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False Localising Signs a J Larner 415 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.4.415 on 1 April 2003. Downloaded from PHYSICAL SIGNS False localising signs A J Larner ............................................................................................................................. J Neurol Neurosurg Psychiatry 2003;74:415–418 Neurological signs have been described as “false FALSE LOCALISING SIGNS ASSOCIATED localising” if they reflect dysfunction distant or remote WITH INTRACRANIAL LESIONS Sixth nerve palsy from the expected anatomical locus of pathology, hence Sixth nerve palsy, either unilateral or bilateral, is challenging the traditional clinicoanatomical correlation the classic example of a false localising sign. It paradigm on which neurological examination is based. occurs in the context of raised intracranial pressure of whatever cause (supratentorial or False localising signs occur in two major contexts: as a infratentorial space occupying lesion, idiopathic consequence of raised intracranial pressure, and with intracranial hypertension, cerebral venous sinus spinal cord lesions. Cranial nerve palsies (especially thrombosis). It was the most common of the false localising signs observed by Collier (12/20) in sixth nerve palsy), hemiparesis, sensory features (such cases of intracranial tumour.2 In a retrospective as truncal sensory levels), and muscle atrophy, may all review of 101 cases of idiopathic intracranial occur as false localising signs. Awareness that signs hypertension (IIH), Round and Keane noted 14 cases (11 unilateral, three bilateral).5 IIH with may be false localising has implications for diagnostic sixth nerve palsy in the absence of papilloedema investigation. has also been reported.6 .......................................................................... The pathophysiological mechanism of sixth nerve palsy with increased intracranial pressure has traditionally been said to be stretching of the he clinical examination of the nervous nerve in its long intracranial course, or compres- system is based on the premise of clinicoana- sion against the petrous ligament or the ridge of Ttomical correlation, with a particular neuro- the petrous temporal bone. Collier, however, was logical sign indicating pathology at a specific “unable to accept this explanation”, his view locus or pathway within the nervous system.1 being that since the sixth nerve emerges straight Occasionally, however, this semiology “breaks forward from the brain stem, whereas other down”, in that neurological signs may reflect cranial nerves emerge obliquely or transversely, it pathology distant from the expected anatomical is more liable to the mechanical effects of locus. backward brain stem displacement by intracra- The notion of “false localising signs” was first nial space occupying lesions. elucidated by James Collier in 1904: on the basis http://jnnp.bmj.com/ of clinical examination during life and subse- Fifth and seventh nerve false localising signs quent postmortem studies, he noted false localis- Dysfunction of the fifth and seventh cranial ing signs in 20 of 161 consecutive cases of intra- nerves has also been reported with raised intra- cranial tumour examined pathologically, most cranial pressure.2 7–16 This dysfunction may be occurring in patients with supratentorial hypoactive or hyperactive, manifesting with nega- 2 lesions. Despite this high frequency (12.4%), tive or positive Jacksonian symptoms, respec- Collier felt false localising signs were being tively; hence there may be trigeminal neuro- 2 7–10 11–13 observed less frequently because of the earlier pathy or trigeminal neuralgia, facial palsy on September 23, 2021 by guest. Protected copyright. diagnosis of tumours, a theme reiterated by later of lower motor neurone type,291415 or hemifacial authors, implying that such signs are a late spasm.12 16 Fifth and seventh nerve involvement 2 feature in the natural history of tumours. Gassel has been recorded in the context of posterior noted false localising signs to be more common in 279 3 fossa neoplasms or more diffuse neoplastic patients with raised intracranial pressure. disease,15 and with IIH.81014Reports of false local- As there have been few previous reviews of 34 ising seventh nerve palsies suggest they most false localising signs, this article attempts a often occur at the same time as, or after, the brief overview of these phenomena and their pos- development of sixth nerve palsies.2914 Brain sible pathophysiology. It does not aim to provide stem distortion resulting in traction on cranial ....................... an exhaustive review of publications on the nerves has been suggested as the pathophysi- subject, most of which are case reports or small 7 Dr A J Larner, Consultant ological mechanism in tumour associated cases, Neurologist, Walton case series rather than systematic studies. Rather, but this seems a less compelling explanation for Centre for Neurology and it selects illustrative examples, particularly where IIH cases. Neurosurgery, Lower Lane, these elucidate possible pathophysiological Fazkerley, Liverpool L9 7LJ, Collier suggested that motor involvement pre- mechanisms. 2 UK; a.larner@ ceded sensory features in fifth nerve palsy, but Structural brain imaging, particularly mag- thewaltoncentre.nhs.uk the clinical features reported in subsequent cases netic resonance imaging (MRI), affording as it Received does the opportunity to study pathological 11 December 2002 Accepted anatomy contemporaneous with clinical exam- ................................................. 13 December 2002 ination, has provided some new insights into the Abbreviations: IIH, intracranial hypertension; MRI, ....................... causes of these signs. magnetic resonance imaging www.jnnp.com 416 Larner J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.4.415 on 1 April 2003. Downloaded from suggest sensory findings are more prominent.7–10 Gassel found phenomenon (or, perhaps more correctly, the Kernohan- motor involvement in only two of eight patients with false Woltman notch phenomenon), in which the free edge of the localising fifth nerve involvement.3 Arsava et al reported both tentorium compresses the contralateral crus cerebri in the clinical and electrophysiological evidence of left trigeminal midbrain.19 Acute subdural haematoma is a common cause. neuropathy in a patient with IIH: examining the blink reflex, Homolateral hemiparesis and third nerve palsy, both ipsilat- no response was elicited either ipsi- or contralaterally when eral to the lesion, may result,20 although unilateral pupil dila- stimulating the left supraorbital nerve, and although trigemi- tatation is the earliest consistent sign of herniation. nal motor function was clinically intact, no response was elic- ited from the left masseter muscle when measuring the Other false localising signs reported with intracranial latency of the jaw reflex.10 pathology Unlike fifth and seventh nerve palsies, trigeminal neuralgia A number of other false localising signs have been reported in and hemifacial spasm have only been reported in the context of association with raised intracranial pressure. Trochlear nerve posterior fossa mass lesions, most usually tumours,11–13 16 but palsy has occasionally been described, along with the sugges- also chronic calcified subdural haematoma. As with the tion that it might be overlooked in cases in which other cranial idiopathic condition, there has been debate about the patho- nerves are affected (sixth, third) because the signs are physiology of trigeminal neuralgia associated with contralateral subtle.21 Although Collier observed no cases of trochlear nerve tumours. Some favour vascular compression of the nerve root as palsy, he denied the possibility that they had been overlooked 11 the proximate cause of paroxysmal ephaptic transmission, clinically, on the grounds that they produce a distressing whereas others implicate angulation and distortion of the nerve diplopia.2 Unilateral hearing loss has been reported in IIH,22 root entry/exit zone as a consequence of displacement of brain although tinnitus is the more common otological problem in tissue caused by an expanding mass lesion in the posterior this condition.5 12 13 fossa. In favour of the latter explanation, two cases have been Unilateral papilloedema may be described as false localising reported in which trigeminal neuropathy was “converted” to when associated with contralateral visual loss and optic atro- trigeminal neuralgia (hence, a lesser degree of dysfunction) fol- phy due to subfrontal or middle cranial fossa en plaque menin- 12 13 lowing removal of a contralateral posterior fossa tumour. gioma (Foster-Kennedy syndrome).23 Papilloedema resulting However, other cases have been presented in which trigeminal from high CSF protein concentration may initiate an inappro- 13 neuralgia did not resolve after tumour removal alone. Matsu- priate search for an intracranial mass lesion. ura and Kondo implicate adherence of arachnoid membrane to “Frontal ataxia”, a cerebellar type of ataxia resulting from the nerve as a contributing factor and advocate its resection in lesions of the contralateral frontal cortex in which fibres of the 12 order to straighten the nerve axis. corticopontocerebellar pathway are said to be interrupted, is Hemifacial spasm as a false localising sign of posterior fossa also a false localising sign, but its frequency is uncertain. tumour seems altogether rarer than trigeminal neuralgia, 12 16 Round and Keane reported four patients in
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