs sustaincd).

f 3. Targct cxpcrimcnt, Rombcrg test, blind gait, gait, diadochokincsis and Bárány test are

norma!. Othcr ccrchcllar tcsts arc normal.

Targ'ct cxperimcnt: thc paticnt is askcd to to uch the tip of his nose with thc tip of his right and

thm his JcCt index fingcr, o r raisc his lcft hecl to thc right kncc (cycs closcd). During the

111o vcmcnts swaying lilight be obscrvcd which may increase hcforc reaching the targct

( inlcntion trcmor).

ln Rombcrg posit ion thc paticnt is standing with foct \ogcthcr anc.l his eycs closcd. Ask him

;ibuut thc Jircct io n of swaying; hc 1-~ askcd similarly with crosseJ lcgs (cornplicatcd Romberg) .

14

Ili ind gait: thc dircction of gail is observcd, when the pati~nt is as~ed .t~ walk with closed cycs.

Gait: wc observc how broad the base of the gait is, how unstcady the p:rogress is. If tJ;ie trunk is

bent back írom standing position, after a ccrtain angle compensatory ílcxion appears in thc -

knecs (Babinski syncrgia) (in cerebellar lcsions it is absent, this is called Babiriski asynergia).

The paticnt is asked to move his hands alternatively (supination - pronation, beat his chcst with

his . fingers). If the movements slow down or hc is unablc to do them we can speak of

dysdiadochokincsis or adiadochokinesis.

Bárány test: the patien~ is asked to strctch his fingers up to the levei of thc examiner's fingers.

Paticnt closes his cyes and drops his arms thcn he has to raise his hands again to the observer's

fi.ngers. The test is repeated several limes. (ln cerebellar lesion we can observe pa~t pointing to

thc focus of thc lesion.)

In cerebellar lesion "scaniilng spcech" can be obscrvcd. The rhythm of the speech is halting,

unusual. (Triad of Charcot: intcntion trcmor, scanning spccch ·and nystagmus.)

Fling back sign: the paticnt f1cxcs his arm in clbow and the q~server tries to stretch -it out, when . ~ . .

the obscrvcr suddcnly releases: the forearm of the paticnt llings back.

Disturbance of wci~ht rccognition: the patien.t on Úamination is holuing an object in both

hands with the samf··weight/ He fccls the object lightcr on the pathologic side. Maintaining tlw

uncomfortable pos1J1on becomes more difficult: pronation can be observed on the supinatcd

.arm, although this phenomenon can also be obscrved in lesion of tbc pyramidal tract. Muscle

tone decreases on the sidc of the focus of the diseasc (cerebellar hypotony), dcep reflexes arc

morc inert.

(Normai detailed description : hccl-to-kncc, fingcr.-to-nose tests ar~. norma!. No deviation during

blind gait. Hc kceps his direction during gait, it has af"'Tiediuin broad ,base and his space is

medium, too, swinging of arms is associated . He compensatcs well during bcnding forward and

· backward up to Babinski test. No dysdiadochokincsis. Bárány test norma!. No íling back sign.)

14: .Vcgctative functions arc normal.

Paticnt announccs: sphinctcrs norma! (bladder, anus), no disturbancc in erection, cjaculation, no

priapism, no complaints of sweating.

Chcck if there is increased dcrmographism, hiccup, hoarsencss, disturbance in thc secretion of.

saliva or gustatory disturbance (pupil reaction has a!ready be~n mentioned).

15

15. Spccch and cognitiYc functions arc in ordcr.

l<hythm, tonicity and comprehensibility of speech arc observed. Visual cognitive achievcment

L' cvaluated on thc basis of recognition of pictures, objeets and symbols (while acoustic

l\111ction is assessed by thc rccognition of well-known sounds /e.g.: trainclatter/). Tactile

rn • 11ition is examined by placing objects into the patient's hands.

1 1. Thc paticnt is alcrt, orientatcd, organised.

'll1c paticnt is alert when hc coopcrates with the doctor during the exai'nination. If he answers

rn 1r questions slowly, sluggishly, and is drowsy, we spcak about somnolence. ln this state, the

p11 ticnt can be woken up and drawn into contact easily.

Th..: paticnt is soporose when hc can be woken up írom his sleep by pain stimuli with difficulty

and afterwards no verbal contact is possible with him.

Th..: patient is comatose whcn he cannot be woken up at all. He might react to pain by pulling

liis cxtremitics but this motor response can be organised also on spinal leve! /hypnoid

dcsoricntation/.

/\pallial dcsorientation is a state in which thc paticnt is seemingly alert but no contact can be

·stablishcd with him /extcnsive cortical lesion may be in the background/.

Whcn it is associated with decortical rigidity, therc is flexural hypertonicity in the upper limbs

1111<l cxtension hypertonicity i11 the Jower limbs.

111 the statc of akinctic mutism the patient seems to be alert, too, but he cannot be drawn into

co ntact and there is no dccortical rigidity either.

(Normai detailed description: his behaviour is conventional, he cooperates wc\I, he is orientated

i11 space and time, his mcmory for both reccnt and remote evcnts is retained, his attention can be

drawn, fixed or switched to different subjects, he does not experience illusions, his thinking is

i11 order concerning both its contents and form, he is emotionally stable, he is in good mood, he

rcports on his complaints realistically. /We examine the dctailed psychic statc in cooperation·

witlJ. a psychiatrist./)

16

Examination of'unconscious paticnt

/It is a gencral rule that rcspiratory and circulatory disturbances _necd immcdiate intervention~ intubation, venous cannula, rnaintcnancc of breathing and circulation./

l. Observc the spontancous position of thc hcad and thc extremitics. The skull must be

cxamincd with spccial c:arc bccause of the possible injuries /subdural haematoma, danger of

some othcr kind of intracranial blceding/.

2. Look far the signs of mcningcal irritation /subarachnoid hacmorrhage, suspicion of

mcningitis/.

3. Condition of pupils

/1esion of mhscncephalon : mydriasis,

damagc to the pontine-tegmcntum: bilatcral maxima! miosis,.pinholc pupils,

hcmispheric space occupation: anisocoria,

ciliospinal reflex: dilatation of pupils on pinching thc skin of the ncck, whilc its loss may

indicate a lesion in the brainstcm/.

4. Thorough fundus examination /papilloederna/.

5. Position of eyeballs:

(1) divergcnt positirn1, crratic eye movcmcnts: pontine-mcsenccphalon 'lesion,

(2) conjugatc deviation:

a/ frontal focus: cycball deviates to thc sidc of thc focus,

b/ ponti ne lesion: deviaÜon towards the side oppositc thc focus.

6.Prcsence of oculoccphalic reflex.

7.Thc following arc typical of hcmiparalysis : the paralys~d half of tik· facc is slightly distcnded

on expiration, thc paralyscd limb falls back fastcr aflcr being lifted th_an thc intact one, thc

paralysed sidercacts to pain to a lcsser extent.

8. Examination of pathological reflexes.

9. Exarnination of sensory disturbances: responses to pain /spinal automatisms/ .

..

17

II. PRACTICAL NEUROLOGY

'111c aim of this chapter is to summarizc brieíly the most essential neurological facts which are

11 · ·cssary for physical examination, assuming the knowledge of functional ncuroanatomy.

CRANIAL NERVES

1. Olfactory ncrvc (1) (physical examination, point 4)

lf' thc olfactory bulb or tract arc compressed permancntly, ipsilateral parosmia develops. The

1 wo sides of thc olfactory system arc connected by the anterior commissure, thus a more central

1rni lateral lesion does not lead to disorders of thc sense of smell. The following symptoms arc

lypical of olfactory mcningioma: ipsilatcral parosmia, optic atrophy and contralatcral

pnpilloedcma /Fostcr-Kennedy syndrome/:

, Optic ncrvc (11) /fundus, vision, visual ficld/

(physical examination, points 4 and 5)

lncrcascd intracranial pressure causcs papillocdcma. ln the bcginning thcre is no visual

di sturbancc. The optic papilla is elevatcd like a mushroom, it is swollen, greyish-yellow, its

111 argins are blurrcd. No vcnous pulsation can be noted /tense vcin/, but striate haemorrhagc

111<1y be observed on the papilla occasionally. Onc millimcter's clevation of thc papilla equals

l.O D.

Longstanding papillocdema lcads to optic atrophy. It is important to emphasize thal the statc of

lhc papilla must be checked before lumbar puncture, though thc absencc of lhe congcstion itsclf

docs not cxclude the possibility of intracranial spacc occupying lesion /dangcr of herniation!/.

Pnpillocdema must be distinguished from papillitis. ln case of papillitis the paticnt's vision

Jdcrioratcs at thc bcginning of the disease. The optic nerve is intrabulbarly inflamed in such

·ases , therc is fine opacity in the vitrcous body and scotomas appear in the visual ficld. ln

jsolated optic neuritis /rctrobulbar neuritis/ the _intlif;nmation of the optic nervc occurs behind

lhc cyc /therc is often no dcviation on thc optic papilla/. Thc paticnt complains of rapid

Jctcrioration of his vision, which may oftcn be the premonitory symptom of mulliple sclerosis.

Thc dccoloration of lhe lcmporal napilla is also lypical of multiplc sclerosis .

• „

18

As a consequcnce of damagc to the optic tract, a variety of symptoms develop depending on the

location of the injury. s.eve~e damagc to the ( 1) optic nervc causc~ amaurosis.

If spacc occupying lesion damages the antcrior medial region of thc (2) chiasma from bclow

/c.g.: tumour of the pituitary gland/ bitemporal hcteronymous anopsia devclops while a

pathologic proccss destroying the lateral region causes contralatcral nasal anopsia. Whcn both

sides are affected, it resi.Jlts in binasal heteronymous anopsia.

ln lesion of (3) the optic tract, heterolateral homonymous hemianopsia occurs. The paticnt

experienccs dcfects of the visual ficld, optokinetic nystagmus is retaincd. If thc part of thc tract

is damagcd whcrc pupillomotor fibres are not yet separatcd, Wcrnickc's hemianopic pupillary

reflex is absent. /ln this case, if we focus the light of thc slit Jamp on the retina parts

corresponding to the damaged optic fibres, no constriction of the pupil occurs whereas it can be

triggcred on the intact retina parts./

ln case of lesion of thc (4) optic radiation the patient docs n6t experiencc defccts of the visual

ficld and central vislon is also rctained. Optokinetic nystagmus cannot be triggered if the

posterior part of the optic. radiation is injured. As thc pupillomotor fibres split carlier,

Wcrnicke's hemianopic pupillary reílex is retained. A lesion to the anterior part of the optic

radiation results in contralateral quadrantanopsia. If the postcrior area is damaged, contralateral

homonymous hemianopsia develops.

When the (5) primary occipital visual cortex is destroycd, Wcrnicke's hcmianopic pupillary

reaction is naturally rctained. The damage of thc occipital polc causes ccntr'al visual

disturbance. ff thc anterior parts of the upper lip of the calcarin fissure are destroyed, it causes

contralateral inferior quadrant hemianopsia whilc the damage of the lower Iip leads to

contralateral superior quadrant hemianopsia. The lesion of ambilateral striate cortex results in

cortical blindness.

3. Oculomotor (Ili), trochlcar (IV) and abduccns (VI) ncrves

(physical examination, point 6)

The oculomotor nervc (Ili) regulates the size of the pupil and it accommodates the curvature of

the Icn_s. Out of the two muscles controlling the pupil's aperture, the contraction of the sphincter

pupillae caus~s thc constriction of the pupil and its relaxation leads to dilat<)tion. The nervc

fibr~s originating from thc ciliospinal centre have a weaker effect (m. dilatator pupillae: its

constrictioil causes dilatation while its rclaxation results iri the constriction of the pupil.)

19

l ' \lhological pupil reactions occur in the following cases:

1, lf' thc optic nerve is damaged on one side, neither direct nor consensual reaction can be

11 11• •cn.:d on thc sidc of the injury. On the side of the healthy cye, however, both direct and

•' )llScnsual reactions arc intact.

' · W crnicke's hemianopic pupillary reaction is abscnt if the optic tract is damaged before the

l.1l ·ra l gcniculate body (whcre the fibres constituting the affcrent stalk of light reflex are still

11 11111ing in the tract). Logically, if the lesion is situated distally from the place of separation,

l 1 hl rcílcx can be triggered from the hemianopic half.

1. l)amage to the spinal (C8-Th 1-2) oculopupillary nucleus as well as to the sympathetic nerve

•, \ ·111ming from this causes Horner's syndrome (ptosis, miosis, enophthalmos). The lesion of the

111 ·Juli a oblongata and the lateral parts of thc pons may also cause Horner's syndrome.

111 case of 11011-rcactive pupil both light and convergence reaction are absent. Argyll-Robertson

11lJ2il is when convcrgencc and accommodation are mai11tained but light reflexes cannot be

tri gcred. lt is essential that in intracranial space occupying processes (increased intracranial

prcssurc) thc pupil is homolaterally narrowed due to irritation of the oculomotor nerve while it

i .~ dil atcd maximally and fixed if thc brainstem is enclosed.

"~" is the rapid spontaneous change of the pupil's 'size. ln case of tonic pupil, the pupils

·onstrict slowly when exposed to light. Convergence and accommodation are also slow and .

t lni c. (When accompanied by areflexia of the lower limb, it is called Adie's syndrome.)

'011ccrning eye movemenl disturbances, we spcak about ophthalmoplegia totalis (the paralysis

Jf thc external or internal eye muscles is ophthalmoplcgi~ externa or interna) when the external

antl internal eye muscles are all paralysed. Diplopia is the subjective symptom of the eye

muscle paresis. Strabismus or sguint means that due to thc weakness of certain muscles, the

antagonists predominate. It is of clinical significance that the oculomotor ncrves can easily be

ua maged owing to increased intracranial prcssure. It is especially typical of the abducens (VI)

11crve which is decussated with the branches of basilar artery and increased intracranial pressure

·ompresses it onto the nerve.

The symptoms of the lesions of the oculomotor nerve must be ·emphasized. While nuclear

damage may be accompanied by partial eye muscle parcsis, injury to the nerve trunk always

lcads to the paresis of each muscle. Therc is ptosis on the side of the lesion, the bulb is abducted

and turned downward (abducent and trochlcar effect), the pupíl is dilated, light reflex may be

•·,

abscnl. (Light rdlexes can theoretically be int;:tct in case of nuclear lesion if the parvicellular

nuclei arc unimpaired. On injury to the trochlear nerve, if the nucleus is damaged, the

contralateral superior oblique muscle is affected whereas nerve trunk Iesions cause ipsilateral

function deficiency (as the fibres coming from the trochlear nucleus run dorsally and then

decussate ).

ln supranuclcar conjugatc gaze deviations, thc movements of the two cyes arc affocted in the

same way so they deviate in the same direction (gaze paralysis and weakness). There is no

vertical or horizontal squint or double vision in conjugate deviation. The frontal gaze centre

(Br.8) is probably the voluntary viewfinder while the occipital one dominates in automatic

(reflex) movements. From the point of view of clinical practice, it is important to stress that ín

cerebral haemorrhagc (or following any kind of attack in the brain), lhe patient's eyes turn to thc

side oppositc lhe hacrnorrhagc (excitement in the cortical oculomotor centre on the damagcd

sidc). Latcr thc cxcitemcnt ccascs and the othcr gazc tract will prcdominatc on thc unimpaircd

side. (Thc patient "gazes" at the lesion.)

Pcrmancnt horizontal conjugatc paralysis or weakness may be caused by damage to thc

tegmentum of the mcsenccphalon and the pons: in this case gaze weakness nystagmus may

occur. (The patient is unable to look to eithcr side for long, thc eyeballs keep returning to

midline.)

Internuclcar ophthalmorlegia develops when the lesion is situated bctween thc nuclei of the

oculomotor nerve and thc abducent nerve. Injury to the medial longitudinal fascicle is in its

background. ln these cases, adduction cannot be performed but convergence is retained·

(functional disturbánce, not paresis of the internal rectus muscles is typical in this case).

Whcn thc pontinc gaze centre is damagcd, the patient is unable to look to the side wherc the

lesion is.

Vertical cye movement disturbanccs occur when thc mescncephalic transition ·is impaired

(nuclcus interstitial of Cajal). Bell's sign can be uscd to differenliate vertical conjugate paralysis

and the parcsis of the cyeball levators. (The bulbs turn upwards when forcing the eyclids to

cfosc.) It is absent on bilatcral lesion of the superior rectus musclc, but in vertical conjugatc

paralysis it is rctained.

21

1. Trlgcminal ncrvc (V) (physical examination, point 7)

111 • fifth nerve consists of a sensory and a motor part. It is important that the corneal reflex

( 11'f" rcnt ophthalmic branch of the ncrve V. connection: pons, efferent nerve VII.) may be

11is ·nt (or reduced) in lcsions of the cerebellopontine angle (acoustic ncurinoma). Thc

l'lwracteristic feature of trigeminal neuralgia is acute pain of short duration which can be

1tln1ulated by touching the critical region of the innervatcd area:

. Facial ncne (VII) (physical examination, point 7)

1 1e íacial nerve has motor. sensory and vegetative functions. We speak about peripheral facial

J) i\ ·csis if Lhe damage occurs in the motor nucleus O( along the facial nerve.

< 'ontrary to this, if supranuclear innervation i~ disturbed (which innervates the nucleus), it is

· ti lcd central facial paresis. The motor facial nuclear segment which innervates the perifrontal

111d pcriocular muscles obtains supranuclear fibres from both hemispheres whcreas thc nuclear

~ ·gment which supplies the perioral n]nsclcs and the platysma is innervated solely by the

·onlralateral hemisphere. lt follows that in casc of peripheral facial paresis, the palpebral fissure

Is wider on lhe paralysed side (lagophthalmos), the furrows becomc smooth, the nasolabial

f'ovc a is shallower compared to the other side. Contrary to this, in central facial paresis bolh

·ydid shutting and wrinkling of Lhe forehead are maintained (due to the above mentioned

hil atcral innervation) whereas "showing the teeth" is morc or less damaged.

On routine neurological examination taste is rarely checked (but in case of lesion of facial

11erve, this examination is of diagnostic valuc in the Jocalization of the disordcr). It is well­

known that the intermcdiate nervc provides Lhc anlcrior two-thirds of Lhc tongue with gustatory

l'i bres by the chorda tympani . The other function of thc facial nerve is the vegctativc inncrvation

or thc salivary gland (except for parotids). If the lesion is situated proximally to the origination

of" chorda tympani the disorder of tastc and salivary secrction appear togethcr.

The patient complains of tinnitus and hyperacusis if thc stapedius is affectcd,

while disturbance of Jacrimation can be obscrved if thc lesion is proximal to the origination of

lhc grcatcr petrosal nervc.

li;Vcstibulocochlcar ncrvc (Vlll) (ddailcd in physical examination, point 8)

7. Glossopharyngeal nerve (IX) (physical examination, point 9)

lt has motor; sensory and vegetative functions.

22

Its motor function is the innervation of the stylopharyngeal and the constrictor muscles. Ifit is

damaged, the soft palate is homolaterally sagging, the uvula is drawn towards the intact side

and dysphagia appears.

The sensory functioh is the innervation of the posterior third of the tongue.

lt adds vegetative fibres to the parotid gland.

8. Vagus nerve (X) (physical examination, point 9)

lt has motor, sensory and vegetative fibres.

(Motor function is discussed in physical examination, point 9)

If thc sensory fibrcs arc lcsioncd, sensory disturbance occurs on a small circumscribed area of

thc ear and thc auditory duct.

Injury to the visceral fibre causes rhythm disturbance in respiration and the heart (oculocardiac

reflex: on pressure on the eycball the heart rate decreases, asystole).

9. Accessory nerve (XI) (physical examination, point 9)

lt has motor fibres only (it innervates the upper third of the sternocleidomastoid and the

trnpezius muscles).

10. Hypoglossal nerve (XII) (physical examination, point 9)

Motor fibres innervate the musculatúre of the tongue. The supranuclear innervation of the

hypoglossal nucleus is bilateral, only the fibres innervating the genioglossus muscle are

decussated and unílateral. If the central _neuron is damaged, the prötruded ton_gue deviates to the

side opposite the lesion because of functional domination of the intact genioglossus.

~ · ..

23

MUSCULATURE (physical examination, point 10)

lt ·r the examination of the cranial nerves we pass on to the muscular system. The basic

ti 11 11 ostic question is the differentiation between paralysis of central origin and of peripheral

l!j J i l.

1. Examining the trophic state of the muscle in case of peripheral lesion: hypotrophy takcs place

11 •l11t ively rapidly and its division depends on the weakness. Contrary to this, ín case of ccntral

11 ·.i1> 11 hypotrophy takcs placc later, it is of diffuse distribution and it can be considered to be the

111 11 sequcnce of inact.ivation.

, /\ major difference is that the muscular tone decreascs in case of pcriphcral lesion, while

d11 ri11g central lesion thc Wernickc-Mann type prcdilcction of tonc distribution can be observcd

11 l ·r a short pcriod of time.

1, Muscle strength dccrcascs in both cases (ín case of paralysis it is not perceptible), while in

p •riphcral lesion the division of paresis obviously corresponds to the localization of thc lesion

11uclcar, radicular, plexal), in casc of ccntral paresis it is distally enhanccd.

1. /\ t peripheral damage, inert or missing deep reflexes can be found but no chronic reflex can

h • ubscrved. ln case of central lesion increased decp reflexes appcar with pyramidal signs.

/\nolher substantial differcnce is that in case of peripheral lesion thcre is fasciculation

·onstriction of tiny myofibrils), whereas ín case of ccntral lesion it cannot be obscrved.

11' pcripheral weakncss extcnds over morc muscles in the uppcr limb then wc can talk about

hrachial plexus lesion. When thc upper plexus is damagcd (Duchcnne-Erb) the shoulder girdlc

11 11d the upper arm are affected, while at the damagc of thc lower plcxus (Klumpkc) the small

lrn nd musclcs are affected.

" 'aroal tunncl ·syndromc" is whcn peripheral lesion of thc thcnar can be observed as a

·onscquencc of chronic pressurc of the transverse carpal ligament on thc median nervc branch.

ln a proximal direction radicular damagc is accompanied by segmcntal weakncss. Organic

lcs ion of the anterior horn of the cord rcsults in peripheral symptoms." A morc cxtensive damagc

~> !" thc spinal cord causcs ccntral weakness (unilateral syndrome: Brown-Sequard syndrome). ln

casc of cross-scctional lesion of the whole spinal cord, bilateral parasagittal lesion or brainstem

J.cs ion (c.g. meningcoma) pai:aparcsis may occur. The lesion at thc middle of the decussation of

lhe pyramidal fibres causes paralysis of the upper limb on one side and of thc lower limb on thc

othcr sidc. This is callcd hemiplegia cruciata .

• „

24

An important localization problcm is the question of paresis that appears in damage to the

brainstcm (alternating character). ln this case damage to the motor nucieus of the cranial nervcs

in the brainstem causes peripheral paresis which is accompanied by central weakness of the

contralateral limbs (hemiplegia alternans).

Weber syndromc: nucleus Ill. lesion+ contralateral hemiparesis (HP),

Benedict syndrome: Weber+ red nucleus lesion+ HP (intensive tremor or hyperkinesis),

Foville syndrome: n. VI. lesion+ HP,

Brissaud syndrome: n. VII. affected +HP (excitement phenomenon and tic),

Millard-Gubler syndrome: n. VIT. peripheral type paralysis, possibly also n. VI. paralysis +HP,

Avellis syndrome: n. IX. lesion paralysis of the soft palate +HP,

Jackson syndrome: n. XII. lesion+ HP.

(The most common is Weber syndrome.)

Proximally thc damagc of the hemispherc and the internal capsule causes contralateral

weakness.

The cortical lesions according to somatotopic localization can result in paresis which extends

over certain musclcs or muscle groups.

REFLEXES (physical examination, point 11)

Further on we discuss thc subject of deep, superficial and pathologic reflexes. The arc of the

deep reflexes (proprioceptive reflexes) consists of two neurons and one synapse. Thc receptor

(muscle spindle) and the effector (working muscle fibre) are in the same muscle (a reflex of its

own). The extension of the muscle causes stimulus. Every striated muscle has its own reflex. In

a healthy muscle we can find missing or inert deep reflexes if:

(1) the afferent sensory fibres have been damaged (e.g. SI root lesion : Achilles areflexia),

(2) the motor neuron of the anterior horn is in'jured (e.g. infantile paralysis),

(3) the motor fibres in the anterior radicle arc damaged,

(4) the motor fibres as well as the sensory fibres are damaged on the periphery

(polyneuropathia, trauma) that is in all parts of the reflex arc.

Supcrficial reflexes arc. ~lici~ed by the stimulation of mechanic reccptors of the skin and the

mucous membranes. Gcnerally, these reflexes are missing (or they change) if the central motor

gyrus or the pyrai:i:iidal tract is damaged (soft palate, pharynx, abdominal skin, cremaster, sole,

anal reflexes) .

•..

25

111 • p:1thological reflexes arc reflexes that cannot be clicitcd in physiological conditions: they

, 111 hi.: sccn in the lesion of any parts of the supranuclear tract syslem (Trömner, Hoffmann,

l111hl nski , Oppcnheim, Gordon, Schaefer, Chaddock, Rossolimo, Mendcl-Bechtercw, knee and

111 l • clonus). (The reflexes rcferring to the damagc of thc brainstem and of thc prcmotor and

11 nnta l lobe arc mcntioncd in physical examination, point 11)

SENSORIUM (physical cxamination, iJOint 12)

Fnr didactic reasons, wc follow lhe distal-proximal direction while surveying the injuries of the

1 11sory tract.

11) Damagc to the peripheral ncrve trunk affccts the region of supplicd by the corresponding

111 •rip hcral ncrve. In casc of chronic alcoholism or diabetes mellitus thcrc is a "glove-like" or

" (() ·king-likc" scnsory disturbancc in thc <lista! region of thc limbs (polyneurotic or

pulyncuropathic type scnsory dislurbancQ).

(. ) fnjury of thc plcxus causcs the symptoms of <lamage lo thc pcriphcral nerve.

l) Thc most common causc of lesion of thc postcrior root is hcrniatc<l disk (other causes can

li ·: inílammation, allcrgy, tumour). A fcature of its symptomatology is that the pain is of

111t.l icular charactcr (dcnnatome division); thcrc„ is Lasegue's positivity, tendcrness at Vallcix's

poinls and sens~ry disturbancc corrcsponding to the affccted dcrmatome, also reflex divcrgcnce.

1 r paresis may takc placc.

l'rocceding a proximal dircction the ncxt localization is

lf) the lesion of the posterior horn of the spinal cord and the central grey matter the usual

·uuscs arc: intramedullary mass lesion, syringomyclia, hacmatomyelia. Dissociated scnsory

disturbancc (heat, pain, tactile sense) develops when the spinothalamic tract (which dccussates

11 i.: ri.:) is injured while maintaining depth perception:·

5) In lcsions of the postcrior cord (tabes dorsalis) apart from thc damagc of ipsilateral dcplh

pcrccption, superficial perccption is kept intact.

..

•..

26

(6) Brown-Seguard syndrome is the hemilateral damage to thc spinal cord which is usually

caused by trauma, inflammation or tumors. On the side of the da_mage and at its levei, sensory

disturbance of segmental dermatome division appears, homolaterally and distally from that,

completc absence of depth perception (spinal ataxia) and ipsilatcral pyramidal lesion takcs

placc. Contralaterally, distally from thc damage therc is hypalgesia and thermohypaesthcsia.

(7) Complete transversc lesion of thc spinal cord (distal from the injury thcre is complctu

scnsory defcct) .

(8) ln the brainstcm. thc medial lcmniscus transmitting superficial and deep senses and th ·

spinothalamic tracts carrying heat, pain and tactile senses run separately, so they can be injurucl

indcpendcntly of cach other. ln case of alternating scnsory disturbance (unilateral pontobulha1•

focus) bcsidcs ipsilatcral scnsory disturbance in the rcgion of thc trigeminal nerve, superfic ial

and dcep scnsory dislurbancc can be obscrved on the contralateral part of lhc body.

(9) Injury to the thalamus (e.g.: focus of vascular origin) causes superficial and deep scnsory

disturbances of the contralateral part of thc body and the face.

(10) Evcn a small focus in the internal capsule can cause hemihypaesthcsia (damage to l1 1 •

thalamocortical tract).

( 11) Thc excitcment of thc sensory cortical arca can cause paracsthcsia and pain on til1

contralateral sidc, cortical damagc in the contralateral part of the body and to the face caU.'•"·

anaesthesia (cortical somatotopy).

( 12) Damage to thc supramarginal gyrus of the dominant hemisphcre causes astereognosi a. (N11

scnsory disturbancc can be shown but the patient is not able to recognizc the object placcd into

his hand with closed eycs . The basic sensory function is sustained but its arrangemcnl

disturbcd.)

COORDINATION (physical examination, point 13)

1 lll' •i!Tcrcnt pathway of thcsc comple~ reílex processes gives information about the position

11 11!1 moti on of the eyes and the head, the tone of the muscles and also about the position of the

1 111hs and the trunk (proprioceptive sensory system, vestibular system). The essence of the

, Jt' • ·ntalion is the coordination of the response of the pyramidal and extrapyramidal systems,

ilt ·cnlrc of which is the cerebellum. The cerebellum is in connection with the pyramidal

y (. ·rn but it rcceives affercntation from the cortex, the frontal region and the motor area

f 1 onto-ponto-cerebellar tract). The fastigial nucleus influences the muscle tension through the

l\\I ·ular formation and the reticulo-spinal tracts. ln clinical practice it is important to know that

1 f ·hcllar diseases with space occupation (tumors, haemorrhages) rapidly compress the Sylvian

11 p1 ·J uct and can bring about severe increase in intracrania1 pressure by the inhibition of the

t ','F now.

EXTRAPYRAMIDAL SYSTEM (physical examination, point 10)

l11c cxtrapyramidal system plays an important role in the coordination of movements (thus in

111 • formation of the motion patterns characteristic of the person, e.g. : in walking), in

, 111otional-mcntal achievements, in the regulaÜon of the vegetative system (secretion of saliva,

p ·rspiration) and of muscle tone. ln case of rigidity the .tone of both the agonistic and the

1111lagonistic muscles increases. lt explains the cogw.heel phenomenon. But extrapyramidal

ltypotonia may occur as well.

<)ne of the most conunon movement di sorder is tremor. (We have to differentiate between

r ·sting, emotional, intentional, static, essential or other tremors, e.g.: tremors accompanying

d•Jirium.)

!{est tremor (or antagonistic tremor) is a characteristic of Parkinsonism and we use different

1tljcctives to describe it e.g. "pill-rolling'', "money-counting", or "feath~r-plucker" .

Wc can often sec intentional tremor in multiple sclerosis (the damage of the dentate-rubral

sys tcm). ln case of an expedient movement before the goal, tremor takes place in rough waves.

bi tatic tremor can be observed in neurotic patients or when the patient is tired. It is brought

'M bout by intentionally fixed position.

, ,

28

Familial or essential tremor can be secn when the upper limb (somctimcs the hcad) trcmblcs, no

intentional motion can decrcasc it and it is of ílexural-cxtcnsional charactcr. Bcsides all thesc,

several othcr typcs of tremor arc known but they cannot be categ?rizcd easily (e.g.: in case of

delirium tremens).

Chorea is an aimless, irregular, acute, whipping motions appearing on thc distal part of the

limb.

Athetosis also appcars distally, but it consists of slow, vermicular, tonic, irregular motions.

Torsion dystonia is first of all in the trunk, it is a slow, tonic, twisting motion.

Oculogyric crisis is a lasting cye-muscle spasm coming in fits .

Ballism is a tossing movcment with large amplitude and sudden appcarancc in the proximal part

of the limb.

Thc motion series deriving from acute contractions in one muscle or muscle group is called

myoclonus (it does not contain nbtable motions).

Tic, which is one form of myoclonus , is a sudden ílash-like motion expanding on one or morc

face muscles.

Different hyperkinesises on thc facc can be observed, likc compulsive protrusion of the tonguc.

perioral hyperkinesis or blepharospasm.

VEGETATIYE SYSTEM (physical cxamination, point 14)

The innervation of thc bladdcr and the rectum, the rcgulation of crection and ejaculation arc in

the lumbosacral region of the spinal cord (damagc: incontinencc or rctention of the urinc amJ

feces, paradoxical ischuria, priapism).

Ileus can be caused by thoracic localization space occupying process.

Horner trias (ptosis, miosis, enophthalmus) can occur on injury to the Th 1 segment. Respiratory

disturbancc and hiccup may take place if there is damage to the C4 segment (phrenic nervc).

Respiratory paralysis is formed at gomphosis caused by tonsillar hcrniation.

Lesion of medulla oblongata causes hiccup and hoarseness,

while pontobulbar damage causes disturbancc in thc secretion of saliva and in thc sensc ol'

taste.

Wcstphal-Edinger and Perli.a nuclei arc located in the mesencephalon (the parasympathcti ·

innervation of the pupil). Thc upper brainstcm, the limbic systcm and certain regions of th ·

brainstcm arc the ccntral controlling arcas of Lhe vegetativc nervous system.

29

1 11 l •1•11 trn l lobulc Jamagc can be causcJ hy parasagi llal mcningioma, which rcsulls in

llll ·1 lt rn al disordcrs of the bladdcr and lhc rectum.

•.

. ..

SPEECH, COGNITIVE FUNCTIONS, PSYCHIC STATE

(physical examination, points 15,16)

30

11' the patient understands speech well, but has speech disturbances it is called motor (Broca)

aphasia, whereas if the dominant part of thc disordcr is in understanding speech, we can talk

about sensory (Wernicke) aphasia.

(Dysarthria is a peripheral innervation disorder as a consequencc of bulbar damage).

Paticnts suffering from motor aphasia might be able to cxpress their thoughts in word fractions,

while paticnts having scnsory aphasia are not ablc to understand their own spccch or the wonls

spoken to them.

ln conduction aphasia (thc lesion of the anglc encompassed by the head of the corpus callosum

and the caudate nucleus), the patient cannot talk spontaneously but has the compulsion of echo

specch (echolalia) .

ln case of total and global aphasia the ability to spcak as well as the ability to understand spcech

is disturbed (it is usually accompanied by alexia and agraphia).

If there is difficulty in finding words (naming objects, phcnomena) it is callcd amncstic aphasi a.

ln case of agraphia the patient does not havc paresis, but he has lost his ability to write.

The state when motor aphasia or visual disordcr cannot be proved, but thc patient is not ablc tn

read is called alcxia.

We can talk about amusia if a musical patient has lost his instrumental or vocal musical sens ·

( disorder of perceptive ability: sensory amusia).

The disorder of counting ability is callcd acalculia.

Agnosia is the problem of the ability to rccognize objccts and symbols (it can be tactile, visual

or auditory).

If the patient cannot recognize an object by touching it, we can talk about astercognosia.

The disordcr of the body image is callcd autotopagnosia (the disorder of the finger sense is

called fingcragnosia).

• „

ln everyday clinical practice an important symptom is anosognosia. lt can be observed in ca · ·

of a focus in the subdominant (usually the right sidc) hemisphcrc (damagc to th •

temporoparictal rcgion), the paticnt docs not rccognizc the paralysis of thc limbs on the lcl'I

s ide .

111 1 'r r (pari ctal lobc damagc in thc dominant hcmisphcrc) means a complex motor disturbance

11 111111 parcsis. ln case of ideokinetic apraxia the patient plans to move, but he cannot carry out

li • ph111. whilc if he cannot plan his movement it is called ideatoric apraxia. (The psychic state

' 11 11111rnri zcd in physical examination point 16).

'·

32

REFERENCES

Bronisch, F.W.: Reflex vizsgálatok. Medicina, Budapest.

Czopf J.: Neurológiai betegvizsgálat. Egyetemi jegyzet. POTE, Pécs.

Csanda E.: Neurológia. Egyetemi jegyzet. SOTE, Budapest.

Heiner L.: A neurológiai vizsgálat. Egyetemi jegyzet. SZOTE, Szeged.

Környey I.: Idegkórtan. Egyetemi jegyzel. POTE, Pécs.

Molnár J.: Az ideggyógyászat tárgyköre. Egyetemi jegyzet. DOTE, Debrecen.

Mumenthalcr, M:": Neurológia. Medicina, Budapest.

Pálffy Gy.: Neurológia. Egyetemi jegyzet. POTE, Pécs.

Poeck K.: Differenciáldiagnosztikai kérdések a neurológiában. Springer Hungariea, Budapest.

Rolak, LA.: Neurology Secrcts. Hanlcy Bclfus, Philadelphia.

Rowland, L.P.: Merritt's Textbook of Neurology. Lea Febiger, Philadelphia.

Simon, R.P„ Aminoff, M.J„ Greenberg, D.A.: Clinical Neurology, Langc, New Jersey.

Szirmai I.: Gyakorlati neurológia. Tertia, Budapest.

Van Allen, M.W„ Rodnitzky, ltL.: Pictorial manual of neurological tests. Ycar Book Medical

Publisher, Chicago.

33

SUPPLEMENT

Nt.:urological history chart (Albert Szent-Györgyi Medical University (SZOTE, ;

cpartmcnt of Ncui-ology).

l'rcsént statc. Ncurological cxamination (SZOTE, Departmcnt of Neurology).

1, Scnsation examination form (SZOTE, Dcpartmt.:nt of Neurology).

Ncurological patienl cxamination with rough skctchcs.

(Bronisch, F.W.: Reflex examinations. /Medicina/ modificd illuslrations).

'·

•..

..

Albert Szent-Györgyi

Medical Univcrsity

Dcpartmcnt of Ncurology

and Psychiatry

NEUROLOGY

Namc:

Agc:

Occupation:

Highest education:

Autoanamncsis (Heteroanamnesis)

HISTORY CHART

Da te:

Patient admitted by:

Prescnt complaint and disease (main complaint separatcly emphasized):

34

lt d ll ual history:

1 ) 11\llllS lfü lCCS of birth:

normal delivery: 0

0

prematurc delivery: 0

acsarca section: protractcd ,delivery: 0

forccps or vacuum dclivery: 0

no data: 0

l 1 11 nl lo speak: intime: 0 latc: 0

1 , 1111\l lo walk: in timc: 0 late: 0

1 h JO I progress:

good:O satisfactory: 0 bclow standard: 0

right-handed: 0 lcft-handed: 0

t li ldhood diseascs and vacéinations:

1°1 •vious diseases:

hypertcnsion:

metabolic diseases (e.g.: diabetes mellitus) :

cardiovascular diseasc:

ostcoarhropathic disease:

gastrointestinal diseasc:

hematopoietic disease:

urogenital discase:

venereal discase:

othcr:

e pcration:

l11jury:

head injury:

spine injury:

Iin1b injury:

35

Loss of consciousness:

Previous diseases of the nervous systcm:

typc:

Infcction during the past week: yes:

yes:

0

Gynecological history:

first menstruation: Last menstruation:

Pregnancy: Delivcry :

Usc of contraceptivcs:

0

no:

family history:

fathcr : mother:

brothers, sisters:

wifc - husband :

Diseases in the family:

hercditary disease:

ncurological and psychiatric disease:

cpilepsy:

malignant discasc:

tuberculosis:

other infectious diseasc:

left-handcdness:

hypertension:

child:

metabolic diseasc (c.g.: diabetes mellitus):

venercal discase:

othcr:

36

no: . 0

0

Rcgularity:

Abortion:

l 11 ' 1w1 1n ·nta l and social history :

Jiv ing conditions:

workp 1 acc:

ni •hl work:

1111t1•1:

ll11111lt1 nts:

tii 11liu 1:

111ti1•1tio ns:

11 •1 ~y :

cigarettc:

1 h J •r •ns itivity to medicine:

coffce:

1111•1 itc: Change of weight: Weight gain

l 1 1 • ·111 ion: Urination: Scxual func_tions: Slcep:

l11tportanl prcvious e-xaminations:

•.

SPECT:

MRI:

CT:

isotope examinations:

ultra-sound:

angiography:

mydography:

XR:

CSF cxarnination:

EEG:

clcctromyography-ncurography:

cvok~d responses (scnsory, motor):

othcr:

37

drugs:

We-ight loss:

Captivity:

Name:

Build:

S kin:

Visible mucous membranes:

Thyroid gland:

Lymph nodes:

Bone structure:

Spinal column:

Muscles:

Joints:

Abdomen:

Lung:

Heart:

Pulse:

pain:

resistance:

RR: . ./ .. Hgmm

Urogenital system:

Present state

Nutritional state:

Tongue:

Tonsils:

liver:

spleen:

38

Date'

Respiration:

Temperature:

11 11 . „1rnp ·:

pr· ·ssurc points:

1\. ·k:

1 111 111 11 ·rvcs:

Olf"action

11 Vision

Visual ficld:

h 111dus:

Pup il s:

111 IV.- VI. Eye movements:

Nystagmus:

Motor branch:

Scnsory branch:

11 ,

11 1. 1-learing:

Weber:

Vcrtigo:

Ncurological cxamination

circumference:

Kcrnig:

Brudzinski:

Masseter reflex:

Other excitation symptoms:

1 •• Pharyngeal pillars: Pharyngeal reflex:

Uvula: Soft palate reflex:

Speech

1,

' II . Tongue

'1 ·1Ísation of taste:

39

40

Motor system:

Reflexes: Pathological reflexes:

Upper limb: Invers radialis:

Biceps: Hoffmann:

Triceps: Trömner:

Radial: Wartenberg:

Ulnar: Palmo-mental reflex:

Babinski:

Oppcnheim:

Gordon:

Mayer: Schaefcr:

Léri: Chaddock:

Abdomen skin reflexes: Rossolimo:

Cremastcr: Mender-Bcchterew:

Lower limb:

Patella:

Achilles:

Plantar:

Deep plantar:

Adductor reflex:

Muscle tone:

Muscle strength:

Movement disturbances:

Coordínation: Finger-nose test:

Knee - hcel test :

Cerebellar tests: Romberg:

Bárány:

•..

41

11111! 1. ~ 1 · 111 :

J lnl v • systcm:

I' 1 lt • 1.1111 ·:

111pl ll liS indicating lobar injury:

11 11\lillll'y:

t t 1'1 lh ·lica l diagnosis:

1111i 11 uti ons to perform:

•..

-\~ 1 1 , ..... 1

Culon suroe l~r.

f'lonlor lat,

Trlgemtnus 1. „~„ ____ „

Occlplt. minor 1'- Occ:lplt. · \ molor 1

1

Oblurolo1\us

Culon. !iUroe meJ.

Cuton. suroa lat.

Plant. lat.

1 1

,\ '· 1 ,..,._„„ I

1 1 , 1" \

-1 I > I I ~ ! ~ \

f f lnlcicost.7,"\ 1 r romi 1

1 lnler- rost. t cost.f / I romi I 1 lot, I \ 1

1 , r

',\ \ \ \

1 I' I 1 j „

.J 1

~ \ ',----\

\ I \1 1 1 1 1, l.'

7:~1· Culon/() lot, \ fem./ \ 1 po•I. \ 1 f 1 r 1 1 1 1 1 !-+ I

1

1 L 1. 1

1 1

'' .... -~l 1

l J f\ I \ I \

\ I \ . ,sz. \ 1

t..s \ \.

1

' I I

I

st

,, 1 j' 1 1 1 1 1 \ti~

Tric eps reflex

, ,

Mayer's reflex

Lé.ri •s forearm symptom

•.

..,

, ,

Supporting reaction

.,

Excitin g abdomen k- . , s in reflex

>.

. ..

, ,

Special thanks to my colleague,

Katalin Jakab, MD

assistant professor of clinical neurology

for her he.lp to compile this material.

Thanks are due to

Délia Szok, MD

rcsident of clinical ncurology

for her editorial assistance.

52

Supporting reaction

•.

,.,

Abdomen skin reflex

•..