nN 3! Consider severity/ decompensation /compl Pericatitis may lea to pericardial effosion and even ta pponade (smallvolume pulse, hypotension, used VP). An ECG might show small complexes. Echocardiography is essential to estimate the volume of fuid accumulated assess cardiac conactiity and guide diagnostic or thera. peutic pericardiocentesis.Periardidis may be part of & ‘myopericarditis in which the Goponin is elevated. Con: surctive pericarditis eauss diastolie dysfunction Consider function ‘Tell the examiners you would establish the limitations provoked by any symptom. tions Discussion What ECG changes may be seen in pericarditis? ‘There is dassically concave, saddle shaped ST elevation, typically more widespread than in ST elevation myocardial infarction, involving more than one coronary tesitory. But it may be normal. Tewave inversion may occur betore the ECG normalises. Atsal epolaristion is affected, leading to PR elevation in aVR (in association with ST depression) and PR depression elsewhere (in association with ST eleva tion). Q waves do nat develop and reciprocal ST depres sion does not accut Cardiovascular and nervous system Table 3.25 Signs Sfererating cance pects For cardiac tamponade Constrictive pericarditis Prominent any descents Tamponade Prarinent de ‘essmauls Sin postve Kasai sigy negate Pals pads prevent Ne peal iock Dubus paadons urconmon Prraral krack How is pericarditis managed? ‘This i symptomatic with non steroidal ant inflammatory drugs. Anticoagulants should be discontinued and any tondenying eauie tested, Steroids may be given if it relapees Which signs help differentiate constrictive pericarditis from cardiac tamponade? Differentiating signs are shown in Table 8.25, How is constrictive pericarditis treated? 1m addition to eating underlying causes, pericardectomy is the definite teatment to release constition, econo Beene) EXAMINATION OF THE NERVOUS SYSTEM - OVERVIEW Context Candidates (and examiners) find neurological examina ton difficalt. They find it difficult to know what to do, ‘what they are looking for and how to interpret their Findings. ‘The nervous system is complicated the human brain comprises one hundred billion neurons, each newron ‘making thousands of synaptic connections with others, and it hae been calculated that the number of possible Permutations of brain activity or information exchange ‘exceeds the number of elementary particles in the known. ‘universe, Not surprisingly, diferent neurologists and cog nitive neuroscientists have diffrent ways of approaching such a complex body system. And more than any other specialy, there is often a sente of inaccessibility to those age olside it. Lists of signs are somewhere in memory, like fragments of jigsaw, but form no real pieure ‘Absent ankle jerks and extensor plantaris alist learned by ote, exoner ated fo a mythical proportion of diffculy. Alnough science is poised to understand a lot more about the human brain, to demystify the walnut shaped piece ofjelly that subserves ll that humans think and do, neurologists and neuroscientists remain in the shallows You may feel you have not set foot in the water, but remember that inthis largely unexplored ocean your inter pretations may be af valid ar anyone's, To make some sense af the nervous system, itis necessary to oversimplity it, and there is nothing wrong with Unat To get glimpses ‘of haw it really worke, two things often help us. The fst 4s to understand things from an evolutionary vantage; this, ‘often helps fo explain why things might beso, The second, is (o understand neurological curiosities, anomalies and disease; these often help 10 explain how the normal brain works. More and more, study of curious diseases is provid ing insights into the murky neuroscientific ocean, exchang ing it for a giant aquarium asthe windows slowly slot nto place "Neurological examination ie best performed in context. Rather than trying to examine everything hurriedly and with litle grasp of what you are looking fr, tis beter tobye seloctive, Patients with different neurological probleme ‘nee diferent types of examination, Levels of the nervous system A basic grasp of how the diferent levels of the nervous system and patterns of signs that arise from disease at dif ferent levels helps candidates know what to do, what to look for and how to interpret thet findings. Interpreting {ndings should be anatomical and pathological Anatomical interpretation of findings Auempt to identify there s one or more than one lesion. and the level or levels involved (Box 3.17), Findings may form a recognisable syndrome such as Horner's syndrome ‘or Parkinsonism, but diseases may also coexist A combi nation of upper and lower motor neuron signs in an older patient is common with cervical myelopathy, multilevel radiculopathy and peripheral neuropathy. Remember that systems degenerate with age and as neuronal reserve eclines so vision, hearing, balance, reflexes and gait can change. In general signs ate mote likely to represent pathology if there are asociated symptoms. If you think ‘pethaps the left iceps jer isa litle les brisk than the sight, it may well be normal Pathological interpretation of findings Consider which dlseases ae consistent with the anatom cal findings. History taking isthe most important part of Deutologial assessment because helps localse the evel Sd site ofa esion and determine te duration ~ inert ient unilateral headache for many yeats is lkely 10 be Inigrain, abrupt hemiparesis and faa weakness crebal itchuemla, wertening. sensory symptome over a. fe ‘months in the median nerwe distribution carpal Cannel ‘drome and so forth, Since histor aking snot postle iN PACES, the examination schemes that follow ate selec tive sequences appropriate forthe cscs that are Uikely to foceur im PACES, With any examination, remember that neurology ls highly observational specialty, Much can be mised by sepping forward instantly to. examine ands on rail res (pergheral ens of he head and nec) Cerebral hemispheres Brainstem vapid system ard cerebellum Spinal cord New senses Neve rot Speetcnenes Nevromssel union Musces ri | EXAMINATION OF THE CRANIAL NERVES Introduction Cranial nerves in context ‘When we examine the limbs we consider upper and lower neuron lesions. Cranial nerves are simply lower (motor, sensory of both) neurons. Examining them in order from Tto XII detracts from the concept that these peripheral nerves connect proximally via their nucle) with central ewes and ditally with neuromuscular junctions and muscles (Fig. 3.17). What we are really doing with so- falled “cranial nerve’ examination is examining the head and neck and when examining head and neck neurology ‘functional approach is more logical than a numerical ‘one ~ examining ‘the eyes ‘visual fields, ‘eye movernents and so on rather than the cranial nerve ‘The value of cranial nerve and long tract lesions in localisation Ceanial nerve nuclei ate where cranial nerves synapse with their supranuclear pathways within the brainstem. Many brainstem lesions may, theoretically, be localised by cranial nerve lesions and long tat signs Cranial nerve lesions Brainstem lesions can be localised in the vertical plane by cranial nerve lesions. The 12 nucle broadly descend from cortex Santen Irtarulear tows Spina card Figure 3.17 Supranuday nudear ard nf ext arangenen of asanN 3! midbrain to medulla (Fig 3.18). In reality these are more than 12 nucle, some nerves with a main nucleus and smaller satellite mucle, Long tracts Brainstem lesions can be localised in the wansverse plane bby signs of damage to long motor and sensory teacte (motor being ventral co sensory) ‘Cortioapnal tract (Fig 3-19) are long motor tacts that descend from the precental gyrus of the frontal lobe, ‘through the internal capsule, cerebral peduncle, midbrain and pons, and decussate at dhe medullary ‘pyramids to supply the contralateral limbs. They are sometimes called pyramidal tacts. Att fibses lie medial to leg fies, Fibres synapse a their destined ventral orn exit sites in the spinal cord, Supranuclear pathways destined to innervate ‘Cranial nerves descend with the corticospinal fibres as far as the brainstem where they decussate and synapse with fnd innervate their respective cranial nerve nuclei and. ‘cranial nerves, which may be pure motor, pure sensory, or both. Supranuclear fibres innervating the lower cranial nerves that mediate speech and swallowing ate often called coricabulbar Sbres (Fig. 3.19) ‘The dorsal columns carying sensory information for accurate localisation of touch, vibration and propriocep- ‘ion synapse and decassate in the medulla and project to the contralateral thalamus and parietal lobe (Fig. 320), ‘The spinothalamic tracts carrying pain and temperature information have already synapsed and crossed lower in the spinal cord and also project to thalamus and parietal lobe (Fig. 3.20). Supranuclear fibres from sensory cranial nervecand their nuclei (eg, the wigeminal sensory nucleus) project to the contralateral thalamus and panctal lobe (Fig. 3.20), The exception is the comeal reflex, whete ‘evolution felt a rapid protective response would be best served by an involuntary relay between trigeminal nerve- mediated sensation and facial nerve-mediated eye closure within the brainstem, There is bilateral supranuclear innervation to the trigeminal motor nucleus, sich that Figure 3.18 Location of carial neve uch in he trasten; 3 cle resent iter, 490 Cardiovascular and nervous system Corea estan Convaltraline en Contalatral supanidear ‘earl ene ans Brann esn ——~ * Conlin sins “Iptlteralaral nave se, 2g Weterssydame [esrtalstera weatress, ‘palatal enor ply) Mol edly decusaton eines Figure 3.19 Coral ves trast lions. Cerebellum not shown fer serlcation (and thr ceria ores wy senry es) Figure 3.20 Sensory pathways om the sinal cord othe pital (tec isthe bonerchewing persists in the face of hemianacsthesia. Chewing Js more important co survival than facial sensation! Al of chit information has localising value (Box 3.18). Implications of multiple cranial nerve lesions -Muluiple cranial nerve lesions may oceur where nerves run closely together (often resulting in the recognised syn romes in Box. 3.19), in generalised disorders. (eg, myasthenia gravis) or as a result of multiple discrete lesions (eg basal meningitis, stokes). Olfactory nerve (1) (Olfactory testing is seldom expected in PACES. 2 cotillion sucha an itral eagle ote may ese Cental ong Yat sins ard conte spare cranial sisi, 3.19 the tongue an face are tected on the sae Side a 3 eripaess the sion must be spans (othe ‘wel and seventh nude, respecte, Howees some canal res indeed mast eee lata prance enaton and ‘ncten i urateced. The geminal motor aces sone example, and facial neve fbessuophng the upe face note ‘par parachites fe chewing aa ee protection cary sania advantages Spare garacutes fo the bulbar cal nes (0, X i) oten exist ut fen requie recites before they Become bileced~ i ot unearmtn fling acral sve to develop speech an suaowingproblens that mprove with renailtaten ashe bra’ plasty declares ssl Brainstem lesions Abrastemlson may case contralateral fng tract ign fhe Iason is above the medularydecsatin ofthe crtossinal tacts and das columns; te spinotalanic acs have already cossed the spine ard any pain ad terperature los cowalteal0 the se of arate Ison wih satel can neve signs becouse te cal neve nel onan atecamaged Sealy {Fc 3.19) continaton s sometimes refered 135 cessed sions lesion or example, athe eel of he mira i lvoe the pons if Vl ots ivohed and te red IX orl ae led A raiser lesion may exe alte, enelnation,spae-ccoyng lesion, basar ary achisen) ‘using bint rar or sensory ong ac anc cranial neve sions Untatealy, il an Vil cerebelopantine ange kin Unio IV. ana VI caveraus Sus son Unto, X an — jugular fear lesan 1%, X, and Xl — babar pay ri | Eyes sual acuity (VA) - optic nerve (1) VA testing is seldom expected in PACES. Problems with VA may arise ffom refractive ertors, anterior eye disease such as cataracts or retinal disease ‘© Ark the patient to close each eye in turn and read the lettets on a near vision chart at 30 em, Vision should be corrected with glasses ifthe patient wears them, buta pinhole could also be used to conzect refractive errors asi filters ost angled rays of light entering the eye. A.6 m Snellen wall chart is more accurate, Normal distance VA i 6/6, meaning that the eye sees at 6 m what it should see at 6 m_ 6/60, (ua levers on the 6/60 line are 10 times larger) ‘means it sees at § m what it should see at 60 m. If letters eannot be seen, bedside teste such a¢ counting fingers, seeing hands movements and perception of light may be performed ‘Test colour vision using a red hatpin, Central vision is colour (cones) and especially sensitive for red. Red desaturation, an impaired ability co detect se, suggests an optic nerve lesion, sual fields (VFs) - optic nerve (II) Different patterns of VE abnotmaliy arise fiom lesions at lifferent sites (Case 3.16). Vs are divided vertically into hnatal and temporal elds such that an object on your right looking ahead iin the temporal field of your right eye and the nasal eld of your left eye. VF defects are described fccording to the patient's perspective and are homony- ‘ost if the samme part of the VF is affected in each ee, Sic just under one arm's lengths away from the patient and at the same level, Cover one of their eyes, lose Your opposing eye and ask the patient to look at you. Slowly introduce a finger or white hatpin in a plane halfway between you and the patient from teach quadrant (Fig. 3.21), ensuring thatthe pin cannot be seen when you start A white pin is ued because peripheral vision is monochrome. Major VF defects ca he screened for using the method shown in Figure 3.218, asking the patent to tell you which index finger or hand it moving, right, left or both ‘© Examine fora scotoma by moving the hatpin (a red cone will detect more significant deficits) slowly at tye level in a temporal fo nasal direction and asking the patient to tell you if it disappears or changes colour In a central scotoma there will be lose of ‘entra Vision, The blind spot 30° into the temporal field ean be mapped in the same way It coreeponde to the optic disc Pupils ~ optic nerve (ll), oculomotor nerve (It) ‘© Check pupils are of equal size and shape Prosis fon the side ofa larger pupil should alert you to a 491Figure 3.21 Vial eld testing (8 conoratin method (8) screening fo ge etc thind-nerve palsy, and on the side of a smaller pupil to Horners syndrome. ‘Place your finger 10 centimetres in ftont of the patients nose and check the accommodation, response (Box 3.20). The eyes should constrict a they converge. 4 Check the direct and consensual light reflexes by shining the light twice in each eye (Fig. 3.22, Box 3.20) ‘© Note any afferent pupillary defect by swinging the light repeatedly (the swinging light test) from eye to ye, dwelling for a second or two on each eye (Box 3.21), Observe paradoxical dilatation ofthe pupil of an atfected eye, implying a damaged afferent pathway (optic nerve). 492 fdrge= yeaa ne ‘Deulometor “i geniculate tree) Seren a fe ‘res ord short ‘lary rerias Shier pul seuce trent pata —— Fran paws Figure 3.22 The lon es, Light reflex Light inpbes vavel lng the optic neve and both otc vac. pronmaaly 10% of res eaching te level te teal (gercalat gagionsuaserve te ght rex andcomectwth both Ecinger-Wesiphal ruc and adocer tirdsteve mc in te peroguedictal mater ef he mata arsympahe es, fertwned around both oaomior aves, are ‘excied’ by the Lg ‘pubes, and stimulate he clay gang, clay reves and imate he aula sphincter muscle of e3er ppl eauing bilateral puplay eonstrcn ‘Accommodation reflex 2 sar efferent chanisn subseresaconeaditn,atough ‘he sferert pathy iin te oral be athe than the ope reve, Thetit-neve nuchal cone the ation of the medal aus muscles and convergence. The clr eves also spl) the ‘ian mul, aetng thelr’ shape fr foeusng. Many mare ‘lin foes ae deat rote cay muscle than co he pupary muscle and te accommadton rele soften regards as 'seongar than te Ight efx Tis may be he reason Ny accommodation 5 reseved othe ureacve Agi Raberton pa.Wis eles onthe fc that the pup rece ua ineraton from ‘he mish, 2 Shing ght the teed eye causes absent or sug rec ana consensual sponses, 8 Shaing gto ch ramal ee stints arma ec and consensual responses, theres complete damage othe afferent catiway of the affected ee, whatever ling the naval ee (dominant ‘espense sexpasee to wl determine te Seo th pls ‘Wen gn is swung bakit the ated eye the nomad ‘up bes and so des the afte pul thee sparta anage tothe affeentcatoay cecavey fm 8 (he dominant ‘espense is sites and srenger than te sluggin eszorse to fo the ated eye sil es, The ter tren 353 ‘et afferent pupa dele An APD i abo known asa Yarcus Gunn publ Eye movements ~ oculomotor nerve (lil), trochlear nerve (IV), abducens nerve (VI) ‘+ Observe the eyes in primary gaze. Misalignment may be due toa latent strabismus (constant convergent or divergent strabiemis in all ditections of gaze), ‘hire -nerve palsy or skew deviation in which the eyes are aligned im different vertial planes (brainstem pathology) ‘+ Observe slow, smooth pursuit movements used for fixation on a moving object (the lioness on the Serengeti eyeing a roaming zebra or gazelle). Do this by gently xing the patient’ head with one hand and ask the patent to fllow the index finger of your ‘ther hand using midline horizontal and vertical movements, not letter I, Look for an ocular paley {dye toa lesion of Ii, IV of VI. Be alert to move than fone lesion, Ark about dauble vision, Also be alert to supranuclear disorders of eye movements that may rot result in double vision such asa lateral-gaze palgy (frontal or parietal lesion when the patent Tooks away from the side of the lesion or pontine lesion when the patient cannot look away from the side of the lesion) ot a vertial-gaze palsy (upper brainstem lesion), * Observe faster saccadic movements, the rapid ‘movement from one point of fration to another (the zebra or gazelle eatches sight of the ioness), asking the patient co look ftom side to side. Tis ‘ay elicit imernuclear ophthalmoplegia, ‘© Note any nystagmus, normal a extremes of gaze + Note any ptosis Fundoscopy Fundoscopy is discussed in Station 5 opine isin vary avon Diverse son [Di secen cervical ct Tid corviaraet, Figure 3.23 Faia sersatan ser Testing the comeal efx. eas 15 inscate he dsb of sensor Fires ro te th eve’, long mucus ra exten or te pons 1) tothe upper cea card (5) theimplcaton of isis that ftuceus srs, nt fh-neve less, roduce later both eu’ tected) ‘nin tn’ patens acl sense ss. Trigeminal nerve (V) ‘The trigeminal nerve is sensory to the face and motor for the muscles of mastication, 4 Feel for any wasting ofthe masseter, the muscles of jaw closure ‘© Ark the patient to clench their teeth (maseetere) and ‘open theit mouth against the resistance of your hand fon their chim (pterygoid) ‘© Test light touch and pinprick in the ophthalenic (V,), maxillary (V,) and mandibular (V,) distributions (a 323), ‘Tall the examiners that you would check the corneal reflex (Fig, 3.24) with a wisp of cotton wool (touching the comea, not the white sclera), its absence often the st sign of a tigeminal lesion est the jave jerk (Fig. 3.25), which can be brisk ith bilateral supranuclear lesions above the level af the pons (eg. pseudobulbar pals). Facial nerve (VI This is ‘oti tor to the face and provides taste to the anterior sof the tongue. © Look a facial symmetry, noting the nasolabial folds and forehead wrinkles and watch spontaneous Iovernents such ae smiling and blinking ‘© Ask the patient to show you thei teeth, whistle of blow out their checks, close thei eyes tightly and 493Cardiovascular and nervous system Figure 3.24 Facil nerve examination. Ask the palin odo the fling: (8) show me your teeth, () pl your cheeks cu (se your eyes Ugh and donot etme open then, and 2) ase your eyebrows Figure 3.25 Fling he jo jt Took up atthe ceiling, again looking for symmetrical ‘movement (Fig 3.24). Bells phenomenon (eye turns ‘upwards on attempted closure) is due to a lower ‘motor neuron lesion ‘Compare power in the forehead and lower face, Since upper facial muscles receive bilateral, supranuclear innervation, unilateral upper motor ‘neuron lesions spare the forehead whereas a facial nerve palsy (lower motor neuron) paralyses the ‘upper and lower face (Case 3.25). Bilateral facial nerve lesions sometimes occu tosis ie not due to a facial nerve lesion. Hearing Hearing testing is seldom expected in PACES, Clinica tests can be unreliable, as demonstrated by formal audiometry Rinne’s test Rinne's test (Fig. 3.264) compares sound from a vibrating 512 He tuning fork on the mastoid (hone conduction) with the extemal auditory canal (air conduction) 49a [Normally sic conduction is beter than bone conduction, ‘one, denser than ai is actualy a better conductor of ‘unimpeded transmis texcernal canal tothe middle ear tion a Rinne positive test Ifbone conduction is bette, this implies conductive deafness (everything other than the sensorineural aspect of hearing is conductive), usually due to middle ear disease of wax, Weber's test In Weber's test (Fig, 3.26C), sound should be heard in both eare equally when the tuning fork is applied to the central forehead or vertex. In_sensorineutal deafness, sound is not detected by the affected ear. In conductive Aeafness sound is louder in the affected ear although this phenomenon is dificult to explain, Censainly, when a tuning fork is placed recy on bone, there is no signii> cant sound transmission through the air and all conde. tion is Uarough bone to the inner eat Any additional slid ‘material in the ear (eg. vax, tympanosclezosis, middle ear brs or even poking a finger into the eat!) is likely to attenuate the normal energy loss at a bone-air interface dnd enhances sound transmission to the inner ea from the vertex Bulbar function - speech and swallowing ‘The lower (bulbar) cranial nerves IX, X and Il are inte- gal to speech and swallowing. The proximity of these nerves implies that several combinations oflesion aze por. sible, and that presenting symptoms may be similar what ver the diagnosis ~ ort of strength in speech and swallowing with hoarseness, nasal speech, nasal egurgita tion of fluids or food particles with aspiration and attacks ‘of choking ~ in other words, a bulbar palsy (Case 3.26) Glossopharyngeal nerve (IX) “This is mostly sensory, relaying information ftom the palate, pharynx and posterior third of the tongue via theFigure 3.26 Rinne’ ret Bone conduction (A) ard a conduction 8. (C) Weber tes placing the turing fr on he teeth s mere snsve ut on tobe done wih cre wigeminal nucleus to the sensory cortex Its motor only to stylopharyngeus. A glossopharyngeal lesion is rare in Jnolation and invasiably part of a wider bulbar palsy ‘© Touch the palate each side with an orange stick ot touch the pharyngeal wall each side with the patient saying ‘AaN’, asking che patient to compare right and. lek. ‘+ Touching the posterior third of the tongue is of less value, ‘©The gag telex (sensory via IX, motor to palate via X) fs untally too grose to test and unreliable, aot present in many people Vagus nerve (X) ‘This is motor to the palate, pharynx, larynx and vocal cords and sensory (o the tympanic membrane, extemal auditory meatus and external ear “© Watch the patient say ‘Aah’ The palate and uvula normally move upwards. In a vagus lesion the paralysed side is immobile and tends to be pulled ‘owards the intact side. The palate fails to elevate snd the uvula i seen dragged across tothe ‘unaffected side. It may be completely it»mobite in bulateral vagus lesions These problems lead to the bulbar palsy symptoms described above. '¢ Assessment should inchide voice and cough as well, as palatal movements. A paralysed vocal cord les lumpy abducted to the midline, giving rise to a hoarse voice and a bovine cough Since sensory fibres feom X ae conveyed in the auricular branch, malignant lesions of the throat may sometimes cause earache, as may the common cold, Hypoglossal nerve (xi) ‘his is motor tothe tongue “© Observe the tongue at rest It is paralysed on the side of lesion and deviates to the side of that lesion. It say alzo be unilaterally wasted ‘On attempted tongue protrusion, the deviation can become more obvious ‘Tongue fasciculation is best observed with the tongue at rest inside the mouth as normal rippling movements can occur when the tongue exerts ital Coordination of cranial nerves in swallowing Pethaps the best test of overall bulbar function is to ask. the patient to drink a glass of watet. Swallowing is a ‘complex process involving many cranial nerves and com prises a voluntary phase, a telex phase and an octopha {geal phase. In the voluntary phase VII holds the mouth shut. IX relay information abot food bolus position to the sensory cortex, V controls chewing IX senses the amival ofthe bolus atthe palate and XI pushes the chewed bolus up and back against the palate. In the reflex phate XII pulls the byoid upwards and forwards to bring the larynx beneath the back ofthe tongue, IX, via stylopharyn ‘ges, atest the hyoid elevators and lifts the larynx for ‘wards and X elevates the palate to occlude the nasopharynx (preventing nasal regurgitation), flips the epiglouis for ‘wards over the top of the elevated and tilted larynx (pe ‘venting food falling into wachea), dlates the hypopharynx {allowing the bolus to fall into the oesophagus) and init ates oesophageal peristalsis, Accessory nerve (X!) This innervates the trapezius and stesnocleidomastoid muscles Test trapezius by asking che patient to shrug thei shoulders against resistance (Fig. 3.274), Test the stemnacleidomastoids by asking the patient to sum their head against resistance (Fig. 3.278). The sight stemodleidomastoid turns the head the lef dnd vice versa, 495. ae Figure 3.27 Tsing the acessery nave: () tapers 8 et serrdedonasio Summary ‘A summary of the cranial nerve examination sequence is the Summary box SUMMARY BOX ~ CRANIAL NERVE _ EXAMINATION SEQUENCE 1 4 Tes: visual acy anthem cour von sng are hatin 1 Tes ale fan ital ren detects major homanyrous eefecs, © Check pupil sze and save $ Tes the tconmesaton cele | © Tes the diet an consensual igh tenes an cece or an 1 ret pilin eee. & Lok atthe eyes primary onze and nen test eye movers © Nese ay icermuarophthalrapeia. © 9 ioe any stags © © tio any poss, © @ Testmasster sent, es toun nal te cisions o te geminal neve antl 1 the earners you woul chek fra crea le, | © Leokat al jmety and tt fc movements sting any | pper and veal sean, © Teli exainers you woul fomaby assess heating inthe presence of symptoms arn the presence of ceebeleponne | pesrpathes, 5 Test palatal senstin 1 @ Tes ul and palatal movenen: 1 © Look atthe tongue atest insice the mouth for dato, | swasing and elton an the ek or mere bau |. Seven of a robutedtng.e | Terthe aeesey nen 496 EXAMINATION OF HIGHER CORTICAL FUNCTION AND SPECIFIC LOBES Higher cortical function Examining higher contialfanction adequately is complex and cannot be performed in PACES. A 30-point mini- ‘mental state examination is frequently performed on the wards, and a l0-point of 4point abbreviated mental test, score an inital clerking sereen (Fig 3.28), Lobe syndromes ‘The cranial nerves send sensory information to the brain and receive motor information fiom it Likewise, the res, Of the body, through peripheral nerves and nerve root, sends sensory infotmation to the cential nevous system fand receives motor information fom it. Some of thie information does not involve the hemispheres ofthe cer. cbral cortex ~ the comeal reflex for example, and spinal feflexes But for most information, the corte it involved, perceiving everything in our world and initiating almost everything we do, Its diferent lobes (Fig. 3.29) have spe: tfc functions The frontal lobe ‘This ica motor lobe plans, iniates and ‘executes’ tasks, known as exccutive function. The precental gyrus puts thoughts into action; itis here that the eacade of messages to move a body part begins. Functions ofthe frontal lobe ate shown in Box 3.22, The posterior parts of the lobe ate ‘most important to motor function, the more anterior parts to behaviour Frontal Jobe disease may result in those features in Box 3.23, The frontal lober aot only inhibit ‘undesitable behaviour but also primitive reflexes that are present at birth. These may be disinhibited by frontal lobe Sisease Connections between different parts ofthe brain explain ‘many neurologial signs. Patients with Parkinsonism may have a positive glabellar tap because of disease involving the frontal lobes exrapyramial connections Flaming, organising, sequencing, abstracting, ination, Jadgeret,se-evavaon and sight Inaton ct movement Speech expression ioling Brac’ speech ae (nthe sominar herihete) olay conta of miition ‘Tremore enigmatic aspects of inking and bebacu such as visdom, telgence arbiter, ral serse and judgement, in ‘eat with al pars ofthe crix ways in which Scene has inte uncesandng equted socal behaviourri | Mini-mental state examination (MMSE) (ONE PONT FOR EACH ANSWER ORIENTATION Year Month Day Dale Tine 6 County Town Disiet Hospial Wad 5 REGISTRATION Esai: names 3 objets (9. apple, el, penny) Pale asked to repet (1 pi reach core). then pale’ eam he rare epeatng ul coret 8 ATTENTION AND CALCULATION Siac 7 for 10, ten repeat fom eau Conte tres: 1008 8 7985, ‘tara: spl WORLD backwards — tow 6 RECALL Askforrames 8 objets armed eater 8 LANGUAGE Name perl and watch Repeat No ads rut Hn ‘Give 2 3-tge command, Scare for esch sage eg, Plas index ngs of iaht handon yur rose andthe on yu a 8 ‘Ask panto read and cbey a witancorerard on poof paper lang ‘hse yeureyes A Dak pant towne a sertonce, Seoe iti eens and hs aublet nda ve Hn ‘COPYING ‘Aske ptt copy a par ofresetingpetagos TOTAL 0 Figure 3.28 Min-nentl sat examinton, The parietal lobe ‘The parietal lobe contains the sensory comex oF post central gyris, Unlike the frontal lobe, the parietal lobe very Imuich senses, and x concerned with appreciating. the world around us, creating a three-dimensional sepresent tion of the spatial layout of the external world, and also ff your body in that three-dimenstonal representation Both the dominant and non dominant parietal lobes ate concerned with recognition and awareness. Rot relay the ppaictal radiations of dhe visual pathways, Disease in a parietal lobe may manifest self broadly in one of two ‘ways (Box 3.28) lesions may cause a single problem or a recognised syndrome (Case 3.30 Agnosias and apraxia) The dom nant parietal lobe is usually lft sided (even in lef-handed 497cov atl ee [rwsstie Figue 3.29 Lobes of he bran people, whose ‘dominant’ hemisphere we often assume as being the right). There is much overlap of dominant and rnon-dominant parietal lobe function, but apraxias ate common after left parietal damage and neglect or sensory visual inattention after right parietal damage. The temporal lobe “The temporal lobe subserves memory (hippocampus and other areas) and emotion, certain aspects of perception, interpretation of numbering and colour, central represen tation of hearing, taste and smell, speech interpretation, tansmission of visual impulses via the temporal visual radiations, and some aspect of behaviout via frontal lobe connections. Lesions may result in memory impairment, auditory agnosia {tempato-parieal connections), catia deafness (iTbilateral) and receptive dysphasia. The limbic system ‘The cerebral hemispheres perceive and initiate, They contact the outside world through sensory and motor pathways. But what of the inside world? There is extreme complexity in the visual pathways relaying what we sec, but we always see a particular object in the same way. A. ronlkey always looks like a monkey, a giraffe giraffe, and ‘we would not mistake one for another But the visual pathways are crude compared with mechanisms of recog nition, learning thought and emotion, The limbic system is a deep part of the brain, part of the medial temporal lobes, where science has more questions than answers, I thas 10 do with memory Itis also thought to be a centre 498 Cardiovascular and nervous system + Executive dunt an apathy (ks of inate an abla {os of somanery) + Akewsia(tficaty with movener) Motorex expressive pha {if dominant hemisphere) + Incontinence 4+ Behavioral and moos dsurbance and sinibition Primitive reflexes + Grasp stoking te palm induces 259 + Faloomertal— fim stroking te hear eminence induces an iplatal grimace + Rooting ~ stking th cheeknduces a grawing mou + Sudkng— ‘outing the is eromeessucting + Snout taping the uper fp makes it pucker upnards ‘+ Gibellar— taping te eehead stmuates ee dese ‘Agnosias ‘Thre is ct in recognising tings, desi ntact sensory pathways percha tothe prea oe. Thse probes with Fecagton ae oten seed agnasae Apraxias ‘Thre isfy performing tats, not becuse of any peoblem vith mor ners oF muses, which ae all tact, but case the arta ue also process inernatenabcu the enone. k ‘wold narmally pass on ths processed nforatin tothe fot abe which in tun weuld normaly ite a cus faci in reigone to Tas relens wth ertorming st are cen tered srs or apanias for smell. Have you nodied that some smells instantly vole distant memories? The occipital lobe ‘The occipital lobe is the common endpoint of the visual nerve pathways. Lesions may result in comical blindaes, Visual agnosia (paieto-ocepital connections) or speci visual processing defecte such s¢ impaired perception of colout or movement, EXAMINATION OF SPEECH AND LANGUAGE Fnsure thatthe patient can hear, then consider in twsn if there is © Dysphasia © Dysarhria * DysphoniaDysphasia ‘Types of dysphasia Dysphasia i a disorder of language ad refers to the ina bility to understand or ind words (Table 3.26) because af lesion i the dominant (usally eft hemisphere As well $e ify understanding or finding won from the brain's lexicon, common ater stokes snd easing frustration to patients dyephasia can be somantcor fuer epeech Ment Bhat televant or nonsensical, sally with Toss of sight, common in frontotemporal dementia) of phonic, i Which a word is almost corteet (eg bat instead of bal). ‘Wernick’ area recognizes sounds a8 language, but & higher concept area is required to convert sounds into reaning, This concept are then connect to Brocas aes, ‘where speech output is generated, A dieet connection, the Sreuate fasciculus, alo. exists between Wermicke’s and Broce’s areas. Transconical sensory dysphasia i similar to receptive dyaphasa but with preserved repetition and it caused by a lesion in the parietal-oceipital concept area ‘Transcortical motor dyaphasia esa to expressive dys phasa but with preserved repetition and isthe result of fn incomplete lesion in Broca's area. Conductive dyspha sia refers to preserved comprehension and output with lose of repetition and isthe result of lesion in the arcuate fasciculus. Difficulty naming objects, or nominal dysphe fia isthe raul ofan angular gyrus lesion, Examining for dysphasia Introduce yourself and ask a few simple questions, eg. Can you tell me your name and date of bith!" © Is there receptive dysphasia’ Give a simple ‘command, eg. ‘Close your eyes/ With your right hhand touch your nose’ and then mote complex, tseo-sep oF three-step commands # Is there expressive dysphasia? Get the patient talking farther, eg "Tell mea lite about where you live * Is there global dysphasia! Ifthe patient cannot perform either task there is global dysphasia (the lesion affects both receptive and expresive areas) ‘+ Is there nominal dysphasiaé Ask the patient to name some objects, eg ‘What i tis” (show pen, tie and ‘vatch). Ifunable to name objects, asks ita. © ri | Assess word-inding ability eg. ‘Name as many Animals as you ean think of! ‘© Assess repetition by asking the patient to repeat a sentence, eA gitafe isa tall, gracefl animal 4 Tell the cxaminers that you would assess reading and ‘writing: similar categories of problem ean aecut with other aspects of language such as reading and writing (dyslexia and dysgrsphia) Dysarthria ‘Types of dysarthria Dysarthta refers to impaired articulation and isthe result fof a lesion in any of the structures coordinating voice production Upper motor neuron lesion (pseudobvlbar palsy) “xirapyramidal lesion, eg, Parkinson's diseare (Cerebellar lesion Lower motor/ cranial nerve lesion (bulbar palsy) Nearomusculae junction lesion (myasthenia) Myopathy Local lesion of the palate, tongue or lips Examining for dysarthria Ask the patient to say some simple and more dificult (eleven benevolent elephants, baby hippopotamss) parses ‘+The sequence ppp, Il, Kk and a cough is a screen for lip, tongue, palate and voeal cord function, ‘igure 3.20 can be used to determine the type of dysar- lia; Box 3.25 describes how to differentiate bulbat from ppeeucobulbar palsy. Dysphonia ‘Types of dysphonia Dyaphonia refers to impaired voice production or phoma thon due toa lesion in the vocal corde of Taryn (uch at laryngitis) or vagal nerve supply, It is common when ‘muscles are weak, as in Parkinson's disease Table 3.26 Recepive ard expressive praia ive dysphas ably to understand een Expressive dysphasi Trail (6 ees, despite comprehension ‘nal fndngs Way be ent, bet werds reannglss Can cause mene Fusion o patients, who knw i thins what they ‘wan fo ay but ata ge he words tf es eee can ans questions a speak sportaresl but often stag, rang mish) Tecan often Weenie’ ara in the tenor lobe ray bea usual ts defect roca area in the onal labe (omnes to Wend’ ara bythe arcuate favceulis) Sys ede inp emma a ls ob "ray wl wo sigush eee and eee i, rd cna a we duce ngage ae: erent a Dyas way levees kth xe rcp cmpern sig mae came sue ass 2 nro lngane ks iy pale wt os waidg 499Figure 3.30 Dysarhra |3| Cardiovascular and nervous system, Bulbar palsy ua aly refs to ntanulea or lower moter newone dase, sal ivbing arial neesX (alate) or Xl torque) wh aca, nasal speech, aa speech escapes the charac ison of ula aby ard nasal regugtation of fui a food wth Choking 2 aspation maybe prominent. Aalegies are 'owning (thoting’ ana sense that ‘verytings inthe way. Te tongue Sens 12089 fr te owt a sees to hang ou wth slay pool, ts abt ee elacng a human's trgue wih a Labrador fogs torguel Patients sete ay it feels asf the moths ru like Bing the oenst ard carat sitet Pseudobulbar palsy Pseuobuba py ees to surat er ver nota rewone ‘dease oth spastic pene. ne ongve appeal and gh and anol beprtwded, hog ible on he Foo of he mouth ‘Analgesia highsithed’, Donald Duck, "ht potato’ or ‘srane’ speech. ilar suprarulearnenation of the wer (cabal nees necessary fr speech ane swalening mens ‘hat bea eatal ee brster lesen ae ace to Inuice 9 psuobubar aky. Cause rele bse intel caps ses 6 denjlnaton. Oar and swaloving probes acral Soke ae duet un baal surance aes, often 3 erbiation of fac and bulbar weakness, bt the spare parte ‘forded by Berl nnenatn ote sling sees means that tis 2 mucratenuates for of poeudeblbat zy.Examining for dysphonia '* Determine whether the patient coughs or produces a sustained ‘eee, Dysphonia with anormal cough Suggests a local (Iaryngeal) lesion. A bovine cough (without an explosive start) suggests vocal cord palsy Summary ‘A summary of the speech and language examination sequence is given in the Summary box ‘SUMMARY BOX - SPEECH AND LANGUAGE EXAMINATION SEQUENCE © srodue yous and ask fe snp questions 9, "an you tel me your rare and eae of Sith? (© Test ‘receptive ejsanasia with 2 simple command, eg'Cse Yost ees ith your ri hand oven our nase and ten more ‘omolx two of thestep conrad 4 “est iorengressie dptas gting the patent tak ore. "Can you el me atl about where you Ie)” © Conde gobal dyishasa Testor remialdsohasin by asking the patent to are some jects unable to name as eta. (© Assess wordncng aly, eg, Nar 3s many animals as you cathe ‘© sess epetton by asking he patient o epeat a sentence fg 'hgrafe all sre anna (© Tel the exainers ha you woul assess reading and wating (© Use me sequence pp, and a cough aap sen ‘orp. tongue pale and vocal cod uncon. “© Aske patito say some chases, eleven beneiclent ‘lepnant baby hipsopotamus. EXAMINATION OF COORDINATION ‘The motor cortex exert voluntary of conscious contol of ‘movement via ite descending motor pathways to cranial nnewes and conticospinal tracts and conscious sensory information travels via the ascending dorea columns, sp nothalamic tracts and sensory pathways from cranial nerve tothe thalamus and sensory cortex “That consciour motor pathways are not enough to control movement is evident from diseases of the extra pyramidal system. The extrapyramidal system adds wncon: cious fine-tuning to every move we make ‘That conscious sensory pathways ate not enough to appreciate the body's position in space is evident by dis caser of the cerebellim. The cerebellum ends sneon: ‘cious feedback to the cortex about every move we make. ‘There i. in essence, a loop (Fig. 3 31). The motor cortex initiates activity, movements are adjusted by the ext pyramidal system, and the cerebelhum provides feedback information about the movements made. ‘When examining coordination, be ware that the domi nant side may have a slight advantage '* Look for nystagmus © Ask the patient to hold their arms outstretched and close their eyes. Look for any oscillation, Mediates rr coral ‘ci Ccartcospal ‘rst Postalinormaion (inocorboler” estar ‘ads) inermsion Net that ale crear sion ilcaut a taied moran CGelrbance andi vers Figure 3.31 Tre op ‘© Ask the patient to touch yout finger, held out about fan arm's length away. Look for an intention tremor ‘or avershoot (past pointing). Then ask the patient to touch their nose. Repeat this movement at fast speeds, the patient touching your finger then their nose repetitively, but with your finger xed, not as a ‘moving target (Fig. 332A). ‘Assess rapid movements by asking the patient © twist their hand, as when turning a doorknob, and to tap the back of their hand quicly (and then rapid alternating movements by turing it aver and back ‘gain quickly), Look for dysdiadochokinesie. ‘+ Assess heel-shin coordination (Fig. 3328) © Gait, discussed separately, is crucial to the assessment of coordination. Cerebellar disease Incoordination in PACES is usually the result of cerebellar disease (Box 3.26) Movement disorders ‘Types of movement disorder are listed in Table 3.27. Dystoni there is focal pathology it tends to be found in the basal ganglia (putamen) oF midbrain, The most common, dystonia is primary torsion dystonia (PTD), Teste t0 501Figure 3.32 Fnge-nose (A) and hel shin (8) test. Cardiovascular and nervous system exclude a secondary cause (eg, Wilson's disease) should be considered in young patients, those with generalised dystonia and those with features not seen in PTD, such a8 additional neurological signs. Types of dystonia ate listed in Table 3.28. A rare group of genetic paroxysmal yskincsias may be dystonic or choreic and include patox: ‘ysmal kinesigenic dyskinesia, parexysmal non-kinesigenic ‘A moenaric fhe pil ‘gro! oferebelar signs is DASHING 1+ Dyssadocotinais with and akenating movemenss ‘Acavn of nbs and action amor Ses speech Hee=shn aca Frat to judge cance yea) wih pas pointing stags {Gat we based Note in igure 3.31 how unreal: dase esses ‘slater sigs A cerebelar hemisphere fees informant the ‘onlaterlcretal erishere but ten that ceetal henisrere exes contol movement bac o he opposes, Ice vem) lesions case mine or tuncal ati. Gat s ‘oad based an the patients ural o tarde stand ea faingo! Tey mig even be unable to situp without ‘ling tone side, Cetebelar henigher eens cause appeal or Kb aaa These pcos may suggest whether ‘ecbela pathology suite ble midis Rerisgherc panel. Ths shoud rata te diferent diagnos to Sacral lesions or or gewaled ist Th 3.27 ype of movener disorder Type of movement disorder ‘Clinical features ‘natio ‘Cal syiores wth branes as the defn entire, almost ays acconpaied by ty and often sgriomes/Parknsenimm by tenet Parsons discssed in Case 3.32 Tenor ' yim oslo of» Boy part produce by aerating o sncrorauscnvacton of anagoie muscles ‘i veors te arse wn pelormance, ane ans rede ana ar sudden predoraany rs. ‘clon ar osu vena Ne esing berets an bes to mary deetes expecaly othe teal gngha, cin eros usvaly imply ceebelar dene: postural vemorcharacesesesental erat To set whether the vemor sly an aton veo le the pater on the bed wr ars ‘uly ugported to aolsh ‘ny usc acthaton,acerebelar vere dsapoeas. A frer way fo assess subtle Vana iso observe wring or Sang, eg an Artimeds spl Wears ae rer dscssed in Case 2.19 Dati hei an scl en fo tn) Susties mud envacon leading equ to twising ad repelive movements or abnormal postures Core Tvolnay or sentavporveabupt, eg ardardam movements Lssaly ate oe, har an fet sal dal Laxgeamaltude moverets alls) are dsatlag fut mil chorea is easy to mis Wybnus Diet sadn, hace Jes due wo active muscle coiacton Suen pauses ae tered asters Causes ici opps, anc, ecepalits and pion disease Tie Tap, biel fe oF sound Usual fects head er arms Suppresele at ergense terion and tessTable 3:28 Types of ena ental basal gana Dyskinesi Dysnesia tity meas dsrdered movement but the tems ten sed sjonymeasiy wit dug-nduced chorea ad dstonia ‘hat oc or example nthe tet tages o Paknson's dene ‘Acute dystonia Prechleperaine, meocpranise and antipsychotic dugs an duce sun, eer ston, cen of the head or neck. Seales erses may acu eater wit an ivavencus archer dug eg progelrel, Tardive dyskinesia Ceminausilunary movements are conmon wth longterm srepochtic, ane det ores dyskinesia, paroxysmal exercise induced dyskinesia and paroxysmal bypnogenie dyskinesia, some linked to wrt ef ceamp Drug-induced movement disorders “These ae outlined in Box 3.27 Summary A summary of the coordination examination sequence is given in the Summary box _ SUMMARY BOX - COORDINATION _ EXAMINATION SEQUENCE © © 00 or asa, 1 Ask ne patent a Fld ter arms cusreened and dose hr ees, locking ran olan. “© se ne pinto tucr you Faget, hel ut bout 2s Tenth aay. Lok oan iin emcee vest ast 1 pomina ‘ype of dystonia Features and causes Fea Feaalinvehonen, 6g cel gstoria (gpasnadcrerals Elerasoasm | arse hom (eveluary spasm tae es) tromansbule distor, lange sta, brachial dona ater’ (cana) an oot ona Segneral ‘ajc regans aed eg canal + cromanceula=/—cewcl tana | ental Gerald Legs ard other areas aly afeced | Me eritonia Unita stn toa lesan ithe Vera oot (nat) Figure 3.33 The long tacts ~ eossecion of one eel of the spinal ‘ar, Showing te mgr acs ung up and down and ties ‘ht conec it a nerve root at that level C5, carcospnal aes 1G dorsal colnns ST, spinothalamic acs. Asses pid movements y asking the patient wi thee har, as when turing a derkrb, and to tp the back of the tard icy ard then pi alternating rovenens By turing iow and bee again que) ook or esiatachoknesis ses ea shin oe, ‘Assess gi, EXAMINATION OF POWER AND SENSATION ~ OVERVIEW The spinal cord The spinal cord ‘The spinal cord extends from behind the Cr vertebral body to the lower end of the Li vertebra, A cord level is thus abou ie designated vertebral toot ext ste (Fig. 3.80, [page 378). The cord is encased by the pia, subarachnoid ‘space, arachnoid, potential dural space and dura, and sup plied by branches ofthe vertebral artezes. Long tracts Knowledge of the long tract of the spinal cord (Pig. 3.33) is essensal to knowing what you are looking for when ‘examining power and sensation inthe limbs and trunk HM Motor (descending) tracts, The corticospinal tacts (CSTs) run downwards and throw off fibres to venteal hora ‘ells. Arm fibres run medially to leg fibres. The CST sup plying each side of the body in fact divides into a lateral, 503CCST, carrying at least 80% of fibres (decusating in the medulla), and an anterior or ventral CST, caning less than 2086 of fibres (not decussating until the spinal cord) For practical purposes, the CST is considered here as one lateral tact, WH Sensory (ascending) tacts, The dorsal ot posterior columns (DC) telay proprioception joint position sense) tnd tibration sense dom peripheral nerves, roots and. doxsal horns, along their gracile (arm) and cuneate (leg) fibres. These bres synapse in the brainstem then oss, oF decussate, from the brainstem to the contalateal thala mus and sensory cortex Ifa dog rubs its nose up your leg sequential segments of cortical representation of homunculus (Fig. 3.68, p. 534) will be stimulated and each will inform you exactly where its nose is. The si nothalamic act (SY) apidly convey pain and temperature Gnd some light ouch) information to the convalaterl Sensory cortex but cross carly, ether immediately o within. 4 few segments in tne spinal cord, ST ate fast pathways, “The diferential crossing of DCs and SITs accounts for the signs in Brown Sequard syndrome. Cardiovascular and nervous system Spinal cord lesions and radiculopathies ‘The level ofa cord lesion or the presence of a radiculopa thy (root lesion) can be determined by knowledge of root ‘myotomes and dermatomes (Box 3.28, Fig, 3.34). Power is most easly astesed in the limbe but sensation can be assessed in the limbs and unk The limbs. Rapid examination screen In the upper limbs, rapid inspection for wasting then, testing for weakness of shoulder abduction, wrist exten- sion and Singer extension should detect subtle upper motor neuron weakness, proximal weakness due to a proximal myopathy and distal weakness due to a lower ‘motor neuron lesion, Inthe lower lime hip flexion and ankle dotsflexion ate the most discriminatory teste of power Sensation can be left unl last when Gndings should be predictable fom the pattern of weakness Spinal cord lesions bra comslete spl cr lesion tere spac weakness of al ‘ui grupo ne ea oh les, Ther sensory sn i aea below te level ofthe lesan sensory vac ar abo Imvhes, Snetimes ely oneal ofthe ois damages themisecn, or Brown-Séeuad syrrome) with pital weakness, andthe Sensory bss sat be dssaate ips ate les of sensation aed by he desl cols and conalateal ss of sensation Cte by he spinctalic vas, Further here ray be detecable wer motor neon ayotanal vweanes atte level fa son tere is drape tothe vera am ler eval eve oe that Iv In T2cLt less af muse groups i the lone bs ae pasa testing poner nas lang vl, Seseng were ‘run dematonal enor ls (bela) sas isthe mos eee vay of assessing the lee of thoracc spine lsios Adora refs are esto undestand when you thnk of 2 tury tle het feng et srulton of loner harace ese ‘es TEL and sin awe three lesions In onba,sacal and ceva lesan denthing der atona les aps deerme tne Tee he les. Eryn dsense he maybe conse pon tthe lee sion, hen Ib ceratores ae ain, inl Cerda root disease i chten considered ths sts thre Cord or rot esas, when bear, ang an abdonnal diagnoses, te ten considered be'oredematoral pin, an thease rot hagls or vera alge eat grove, Radiculopathies bra radclpaty there ic cree myotomal weakness and eratomal ses es hee mtorr othe muses supa by 2 articular eve roo, no mater haw the ere resin that root are aly stauea via the Ib plenses and perpheral rei not ess, aleced usc ave ak and acid ne ay fies ile tat rot ae lst. The term dematoe refs fo the a3 sn snp by 2 rere oat 9, 3.34), Detmatames vay between nd dua ad era in indus. ‘Myotomes Movements supped by specie roots are + C5 shoule ation (= eps ees) + €6~ ew flson (+ supra etn) + CT=ebow exensin (+ tie le) (C8 figefleson and exerson 71 = movers ofthe smal muscles of he hand 2 hip esionadducion knee exensan (ene eed LA ankle erin (ne fe) Sane dosifnen Si ~ ankle plantar Teadon/evesion ane re “General tw, and sometines more, oats contoute to» patil movement but oe sted above) rakes the mar Censure, Reterence sources vay in asrbing ree acts to arti movers, an in vat hte is considerable blag Naraton seen nid, Ther a eght cea ots But fever vrebrae. Root Cl eis above he C1 velba 3d C8 bao ‘he C7 vere. Al hoa and ba ot at elo te Aesignated vertebra and sacal ‘ot fom farina ithe aco Lumbar and saea roots vel a fong stance fom he cord Segmer of erg th et te Dermatomes Dermatomes ae shown in Figate 3.34Supracaviub Cresrlex cere Lateral claneous rene! am edit etareous reve am Medal estareous rave! es Lateral etaneous rave! es Redilnene ecan nerve Hletgunal nove ‘tater reve Lateral cutaneous rereo! ca Saphenous neve Surrerve Figure 334 Deratomes Examining power Whilst the above i a useful screen when you do not suspect neurological disease, a more complete examina tion is required in neurological cater The key to examining {he Tks in extmining pov, Wm Grading power. There are numerous ways of grading power (Table 3.29), but its also tefl to desexibe weak ness in terms of functional los, im Five patterns of weakness. Its important diagnost: cally to consider five patterns of weakness {Table 3.30). Fach has characteristic signs. Recognising the pattern offers 4 clinical corlat. Ihe clinical correlate connects the site fof the lesion, determined trom the pattern of weakness, to numerous possible pathologies or diagnoses. Generally, reaching the clinical correlate is by clinical examination, land determining the pathology by history and invest: gation. When examining limbs, aim to identify the clini fal conelate before considering possible diagnoses Unarnere 4 fet teraralnere edalardivemedie ‘Rksneas rane Tgh ouletaneous ere falar arene Poser caren Mast evaees Medaletaneaus ewe feat bate neve Paster cutaneous rere a gh Lateral euesur ete a 0h Lateral etaoous ere eal Surlrene Table 3.29 Medial Research Counel cing ol poner Grade Defini 5 Nomad 4 ‘ive everent against gravy ad eine birt fl svengin 3 ‘aive reverent against gray Bu not aganstresisane 2 ‘Aaive neverert wih vy elminated 7 Flickr of movenent or voitary contain ° Ne vile palpable novenent Sometimes multiple patterns of weakness occur, eg. crv ‘al mysloradiculopathy, cervical myelopathy with periph cral_neutopathy, diabetic peripheral neuropathy with mononeutite multiplex, 505SEEN) 131 cardiovascular and nervous system, Tale 3.30 Five patens of weakness ttern of weakness teristic signs Clinical correlate Possible pathologies or diagnoses Upper near imide gouge nth amps bot Fceaied one er parley Monopness one mb) Sake revon Cough am feos dite Enhonged ees eee Wederess Stenger an eros and leg_——_Extese (pg) plantar Mewar rand aad ase tne Senge ta ey fexos}— rapanse one) ‘eat aut nt ht ttes Ba nb may ape tae bese ony 9 ap he nese cl omnes damage 3 269 ‘natn Cate 3.27) ts maybe seca 0 awa grin heen Fes, sens ‘aint ard Fon tee dese rate she Sone onthe Romineks 3p ae ‘eg. canal resrpahes ‘rere spaey populated, wrereas Toner inh cr they havea Conlatel bunched together, is analogous to eras) ‘up ung high ne cove lore Telqiseparess (ll Cena they head to werk onthe stony Tou'lnbs tg. nigh myelopathy ‘hats imately he intemal capsule ‘cove co lesion, Shier raster or ‘eral hensshete lesan) Paraparesis ith lps Denyelration ‘due to spl cord Silane rele lage WS ER SER AEG YI ROMIAY ete va me “iaisenseai Saunton ist ter se ee eran Pree aa se SS" severance Sat a eat Site of weakness depends on the root, sychome San a soavantiy Gale pee ean ior Totnes ery sete soon sisi ately Chore loci ‘ Epc Fab dpe me aoa adil ines 13 etn sey aod Ton nape pinas emule Wiese PeedTatnty Minoan eS Teen aS mos Sonicare cone mae see ets wee oi weieind te x fingertias starting to be oot etae Sls ts won tov ‘eae, ‘ami ek ee a Sa Task Seances =e West eas ee Ts Sans "yn hy water onanExamining tone |Alitde resistance is normal, Increared tone is due to upper ‘motor neuron lesions. Increased tone due to spasticity is best elicited by rapid movements and is present if resist ance increates suddenly ("the catch’ or lasp-kenife), eg. the hncel ings up from the bed when the knce i lied quickly. Leadpipe igiity is when tone is increased throughout ‘movement. Extrapyramidal cogwhel rigity, with regular Intermittent breaks, is best elicited by slow movements Peratonia or Gegenhalien refers to resistance due to frontal lobe damage and is common in cerebrovascular disease. Flaceid tone, with loss of resistance throughout move- ‘ments, indicates lower motor neuron lesions. The heel {does not liftoff the bed when the Knee i lied quiet Examining reflexes Reflexes are monosynaptic responses to the stretch of muscle fibres, mediated in the spinal cord. Reflexes and tone have a further inhibitory input from higher neurons in the muscles they supply. In lower motor neuron lesions, reflexes are reduced or absent. In upper motor neuron. Jesions there is disinhibition from higher neurons and reflexes are increased. Always use a long tendon hammer, dnd let it sving with its own weight onto the muscle Patients should be relaxed, which is best achieved by not telling them to relax! Reflexes are graded as in Box 3.23, Increased reflexes occur in upper mofar neuron lesions Absent or reduced (more difficult to judge) reflexes occur in lower motor neuton lesions. The term inverted seen merely implies the absence ofa reflex at one, or sometimes ‘more level (¢ C5 and Cé) and brisk reflexes elow and Indicates a spinal cord Iesion at the level of the absent reflexes Examining sensation Usually, examiners will stop you before you embar sensory examination, The exceptions ate with a radicw lopathy, a specific mononeuropathy or peripheral neuro- pathy. The modalities totes for are proprioception (joint positon sense), vibration, temperature and pinprick. m Proprioception. Grasping the sides ofa finger or big toe, move it up and down, demonstrating to the patient, before asking them to close their eyes and report the direc- tion of movement being applied (Pig. 3.35) Vibration. A 128 Hz tuning fork may be applied over the first metatarsophalangeal joints, medial malleoi, knee, greater wochanters, anterior superior iliac spines, ribs, sternum, wists, elbows and shoulders (Sig. 3.36) = Absent + Present onl wth enforcer + Donnie 4} Nomal $+ Hyperactive ee Cams Figure 3.35 Tsing propcepan i Finger (A and toe Figure 3.36 Testing wbraton sense 507Sie Tale 3.31 Patens 6 sensry ss Lesion Pattern of sensory loss Paretallebe ion Seco nation or neglect Recogtin ofall ypes of sensation ma be a, ut par casavon rwo-point dscimiaton ost Herisensoy los of al modatis of Seaton Thala sien Tranten Teen ess of pan ard enperature on ace and opposite eof ody i ater red syatome Spinal rd sions Complete ransiese Compl sso all sensory lesion rods below eon run Stquard Loss of ai ard tencertre Trmiecion Sensatonconraatealy and Proprceptonandvraton sense Ips telly Slow leon Loss of ain ard tencertre sensatn tera ew kin Wh other medals preserved (estacited sensory fo) Loss of ronrioepton ana vibration Sense blataly below sion Cental ard eon, a. sngomyel Data clue leon, 9, bes dosals oer sal Loss pain ard temperature rene ‘senso eatery bel kin th preserved ropioeptian and vibratn sense adeckpathy Dermatonal bss oreneuepaty Sess bon of pee Peiohealnexopaty, Peripheral symmetial senses Temperature. A cold tuning fork test the spinotha lame tacts W Light touch and pinprick. Using a disposable new- ‘ological pin, fist confirm on the patient's sternum that the difference between sharp and blunt is appreciated Light touch may also be assessed, with cotton wool, and nota stroking movement. ‘Light is the operative word ~ many candidates apply touch that pachyderms such as elephants or hippos would deteet! Pinprick and light touch loss are often the frst to be noticed by patients but the other sensory modalities may bbe mare discriminating For all sensory modalities you can. interpret pattems of sensory loss (Table 3 31) EXAMINATION OF THE UPPER LIMES Inspection Note any obvious wasting, fasciculation, tremor or unusual poxure. The face may reveal asymmetry, wasting, Parkinsonian expression, Homers syndrome, nystagmus and s0 01, Cardiovascular and nervous system Tone ‘Take the hand af if to shake it and hold the forearm Pronate and supinate the forearm, then roll the hand at the wrist and finally flex and extend the elbow. Repeat movements a different speeds. Power Instruct the patient ‘Hold your arms out in front of you and close your eye’ and look for * Upper motor neuron weakness (the arm falls) Dnt (the arm wanders in the presence of a parietal lesion) * Overshoot (when the arm is tapped with eyes closed Ic falls co tediscover is point of origin) and the action temor of cercbellar disease If there isan obvious upper motor neuron weakness it Js not necessary to examine every muscle group. Pull exam ‘nation would begin by asking the patient to shrug their shoulders adducting the scapulae (C34 roots and tape: ius mules), brace back their shoulders (C4,5 roote and thomboids) and push forwatd against resistance (C5-7 roote and serratus anterior muscles) but there instructions ate seldom necessaty, Examining shoulder movements Refer to Figute 3.37, Examining elbow movements Refer to Figuse 3.38, Examining wrist movements Refer to Figure 3.39, Examining finger movements (that do not involve small muscles of the hand) Refer to Figure 3.40, Examining the small (intrinsic) muscles of the hand Refer to Figure $41. These muscles all originate within the hhand and are supplied ffom the TI nerve roots via the ‘median and ulnar nerves, The median nerve supplies jst four small muscles ‘LOAF’ ~ lateral two lumbrials, oppo zens pollicis, abductor pollicis brevis, flexor pollicis brevis, whiel ate the thenar muscles) and the ulnar nerve sup- plies all other small muscles ~hypothenar muscles, medial {wo lumbricas,interortei which abduct and adduct the fingers, and adductor polis Refi With the patient® arme relaxed and rested lightly on the abdomen, test the apper limb reflexes (Fig, 32)“Abduction ~second 30" Meat OnSite vue 1 de act See ae ee | cmp ion Ses so Roots} C8, 6 (mostly C6) dont let me os (= oa ae . up ke this ‘Flaxion with elbow half pronated ike 80; dort let a SN —— pena eam DM T — Terao _ icon a) ke Ts walt net oct Spat sore ina ye iron) | Resse show sec tags ee toon saan nate a. pectela se Ri ten uc Sop = — ‘| Pronation 5aroton Rony nyt yew Tnaieaaton || | iar Shovnote ‘ee ou } wa Sascapane | {mesa ec eh tar dy ‘Nowe(s): Suprascapular | Muscle(s; Subscapularis | [ands 7 ‘exarining the hand) } \\y wD Figure 3.38 Examining elbow movers ‘See C5 ened by abuso, lal al iPomaton Figure 3.37 Bamiing shoulder movenens 50911 eres — = Fenn Soe, | Ee a= = Ss No Haan eae | st tom andar tas es Pec 18 monty) a | Neve) eden Fon of ta phage jo tine tinge sup rt eae Te FP toner adm ges fre as ‘eapedy maaan ne. ied eden ene ot anit ge ‘ec as feppeaby ore Sroecbyaeene | | mca A 7 font) Nee) ai cme postr oson toxin nang cesarean Janet inger Sos tocer) evo Mean ci i eters: sc) Per oto spre ‘ec aal tems cas I eri deh 6) Figon opting tot un NT] ri maaan us): Flexor poles longus Figure 339 Examining wit movers Now had ihem sai ov, ent etme bend am Coordination Rec) -Arapid fnger-nose tet should tell you whether or not to Nov Radial ipotror pursue cerebellar examination as oulined in Examining ‘noes ‘coordination sts: Longa shot ‘toes elon Sensation efecto "Examining power and sensation ~ overview. [Extension of metcarpophalangeal Jone of ges Summary Masel) Extensor dgtorun ‘A summary of the upper limb examination sequence is given in the Summary box, SUMMARY BOX ~ UPPER LIMB ‘iron oan inane EXAMINATION SEQUENCE seas saint sl): Extensor polis longus Look or wasting, asco, ero or unusual postr ees tae Famine shoulder movenens (Fg 3.37 bbamie eheow movener (5, 3.38) Extension of thumb at ame wrst movenent (93 tacarpoptalangeal joint aamine finger movers 3.0) ass Extensor polis brevis Famine the small muscks ofthe mand (ig. 3.8) amine bees, vieps and supine ene, baamine cootdnaten wih a api inger-rose est amie cena, eoreeeceesy Figure 3.40 fuming finger movements. FP, exe igre protons, 510ri | Flexion of finger metacarpophalngeaoints | ["abducton of tngars as) Tt Passe movement Neth Madan feat spread you ‘ral Ne Unar a muscle): Latrat wo tambials ‘Sm ae (dex erd rel ges) sch nerossl “helms he etacap fore noes dhalrgal ns whee posal Sone repalargzal oc rtergaargcal Bpabecinlsnetersonanvben | eget gare Teach ets clyour| (my hand liege wn your ais DE pliers ‘ave eng rat deratnicsseous ‘Sal ‘Oppetion of thumb sc Fist doralntarosseous Ress) TY Neves) Median Stall srscls:Opponens polis Creston ales abucion at ares the pal. fexan an tation ‘ely sing abc dg ini 1 Sral Lotyou ps face | pci): Abdur gt ini Pon you te calito Fou 0 open aera my hand she caing A ent atm path thom owe \ ‘Rssctn fm “Rabacion opens Ness) Medion Yep a Posse movenent ‘Sat feashor fous) Tt tele Abaco pos brevis Nea Dar ‘Seal - musi afa arrose adil whe Teuhyorpame] | wihyourtumbs | | ips ic of paper between your 7 rg: entre pit ay Flexion of hum ‘vel tesing pr ros Bott al ruses Palmar inerossel Neves) Median Sra mul: Palmar iter Sra rush Fexor pli brevis en soaring aap Soars agar, | [Sep i hat tape thet ecu beg ean and |_| 4or® bie pull any arg at borg tos Devons ° everet Fieon of figar to patent i, ‘metacarpophalangeal joints Bip Roath 74 Actvely esing thumb adduction (1 | Newe(s: Ulnar ‘adductor is paralysed, um flexes — G OS | mt edit te ant 7 | Froments san) . usd Media Wo unbiais «| Sint usc Adc pote firgandide Fngers tres) Aas pol Figure 3.41 framing the smal muses ofthe hand 51= Eling tne iepsretex 6 (rosy 5) ~ ‘aac wa substance ling ta fgar ex C8 fever dglorum pounds nd Rox Sarum supeicals covet va median and ura raves Figure 3.42 Testing upper nb eens. EXAMINATION OF THE LOWER LIMBS Inspection Note any deformity or positional abnormality. Look for ‘wasting and faeciculation Tone Roll the legs, externally and internally rotating the hips (Fig, 3.434). Hick them up from behind the lees ~ the ‘heel wil Oy’ if thee is spasticity and remain in contact ‘withthe bed at al times ifthe leg i laceid. Normally there is only minimal departure of the heel from the bed (Fig. 53.43B). Check for ankle clonus. With the knce semifleed and the foot relaxed, suddenly pull the foot dorsally and hhold it, looking for sustained contracions at the ankle joint Pig, 3.43C). More than three beats is abnormal. Power ‘The patient should be lying supine. Examine sections of the lower limbs as follow. 512 Eling the ticeps etx C7— cat sacl nove 121 [EERE aeapeee _ Eleting the spina rtax C56 (nosy 8) - Sl igo and ebow inion as braciraals {not sunt) conaet a radial nore Hetinans sin Examining hip movements Refer to Figure 3.44 Examining knee movements Refer to Figure 3.45 Examining ankle movements Refer to Figure 5.46, Note that the sciatic nerve has «wo divisions, the common peroneal (lateral popliteal) nerve and the tibial (medial popliteal) nerve, The common per real nerve has two subdivisions, the deep and superial peroneal nerves Examining toe movements Refer to Figuse 3.47, Reflexes ‘With the patients legs relaxed, test the lower limb refleses (ig, 3.48)Hovng ike he koe up rom the bo et fo excuse a marae bxreae en (rain Frag ton ben and aghion be i gat betel fan ioe 8 © 7 Figure 343 Teng en te ntsc en a8 Fon ihe op Fon bo net et oe cs Pa cate crt > east Now push your stn ou gst ny hard ard ¥y fo stages yu bg Ta ri | ityour og up towards he ling sth ler io 90" auratcaly assessud ding Nts abo shiovedith patorts able Flexion Real) Lt, 2 (most L2) Nerves): amoral {ost down now dontletme sito Extension Fulton best tested poe (ot shown but corolatesexanston Sequnce so ease paornet supine wins inatcton shown bare Root 5, $1 Neri: nerior gluteal nerve aso) Glutous maximus [Now push your igh] down nite bes agains restance) ‘Abduction eae LAS Nowe): Superior gluteal narve scl): Guts mediusininimus {ateal tan ofhip also |“ Push your high eter voles thse muscles) |_| apainsmy hands NC Push youths iar agains hands Reais) 3,4 (mast L3) Nerves}: Femoral sels): Quadricps femoris Figure 3.45 framing knee moveres “Reduction Roos) L2,3(mosty 2) Neve() obturator Muscles) Adductors Figure 3.48 Examining hip movements 51311 eres Dorsifxon Real) Le, sty L5) Nave): Seite -aconmon prose rari deap parancal ave rgely response for dereexon) asl: Antrir tia (ilar) PDy Te cock you catback gant my handie your test the clog Plantar exon Feats St Neves}: Slate abner usels)Gastrocnemistsoleus Tow posh your foc down gant Flexion Roo): 8,2 (mostly 1) ) Nene) Seiate \arlee Small muscles of foot and flexor digitorum lngos Extension Hew Real): 5, $1 (most U5) Stghten Nene: Seale hem aut lasses Extensor digtorum longus extends tos Extonsor haus longus extends big toe Extonsor halucs Brevis (he ran asco haat doris the foot Roos): 4 5 (mosty La) Nea): Slate va bid neve uss} Postarior bial bas postr) version Root) L584 ~via common pean (supteial peorcl sunt ‘telomere and largely respenable a ovrion) Muss: Proneuslongusbrevis ‘Nek tha orton ard pla fxon are ost ssasod by patent Stacg on hols and tos respectvoly Figure 3.46 Eramiing aide movenens Coordination ‘ak the patient to run their heel smoothly wp and dows the shin and watch for any tremor or difficulty coordinat ing thir movement Sensation Refer to ‘Examining power and sensation - overview! Summary ‘A summaty of the lower limb examination sequence isi the Summary box 514 Figure 3.4 ining toe movements ‘SUMMARY BOX - LOWER LIMB EXAMINATION SEQUENCE ook fr eeormty or any postanalabnomaly, wasting ane ‘and examine for demas Eanine nee mover rine ake mverents Fi. 3.46 rine toe movement (9.3.4), sine knee and al efx, sss he paar Examine cootaton ith aap hee-hints, EXAMINATION OF GAIT Gait abnormalities ‘Examining gaits an estenial past of lower limb and more generalised: neurological examination. Common abnor ial types of gat are illustrated in Table 2.32 and whilst these may become eaty to fecagnise a uggested requence for detecting these i given in the Summary box ‘Most gaits are symmettcal. Asymmetsc gaits may be due to hemiplegia, foot drop or pain Summary A summary of the gait examination sequence is given in the Summary boxTable 332 Conman abrarwal peso cat Gait Signs What to look for next ‘Spas ‘kad 35 if adie tough mud with Upper nator newon sans Soke foot ned innards Henpleia Deryelration May be pa of nenpecia cr paraplegia — Sensory paral inhemiple pes om fected side ted pward fase spastc leg of the ear in paraplegia gat is scisvng, as fe Ings ar ying ta css cur each ther evbalor Wide based ‘ther cerebar e ‘Nese Luring as onthe deck of a ship Cereb degerration Pwensanan Shor, sling se Lack am sing Steapeg pote a though shang steps aie haying to fae up wh = soaleg ‘ier sr of Patnsn’s sasee9. bashiresa, hypanima gi, asymm sing enor Paknons daeare Sipe S28) =e BS? S| ape Semetresvual ads crpesate and ‘vee aul ban processing of walking rece Frontal lobe dsease ‘esinan ga arhe&patt pas Sar seps “sess cetoroacube ak Dis alba Presets arm weg faces danse pig sosure Sensory atc Foot sens osama down ono the fost Pose Ronbegs san “Sibaete combined ‘staging gat Movements oleh bea) roveltan ‘2 Imgaeeaopioceion and degeneration of cord ithe postion space ‘ration seve ‘hoes sass Wie based and agpebesive,oatent Inder ata Teling tofu aid unsure sess eral myelepathy gr sepaing Foot dep Sigas of @riren peoneal Common peroneal Fate Is leg or bends nee to aid neve paby reve ply Tortotseapng groan eeay mater ad sesay neuropathy 1 Seatenere lesen la Sraseuloaty Wadsng Wide based gat ith wight sing For specon for Tel uses of Cushngs snore Sie to side of pes as patert wales groxral myopathy eg, Taytoxcoss foraarde Cushing's sytome Polmyests apa Patent cannot wa ‘ter apne Normal pesure Nevomscl stem works Ober tora be signs hyeocenalis 51511 eres leting the koe reoxL,4— ste the quaicps ard wach contact nathan exten a Jae Rerorcoment maybe usd to enhance eles which are dub eet {askpatenttsdasp hands tg as shown er dans tah) Fling he ankle reflex of recurbar palo (nd your kre sghy and a fp fhe si) 5,84 ost S1)~ se te tiles tendon, Fave ncn aloes nen al ml by aung te aroun of alee aed wach or lara ese ard ca cancion “pl ‘Mate rte ito ste tho ace oth fot to stimulate suten Behl skeeh Plantar response sap th utr barr fe foot fr heals ne and than aco sale fh orto With he oa ol noma a xr {poste Babin’ Sgn ype mar nurn sion, or weave) ‘Alomatiesimalipsde simu th lara aspect oft foot (Chak sor) or ain Figure 3.48 Lowes Ib eles, 516 thu ard index ingrown te mesial aspect ofthe tia (Opps eex) both sm arly of sf present SUMMARY BOX ~ GAIT EXAMINATION SEQUENCE © bserve te pain waking, ' Note any sora award ering of eto ong spas, ‘© Observe te pain wring ard mete any oss of rm swing (Warnsoniany oe peste “© ‘Ober te ptr sancng (and then walking) onthe ees and toes (igh stepping oo op “© Observe gatent walking eel ae or tander walking (eet (© Check Ramberg test ens tail sis on pase ifthe paver ior unseay wit ges hss than open "pseudo sambergsm i conan becuse, without son, Urseaies avs ate ore = and 3 rb peste Ronbers et assacced wih sopaceptve and vraion sense mpaementacaring in dvs alan dea ad sre berphenl newovates. “© bsere te patient sqiating (rina myopathy Es CASE 3.16 VISUAL FIELD DEFECTS Instruction Please examine this patient's eyes/visual elds and comment on your findings. Recognition ‘There is (depending on the ste ofthe lesion} + Aefifsight central sotoma + Tune! (more cometly funnel) vision © Unitaeralbtnness + Bitemporalhemianopia © Aleffright homonymous hemianopia # Alefifnight homonymous quaamtanopia © Los of sion inthe left/right ee with macular sparing Interpretation Confirm the diagnosis ‘What to do nest depends upon the defect (Fig. 3.49). What to do next — consider causes/assess other systems Central scotoma “This indicates disease ofthe macula or nerve fibres from the optic neve head (optic dsc) that supply it Look for tvidence of disease a the macula or dae auch a diabetic racalopathy oF optic atophy Five signs of optic nerve damage ae listed Box 3:30,