MRCP PACES MANUAL - Pastest
MRCPPACESMANUALLouise Pealing MA Hons (Cantab) MBBS MSc MRCP MRCGPGeneral Practitioner and Clinical Research Fellow, Nuffield Department of PrimaryCare Health Sciences, University of OxfordBenjamin Mullish MB BChir MA (Cantab) MRCP AFHEASpecialty Registrar/Academic Clinical Fellow, Gastroenterology and Hepatology,St Mary’s Hospital, LondonPhilip J Smith BMedSci (Hons) BMBS (Hons) MRCP MSc (Nutrition)Gastroenterology Specialist Registrar and MRC Clinical Research Training FellowGastroenterology Department, University College London Hospital, LondonEdited byDouglas C Macdonald BM (Hons) BSc (Hons) MRCP PhDConsultant Hepatologist, Royal Free London NHS Foundation TrustRoyal Free Hospital, London
ContentsPrefaceIntroductionSTATION 1 Respiratory and Abdominal Examinationsvivii1The abdominal examinationAbdominal scenariosThe respiratory examinationRespiratory scenarios374752STATION 2 History-Taking Examination71History-taking scenarios77STATION 3 Cardiovascular and Neurological ExaminationsThe cardiovascular examinationCardiovascular scenariosThe neurological examinationNeurological scenariosSTATION 4 Communication skills and Ethics’ Examination169170175220241353Approach to the communication skills and ethics stationCommunication skills and ethics scenarios355359STATION 5 Integrated Clinical Assessment393Approach to Station 5Integrated clinical assessment scenarios398407Abbreviations599Index605v
Station 3Neurological scenarios1.Multiple sclerosis17.Median nerve palsy2.Parkinson’s disease18.Ulnar nerve palsy3.Motor neuron disease19.Radial nerve palsy4.Hemiparesis20.5.Spastic paraparesisCommon peroneal nervepalsy and L4–5 root lesions6.Cervical a22.Ophthalmoplegia8.Myotonic dystrophy23.Visual field defect9.Myasthenia gravis24.Dysphasia10.Muscular r and pseudobulbarpalsy26.Brain-stem syndromes12.Friedreich’s ataxia27.13.Cerebellar syndromeCerebellopontine anglelesion14.Peripheral neuropathy28.Jugular foramen syndrome15.Facial nerve palsy29.Old polio16.Wasting of the smallmuscles of the hand30.Involuntary movements andHuntington’s disease
306MRCP PACES ManualSCENARIO 17. MEDIAN NERVE PALSYIdentifying clinical signsThe median nerve serves the intrinsic small muscles of the hand not served by the ulnar nerve.The median nerve also serves muscles of thevolar surface of the forearm, which includes themain wrist flexors.The most common median nerve palsy appearingin the PACES examination is a carpal tunnelsyndrome. Indeed this is the most common peripheral mononeuropathy. However, there can bemore proximal lesions of the median nerve thatoffer more objective clinical signs.Distal median nerve lesions (carpaltunnel syndrome)Inspection: the hand shows thenar wasting (alate sign) with hypothenar and first dorsal interosseous sparing. The thumb is externally rotatedand adducted into the plain of the palm (Figure3.18) due to weakness of opponens pollicis andabductor pollicis, and some refer to this as ‘apehand’ deformity (but it is best to describe theposition of the thumb). The index (first) andmiddle (second) fingers may also be held inextension due to weakness of flexor digitorumprofundus I and II and flexor digitorum superficialis, and unopposed action of the radialnerve-innervated finger extensors. Some call thisthe ‘papal sign’. Look for surgical or traumaticscars at the wrist, palmar crease, forearm orelbow.Motor function: there is weak thumb abduction(abductor pollicis brevis), tested for by asking thepatient to place the hand palm up and point thethumb up to the sky perpendicular to the planeof the palm and test against resistance of yourthumb. There is weakness of thumb opposition,tested for by asking the patient to oppose thethumb with the little finger and stop you pullingthem apart. There may be normal flexion at thethumb MCP joint due to intact ulnar nerve innervation of flexor pollicis brevis. There is normal flexion of the thumb at the IP joint due tointact innervation of flexor pollicis longus in theforearm. Arm pronation and wrist flexion arealso normal if the median nerve lesion is distal.Sensory loss: there is sensory loss in the palmaraspect of the thumb and lateral two and a halffingers but normal sensation over the thenareminence (supplied by the palmar cutaneousbranch of the median nerve which does not passthrough the carpal tunnel).Additional tests: you can ask to perform Tinel’stest – tapping over the median nerve at the wristmay cause paraesthesia in the distal median distribution. Phalen’s test involves flexing the wristto 908 for at least 60 seconds, which may causeparaesthesia in the distal median distribution.The median nerve compression test involvespressing on the palmar aspect of the wrist for upto 60 seconds, which may cause paraesthesia inthe distal median distribution.Figure 3.17tributionMedian nerve cutaneous dis-Additional signsExamine for signs of other diseases associatedwith carpal tunnel syndrome such as:
The Cardiovascular and Neurological Examinations307Median nervePronator teresFlexor carpi radialisPalmaris longusFlexor digitorumsuperficialisAbductor pollicis brevisFlexor pollicis brevisOpponens pollicisFirst lumbricalFigure 3.18 Pronator quadratusSecond lumbricalRoute and muscles innervated by the median nerve Hypothyroidism: goitre, slowly relaxing Anterior interosseous nerveFlexor digitorum profundus I & IIFlexor pollicis longusreflexes, pretibial myxoedemaAcromegaly: supraorbital ridge, prognathism,interdental separation, bitemporalhemianopia, large doughy hands,hypertensionRheumatoid arthritis: deforming arthropathy,elbow nodules, steroid skin changes,episcleritis/scleritis, interstitial lung diseaseDiabetes mellitus: finger-prick testing,peripheral neuropathy, retinopathyGout: deforming arthropathy and gouty tophion hands, ears and feet.Anterior interosseous nerve palsyThis nerve has branches to flexor digitorum profundus I and II, flexor pollicis longus and pronator quadratus. It is typically affected by amidshaft fracture of the radius, excessive exerciseor penetrating injuries of the forearm. There isweakness of the thumb and index finger flexion,best shown with the ‘okay’ sign, ie flattened dueto failure of distal flexion (see Figure 3.17). Thethenar eminence muscles are spared. There is nosensory loss.Di¡erential diagnosisProximal median nerve lesionsPronator syndrome: compression of the mediannerve can occur as it passes between the twoheads of the pronator teres, high in the volaraspect of the forearm. It can present with purelysensory symptoms of pain over the volar surfaceof the forearm at rest or with forearm pronation.There will be sensory loss within the mediandistribution including the thenar eminence (unlike carpal tunnel syndrome). Elbow lesions:Fracture: supracondylar fractures are mostcommon Dislocation Compression: ligament of Struthers Forearm lesions: Fracture: midshaft radial fracture causinganterior osseous nerve palsy Injury: penetrating injuries of the forearm
308 MRCP PACES ManualCompression: pronator teres syndrome Wrist lesions: Fracture/traumaCarpal tunnel syndrome (CTS).Clinical judgement andmaintaining patient welfareCTS is caused by compression of the mediannerve within the carpal tunnel, which is boundby the carpal bones below, flexor retinaculumabove, radially by the scaphoid and trapezium,and medially by the pisiform and hamate.It is most commonly idiopathic, but associatedconditions include: pregnancy, menopause, hy-pothyroidism, diabetes, acromegaly, rheumatoidarthritis, gout, renal failure, multiple myelomaand amyloidosis.InvestigationsElectrophysiology: nerve conduction studies andEMG.Imaging: seldom needed, but MRI might be considered.Management Treat any underlying associated conditions Physiotherapy and splint the wrists with adegree of dorsiflexion Steroid injections into the carpal tunnel area Surgical decompression of the carpal tunnel.
The Cardiovascular and Neurological Examinations309SCENARIO 18. ULNAR NERVE PALSYIdentifying clinical signsThe ulnar nerve serves most of the intrinsic smallmuscles of the hand. However, the ulnar nervealso supplies two important extrinsic muscles ofthe hand: flexor carpi ulnaris and flexor digitorum profundus 4 and 5; it is important to remember this when considering a claw hand deformity.Clues pointing towards an ulnar nerve lesioninclude unilateral signs, clawing of the hand andwasting of the hypothenar eminence with sparingof the thenar eminence.Distal ulnar nerve lesion (distal to theelbow)Inspection: with the hands held prone there isdorsal guttering and marked wasting of the firstinterosseous between the thumb and index finger. The hand shows a claw deformity (you mightwant to say a clawed appearance) with hyperextension at the fourth and fifth MCP joints andflexion at the fourth and fifth PIP and DIP joints,due to paralysis of the medial lumbricals. Thereis slight ulnar deviation of the fifth finger (knownas Wartenburg’s sign) from unopposed action ofextensor digiti minimi (which inserts into theulnar side of the little finger and is innervated bythe radial nerve). With the hands held supine,marked hypothenar wasting with sparing of thethenar eminence can be seen, and no wasting ofthe forearm muscles. Look for scars or deformityfrom trauma, surgery or arthritis around the forearm and wrist.Motor function: there is weak abduction (dorsalinterossei) and weak adduction (palmar interossei) of the fingers. There is weak thumb adduction (adductor pollicis) as demonstrated byattempting to grip a piece of paper held betweenthe borders of the index finger and extendedthumb. Grip can be maintained only using thumbflexion (intact flexor pollicis longus served by themedian nerve), known as Froment’s sign. There isintact flexion of the fourth and fifth DIP joints,as shown by the marked ulnar claw appearance(it is difficult to test actively when the fingers areheld in fixed flexion). There is intact medial/ulnar flexion of the wrist.Sensory loss: in the ulnar distribution over thefifth finger (see Figure 3.19), adjacent ulnar sideof the fourth finger, ulnar side of the palm anddorsal aspect of the hand. (In distal ulnar nervelesions this sensory loss may be variable orpresent only in the fifth finger.) Test along theradial side of the fourth finger and up the ulnarborder of the wrist and forearm to check that thisdoes not represent a C8–T1 lesion instead (muscle wasting would also be different, see Scenario16).Additional tests: you can ask to perform Tinel’stest tapping along the course of the ulnar nervefrom the wrist along the ulnar border of theforearm and up to the elbow, which may elicittingling from irritation of the nerve.Figure 3.19butionUlnar nerve cutaneous distri-Proximal ulnar nerve lesion (at theelbow)Inspection: with the hands held prone there isdorsal guttering and marked wasting of the first
310MRCP PACES Manualinterosseous between the thumb and index finger. The hand shows a mild/no clawed appearance with hyperextension at the fourth and fifthMCP joints but only mild flexion at the fourthand fifth PIP joints and no flexion at the DIPjoints. This is known as the ulnar paradox, withproximal lesions resulting in less clawing. Thereis slight ulnar deviation of the fifth finger knownas Wartenburg’s sign (see above). With the palmsfacing up, there is marked hypothenar wasting,with sparing of the thenar eminence. In addition,there is wasting of the ulnar border of the forearm. Look for scars or deformity from trauma,surgery or arthritis around the elbow.Motor function: there is weak abduction (dorsalinterossei) and weak adduction (palmar interossei) of the fingers. There is weak thumb adduction (adductor pollicis) with Froment’s sign (seeabove). There is loss of flexion of the fourth andfifth DIP joints (loss of flexor digitorum profundus with high lesions) as shown by holding thefourth and fifth MCP and PIP joints extended andasking the patient to try to flex the fourth and fifthDIP joints (this takes practice to demonstrateeffectively!). There is weakness of medial/ulnarflexion of the wrist (flexor carpi ulnaris) notfound in distal lesions (see above).Sensory loss: this occurs in the ulnar distributionover the fifth finger, ulnar side of the fourth finger,ulnar side of the palm and dorsal aspect of thehand (see Figure 3.19).Additional tests: you can ask to perform Tinel’stest, tapping along the course of the ulnar nervefrom the wrist up the ulnar border of the forearmtowards the elbow, which may elicit tingling fromnerve irritation.The elbow flexion test can be used to test forulnar nerve compression at the elbow, particularly in cubital tunnel syndrome. The elbow isflexed fully with the forearm supinated, and within 60 seconds the patient starts to feel pain ortingling in the fourth and fifth fingers.Di¡erential diagnosisElbow lesions Fractures: Supracondylar fractures are most commonand late complications of fracture/surgerycan include cubitus valgus deformity ofthe elbow joint. Dislocation: Arthritis: bony spurs and narrowing of theulnar groove Compression: cubital tunnel syndromedescribes constriction under the fibrousarch of the two points of insertion offlexor carpi ulnaris. Certain occupationsare more at wrist such as secretaries (fromleaning on elbows) and decorators (fromrepeated elbow flexion and extension).Wrist lesions Fractures Ganglion Tumour Mononeuritis multiplex.Clinical judgement andmaintaining patient welfareInvestigationsImaging: plain radiograph of elbow joint, ultrasonography of the cubital tunnel or MRI.Nerve conduction studies localise the site of thelesionBlood tests: FBC, CRP, ESR, anti-nuclear antibodies(ANAs), anti-DNA, pANCA (perinuclear antineutrophil cytoplasmic antibody or ANCA), cANCA (cytoplasmic ANCA), rheumatoid factor, hepatitis B and C serology (mononeuritis multiplex).ManagementConservative: avoidance of aggravating factors,physiotherapy, splinting, NSAIDs.Surgical: transposition of the ulnar nerve and/ordecompression of the cubital tunnel.
The Cardiovascular and Neurological Examinations311SCENARIO 19. RADIAL NERVE PALSYIdentifying clinical signsThe radial nerve serves the extensors of theelbow, wrist and fingers. With knowledge of theanatomy of radial nerve innervation it is possibleto describe the level of the lesion giving rise toclinical signs (see Figure 3.20).Radial nerve lesion at the axillaInspection: there is wrist drop and slight fingerflexion but with no wasting of the hand muscles.Look for surgical or traumatic scars anywherealong the route of the radial nerve from the axillato the wrist.DeltoidTeres minorTriceps, long headTriceps, lateral headTriceps, medial headRadial nerveBrachioradialisExtensor carpi radialis longusExtensor carpi radialis brevisSupinatorExtensor carpi ulnarisExtensor digitorumPosterior interosseousnerveAbductor pollicis longusExtensor pollicis longusExtensor pollicis brevisExtensor indicisFigure 3.20Route and muscles supplied by the radial nerve
312MRCP PACES ManualMotor function: there is weakness of all radiallyinnervated muscles: Weakness of elbow extension and flexion(midway between supination and pronation) Forearm supination (tested with arm by theside and attempted supination of forearmagainst resistance applied to the patient’shand) Wrist extension and finger extension at theMCP joints.Both triceps and brachioradialis (biceps) deeptendon reflexes are absent.Sensory loss: this occurs over the triceps, posterior forearm and first dorsal interosseous.Radial nerve lesion in the spiral grooveof the humerusInspection: there is wrist drop and slight fingerflexion but with no wasting of the hand muscles.Look for surgical or traumatic scars.Motor function: there is weakness of all radiallyinnervated muscles below the triceps. There isweakness of elbow flexion (midway betweensupination and pronation) but elbow extension isintact (triceps innervation above the spiral grove).There is weakness of forearm supination, wristextension and finger extension at the MCP joints.The triceps reflex is preserved but the brachioradialis (biceps) deep tendon reflex is absent.osseous nerve dips beneath the fibrous arcade ofFrohse (‘supinator arch’) which is the commonentrapment area). There is intact elbow flexion(midway between supination and pronation) andintact elbow extension and forearm supination.There is weakness of wrist extension and fingerextension at the MCP joints. Triceps and brachioradialis deep tendon reflexes are intact.Sensory loss: there is no sensory loss because theposterior interosseous branch is a purely motornerve.Radial nerve lesion at the wristInspection: the arm and hand appear normal.Look for surgical or traumatic scars around thewrist.Motor function: there is no motor weakness(because the radial nerve serves only extrinsicextensor muscles of the hand from above thewrist).Sensory loss: there is sensory loss in the firstdorsal interosseous only (as the sensory branchbecomes superficial at the wrist).Di¡erential diagnosis Axillary lesions:Fracture/dislocation of humeral headCompression: use of shoulder crutch or‘Saturday night palsy’ from prolongedhanging of the arm over the back of achair (when intoxicated) Spiral groove lesions: Fracture: mid-shaft fracture of the humerus Compression: wheelchair users restingback of their arm against the chair Posterior lesions: Compression: from the arcade of Frohse/supinator arch Interosseous lesions: Tumours/lipomas or ganglia near theelbow Sensory loss: there is sensory loss over the posterior forearm and first dorsal interosseous. Theremay be variable loss of sensation over the triceps.Radial nerve lesion con ned to theposterior interosseous nerveInspection: there is wrist drop and slight fingerflexion but with no wasting of the hand muscles.Look for surgical or traumatic scars.Motor function: there is weakness of radiallyinnervated muscles below the supinator (the supinator nerve comes off before the posterior inter-
The Cardiovascular and Neurological Examinations Wrist lesions: Fracture: at the distal radiusCompression: tight bracelets/handcuffs/plaster casts.Clinical judgement andmaintaining patient welfareInvestigationsElectrophysiology: nerve conduction studies andEMG.313Imaging: ultrasonography/MRI may rarely be considered.Management Conservative management of ‘Saturday nightpalsy’ with spontaneous improvement Physiotherapy and splinting for mildcompressive lesions Surgical correction of fracture/dislocations.
314MRCP PACES ManualSCENARIO 20. COMMON PERONEAL NERVE PALSY AND L4 5ROOT LESIONIdentifying clinical signsCommon peroneal nerve palsy is the most common cause of foot drop. However, a lesion inany of the areas, including the motor cortex,spinal cord, lumbar nerve roots L4–5, lumbosacral plexus and sciatic nerve, and peripheralneuropathies or myopathies, can cause foot dropwith different associated clinical signs. Knowledge of the anatomy of the common peronealnerve will help determine the level of the lesion.The sciatic nerve (L4, L5, S1–3) divides into itsterminal branches, the tibial nerve and the common peroneal nerve, two-thirds down the posterior thigh. The tibial nerve serves the posteriorcompartment of the lower leg, producing plantar-flexion and inversion. The common peronealnerve (Figure 3.21) serves the anterior part of thelower leg, winding around the neck of the fibulaand dividing into the superficial peroneal nerve(foot eversion and sensation to lateral lower legand dorsum of foot) and the deep peroneal nerve(foot and toe dorsiflexion and sensation to thedorsal web space between the hallux and secondtoe).Common peroneal nerve palsyInspection: there is foot drop with a highstepping gait. There is wasting of the anterolateral compartment of the lower leg. Look forsurgical or traumatic scars near the knee andneck of the fibula. Look for any ankle supports/adapted footwear.Lateral cutaneous n. of calfCommon peroneal n.Cutaneous distributionDeep peroneal n. (cut)Common peroneal nerveSuperficialperoneal n.Peroneus longusSuperficial peroneal nervePeroneus brevisMedial cutaneousbranchLateralAnteriorDeep peroneal nerveserving web spaceLateral cutaneousbranchFigure 3.21distributionRoute and muscles supplied by the common peroneal nerve and cutaneous
The Cardiovascular and Neurological ExaminationsMotor function: there is weakness of ankle dorsiflexion, and hallux extension (deep peronealnerve) and eversion (superficial peroneal nerve).Test for eversion in a passively dorsiflexed footbecause the everters cannot exert their action ifthe foot is in plantarflexion. The ankle jerk isintact and plantar reflex is downwards. There isnormal plantarflexion and inversion. In mildcases, weakness may be seen only when askingthe patient to walk on the heels.Sensory loss: over the lateral calf and dorsum ofthe foot, but sparing the little toe. The little toehas sensation from the sural nerve, a branch ofthe tibial nerve.Super cial peroneal nerve palsyInspection: there is wasting of the lateral compartment of the lower leg but no obvious highstepping gait. Look for surgical or traumaticscars near the knee and neck of the fibula. Lookfor any ankle supports/adapted footwear.Motor function: there is slight weakness of ankledorsiflexion which might be seen only when thepatient is asked to walk on the heels. There is noweakness in hallux extension, but there is weakness of eversion. There is normal plantarflexionand inversion.Sensory loss: over the lower lateral calf anddorsum of the foot, but sparing the little toe.Deep peroneal nerve palsyInspection: there is foot drop with a highstepping gait. There is wasting of the anteriorcompartment of the lower leg. Look for surgicalor traumatic scars near the knee and neck of thefibula, anterior lower leg. Look for any anklesupports/adapted footwear.Motor function: there is weakness of ankle dorsiflexion (deep peroneal nerve) and hallux extension but intact eversion (superficial peronealnerve).315Sensory loss: only in the dorsal web space between the hallux and second toe.Di¡erential diagnosisMyopathy: tends to give rise to proximal weakness but there are distal variants. Signs will bebilateral. All foot movements will be weak including plantarflexion and hallux flexion. Theankle jerk may be reduced. There will be nosensory loss. There will be myopathic signs in theupper limbs and possibly the face.Sensorimotor peripheral neuropathy: there isalso weak plantarflexion and a stocking patternof sensory loss including the little toe. Signs willbe bilateral. There may be dorsal column signsand a positive Romberg’s test and sensorimotorsigns in the upper limbs.Neuromuscular junction disorder: signs tend tobe bilateral with upper limb and facial involvement. Weakness will affect plantarflexion and befatigable. Reflexes and sensation will be normal.MND: signs are bilateral, although in early disease there can be asymmetry. There will be amixture of UMN and LMN signs with increasedtone, brisk ankle jerks, possibly upgoing plantarreflexes, marked wasting and fasciculations.There tend to be signs in the upper limbs andface. There are no sensory findings.Sciatic nerve lesion: a peripheral nerve lesionaffecting the sciatic nerve can cause foot drop,but also weak plantarflexion and inversion, weakknee flexion (with preserved knee extension) andhip extension. The ankle jerk is absent with apreserved knee jerk. Sensory loss will be alongthe posterior thigh, lower leg and foot, sparingthe medial side of the lower leg. Injury to thesciatic nerve can occur through hip surgery, misplaced gluteal injections and pelvic pathology,such as trauma, haematoma, abscess or tumours.Lumbosacral plexus lesion: presents similarly to asciatic nerve lesion but with femoral nerve involvement. This will cause additional weakness in
316MRCP PACES Manualhip flexion, abduction and adduction, and kneeextension. The knee and ankle jerks are lost.There will be more extensive sensory loss including the anterior thigh and medial lower leg.L4–5 radiculopathy: leads to similar findings as acommon peroneal nerve lesion. In addition therewill be weak hip abduction and adduction andvariable effects on knee flexion and extension.The knee jerk (L3–4) may be lost but ankle jerks(S1–2) preserved. Sensory loss will include themedial part of the lower leg (L5). The patientoften has back pain because nerve root compression usually arises from lumbar disc herniation(less commonly a tumour). Straight leg raise,stimulating nerve root irritation from stretching,will reproduce symptoms.Spinal cord lesion: this can cause weakness infoot dorsiflexion but will also cause weakness inother muscle groups of the leg depending on thelevel of the lesion. Foot drop is not so obviousdue to the UMN spasticity. Lesions can be unilateral or bilateral. Sensory signs will depend onthe location of the lesion in the cord and theremay be dissociated sensory loss, giving rise tothe Brown–Séquard syndrome if the lesion isunilateral.Cortical lesion: a tumour or stroke affecting themotor cortex, such as a lacunar infarct or parasagittal meningioma, can rarely cause localisedlower limb weakness and foot drop. There willbe UMN signs.Causes of common peroneal nerve palsy Trauma Fibular fracture Knee surgery Compression: plaster cast, leg crossing,weight loss.Clinical judgement andmaintaining patient welfareInvestigationsElectrophysiology: nerve conduction studies andEMG.Imaging: MRI might be considered.Management Avoidance of aggravating factors such as legcrossing or squatting Physiotherapy and splinting of the ankle/foot Surgical repair or release if there has beentransection or tethering.
The Cardiovascular and Neurological Examinations317SCENARIO 21. NYSTAGMUSNystagmus will usually be a sign as part ofanother disorder such as cerebellar syndrome orMS, but rarely it can form the full case in thePACES neurology station.Nystagmus is an involuntary rhythmic oscillationof the eye(s) that may be physiological, congenital or acquired. It represents a problem with theneural mechanisms/centres involved in maintaining image fixation on the fovea for optimal visualacuity.Identifying clinical signsNystagmus is usually described with reference to: Monocular or binocular/conjugate Position: primary (looking forward) or onlygaze related Type: pendular (equal velocity in eitherdirection) or jerk: a slow drift then fastcorrective phase – the direction of nystagmusrefers to the fast phase Plane: horizontal, vertical or rotatory/torsional(sometimes it is easier to tell by looking at thepull on the conjunctival vessels).wards the side of the lesion. There may bedysarthric speech.AdditionalFinish your exam by asking to test the cranialnerves, particularly looking for any abnormalityof cranial nerve V (corneal and facial sensation)or cranial nerve VIII which may suggest a lesionat the cerebellopontine angle (see Scenario 27).Ask to examine the fundus for optic atrophywhich may be present in MS.Ask to examine the upper and lower limbs,which may show pyramidal weakness consistentwith MS, or dorsal column signs in alcohol misuse or vitamin B12 deficiency.Romberg’s test is not a test of cerebellar function,but rather of dorsal column/proprioceptive function. A patient with a cerebellar lesion cannotusually stand steady, feet together with arms bythe sides even with the eyes open, so Romberg’stest cannot be performed.Di¡erential diagnosisUnilateral cerebellar pathology and nystagmuswill tend to be caused by structural lesions:Cerebellar nystagmus Cerebrovascular events, eg lateral medullaryThis is a binocular/conjugate, primary and gazerelated jerk nystagmus which is in the horizontalplane, and the direction of the nystagmus (fastphase) is towards the same side as the cerebellarlesion and maximal on looking towards this side.The nystagmus does not fatigue with continuedgaze to the affected side. There is also loss ofsmooth saccades. Demyelination, eg MS Cerebellar/posterior fossa tumours, egsyndromeastrocytomas, haemangioblastomas,medulloblastomas and metastatic disease(breast, lung, skin, kidney).Bilateral cerebellar nystagmus will be caused bysystemic pathology: Toxins (alcohol, chemotherapy andFurther cerebellar testing will show homolateralpoor finger–nose pointing with dysmetria andintention tremor, dysdiadochokinesis, poor heel–shin coordination and an ataxic gait falling to-anticonvulsants) Autoimmune and paraneoplastic processes Inherited disorders involving cerebellardegeneration, eg olivopontocerebellar
318MRCP PACES Manualdegeneration and Friedreich’s ataxia (seeScenario 12).Vestibular nystagmusPeripheral vestibular nystagmus: this is a binocular/conjugate horizontal or rotatory/torsional nystagmus which is a primary and gaze-relatedunidirectional jerk nystagmus with the fast component maximal to the opposite side of thevestibular lesion. With upward or downwardgaze the nystagmus remains horizontal and inthe same direction. With continued gaze awayfrom the side of the lesion the nystagmus fatigues. There are no cerebellar signs. The gaitmay be unsteady, falling towards the side of thelesion, and the patient may describe vertigosymptoms. These are often worse when testinggait. Tinnitus and deafness may be found on theside of the lesion.are no peripheral symptoms such as tinnitus ordeafness and no cerebellar signs.Di¡erential diagnosisThe central vestibular system includes the vestibular nerve nuclei and their projections to the cerebellum, extraocular nuclei via the mediallongitudinal fasciculus, the spinal cord via thevestibulospinal tract and projections to the cortex.Causes of central vestibular nystagmus includebrain-stem stroke and vertebrobasilar insufficiency, brain-stem tumours, demyelination suchas MS, syringobulbia (see Scenario 7) and basilartype migraine (some classify this as a cause ofperipheral vesti
MRCP PACES MANUAL Louise PealingMA Hons (Cantab) MBBSMScMRCPMRCGP General Practitioner and Clinical Research Fellow, Nuffield Department of Primary Care Health Sciences, University of Oxford Benjamin Mullish MBBChirMA (Cantab) MRCPAFHEA Specialty Registrar/A
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