Understanding Neurology

222weakness, wasting, or reflex loss should be assessedfor. Nerve stretching manoeuvres (e.g. straight legraising) may exacerbate pain, as may certain postures(bending over). Percussion or compression of nervesover entrapment sites (Tinel’s sign) may increaseparaesthesiae or numbness, and/or cause pain.Multiple focal sites can be affected in mononeuritismultiplex, often sequentially, sometimes flitting, and itis frequently due to vasculitis. Multiple spinal roots canbe affected by infiltrative disease within the spinalcanal/dura, often affecting the lumbo-sacral roots as inlepto-meningeal carcinomatosis.Distal limb sensory loss, progressing proximally, isa feature of dying-back polyneuropathies, such asthose due to vitamin deficiencies and diabetes.Pathologically, there is axonal degeneration affectingthe axon most distal to the cell body initially. Usuallythere is sensory loss to the level of the knee before theupper limbs are involved. Exceptions to this ruleinclude the sensory neuronopathy associated with thesicca syndrome and paraneoplastic sensory neuropathy(dorsal root ganglionopathies). Reflexes are frequentlylost early in peripheral polyneuropathies. A pseudoneuropathic(peripheral) pattern can be seen in cervicalcord compression whereby patients present with distallimb paraesthesiae. On examination however, therewill be upper motor neurone signs (i.e. brisk reflexesrather than depressed or absent reflexes). Distal limbparaesthesiae can also be a feature of multiple sclerosis.Sensory loss affecting the perineum suggests aconus medullaris or cauda equina lesion. This isassociated with loss of sphincter control, i.e. bladderand bowel dysfunction. Sensory loss with a level onthe trunk indicates spinal cord disease. Often patientscomplain of pain or heightened sensation at the upperlevel. Causes include cord compression (e.g. tumour ordisc protrusion), inflammation (transverse myelitis),and vascular disease (anterior spinal artery syndrome,posterior column function preserved). Hemicordsyndromes can present with ipsilateral posteriorcolumn (proprioceptive loss), and contralateral spinothalamicloss (Brown-Séquard syndrome); there maybe ipsilateral motor loss. Central cord lesions (e.g.intrinsic cord tumours and syringomyelia) tend tocause bilateral spino-thalamic loss initially, due tointerruption of the decussating fibres, followed bymotor loss. These lesions may present with asuspended sensory loss, i.e. with preserved sensationdistally. An example of this is a syrinx affecting thecervical spinal cord that presents with ‘cape’distribution spino-thalamic sensory loss.The hallmark of brainstem sensory loss is crossedspino-thalamic sensory loss, i.e. trigeminal (facial)sensory loss ipsilateral to the lesion, with limb/trunkloss on the contralateral side. The lateral medullarysyndrome of Wallenburg is a good example of this.Thalamic lesions are associated with hemipaindisturbances (thalamic syndrome, is often burning innature), often with retained simple sensations.Cortical sensory syndromes are again characterizedby unilateral symptoms (unless bilateral corticallesions), intact simple sensations (appreciated at thethalamic level), but impaired integrated sensorymodalities (Table 60).The handSensory examination of the hand deserves particularattention. Peripheral nerve lesions, especially thosedue to trauma (acute and chronic), and less frequentlyas a result of vasculitis and granulomatous disorders,are especially common in the upper limb. Partial andchronic lesions often present with sensory symptomsprior to the onset of weakness and wasting. Radicularand brachial plexus lesions are more unusual, andoften have coexisting motor features at presentation.The hand receives its sensory innervation from threeperipheral nerves: median (C5–T1), ulnar (C8, T1),and radial (C6, 7, 8) nerves, derived from three spinalroots (C6, 7, 8) (163, 164). The median nervesupplies the radial three and a half digits andassociated palmar surface; the ulnar nerve the littleand half of the ring finger, as well as the ulnar surfaceof the palm. Sensation from the dorsal surface of thehand and digits as far as the distal phalanges ismediated via the radial nerve (may be more proximalin ulnar innervated digits).Sensory loss splitting the ring finger is a usefulfeature to distinguish median and ulnar nerve lesionsfrom more proximal lesions (plexus and root), but ina small percentage of people the ring finger issupplied by either nerve completely. The median andulnar nerves supply the intrinsic muscles of the hand:the median nerve supplies the two radial lumbricalmuscles and the muscles of the thenar eminence barthe adductor pollicis and flexor pollicis brevismuscles; these and the rest of the intrinsic handmuscles are supplied by the ulnar nerve. Themyotomal innervation of the hand muscles is via theC8 and T1 nerve roots. Thus, wasting in specificmuscle groups may be an aid to diagnosing focallesions and may precede frank symptomaticweakness. Advanced ulnar nerve lesions will produce