False localizing signs occur when neurological signs and symptoms are caused by damage distant from the primary site of pathology. They challenge traditional models of clinico-anatomical correlation and localization. Common causes of false localizing signs include increased intracranial pressure and spinal cord lesions. Examples include cranial neuropathies, hemiparesis contralateral to supratentorial lesions, and radicular symptoms in idiopathic intracranial hypertension. Recognition of false localizing signs is important to avoid mislocalization and consider potentially life-threatening underlying causes.

1. FALSE LOCALISING SIGNS IN
NEUROLOGY
Indian Journal of Clinical Practice, Feb 2013: 553-559.

2. SPECIFIC LOCALIZING SIGNS
 Signs elicited during neurologic examination are thought to be
SPECIFIC / FOCAL LOCALIZING SIGNS if their presence indicates a
lesion at a specific area in the nervous system.
 The neurologist must decide whether the symptoms and signs
could all arise from one focal lesion, or whether several
anatomical sites must be involved.
 The Principle of Parsimony, or Occam’s Razor, requires that the
clinician strives to hypothesize only one lesion.
 The differential diagnosis for a single focal lesion is significantly
different from that for multiple lesions.

3. OCCAM’S RAZOR

4. FALSE LOCALIZING SIGNS
 In contrast, Clinical features caused by damage far from the
primary site of abnormality are called False Localising Signs.
 Reflect dysfunction distant from the expected anatomical
location of pathology
 Challenge the traditional clinico-anatomical correlation
paradigm on which neurological examination is based.
 Falseness exists with the Interpretation of the findings.

5. HISTORY
 The term derives from the era before neuroimaging
studies, when clinical examination was the major means
of lesion localization.
 James Collier first described cerebellar tonsillar
herniation in 1904
 Subsequent scientists noted them to be more common in
raised ICP.

6. PATHOGENESIS
 Presence suggests that intracranial shifts are marked.
 Indicating the presence of markedly raised ICP, or large
space occupying lesions in the skull.
 The “False”hood is in the interpretation.

7. PATHOGENESIS
 False localizing signs occur in two common contexts:
 As a consequence of raised ICP, which may be:
◦ Secondary to or symptomatic of intracranial pathology (tumor,
hematoma, abscess), or
◦ Primary, or Idiopathic (IIH), and
 Spinal Cord Lesions
 Course: acute (intracranial hemorrhage), or chronic (IIH,
tumor)

8. CORTICAL FUNCTIONS
 APHASIA
 Subcortical aphasia may result from lesions of:
◦ Basal ganglia,
◦ Anterolateral nuclei of the thalamus, and
◦ Peri-capsular white matter of the dominant hemisphere.
 Lesions of post limb of the int capsule (ICp) typically
produces aphasia with:
◦ Rapid fluent speech with paraphasias and extended jargon,
◦ Poor comprehension, and impaired repetition.
J Neuropsychiatry Clin Neurosci 27:2, Spring 2015

9. CORTICAL FUNCTIONS
 Lesions of the ant limb of int capsule (ICa) (and often the
genu [ICg]) typically produces aphasia with:
◦ Grammatical but slow dysarthric speech,
◦ Impaired syntactic comprehension, and
◦ Impaired repetition for low-probability sentences
◦ Impaired articulatory agility, buccofacial apraxia.
◦ Concomitant neuropsychiatric disturbances (executive
dysfunction, diminished motivation, emotional lability)
J Neuropsychiatry Clin Neurosci 27:2, Spring 2015

10. CORTICAL FUNCTIONS
 An atypical variant involving posterior shift of corticonuclear,
corticospinal, and sensory fibers within the ICp would
concurrently permit broader distribution of frontopontine,
thalamofrontal, and thalamostriate pathways from the ICa
into the ICg and the anterior portion of the ICp.
 Variant capsular anatomy of this nature offers a parsimonious
explanation for this patient’s clinical presentation with
poststroke subcortical aphasia and neurobehavioral
disturbances without motor or sensory deficits.
J Neuropsychiatry Clin Neurosci 27:2, Spring 2015

11. J Neuropsychiatry Clin Neurosci 27:2, Spring 2015

12. CRANIAL NERVES
 MECHANISM OF CRANIAL NERVE SIGNS:
◦ Extrinsic compression of the nerve on the tentorial margin or petrous
temporal bone, M. C. Localising.
◦ Kinking or Stretching of the nerves in their intracranial course, over the
clivus, just posterior to the clinoid, due to raised ICP, M. C. False
Localising.
◦ Supratentorial pressure causing the brainstem to buckle as it descends
because of caudal tethering of the neuraxis at the first dentate
ligament (“dynamic axial brainstem distortion”)

14. CRANIAL NERVES
 There may be Hypo- or Hyper-function of a cranial nerve,
 Manifesting as negative or positive symptoms, resp.
◦ Negative symp- Sensory Neuropathy or motor weakness
◦ Positive symp- Neuralgia
 PATHOPHYSIOLOGY:
◦ Vascular compression of nerve root causes paroxysmal ephaptic transmission,
◦ Angulations and distortion of nerve root entry/exit zone due to mass effect
produces focal neuropathy
◦ Adherence of arachnoid membrane to the nerve

15. CRANIAL NERVES
 PAPILLOEDEMA cannot be reliably used as an indication
of elevated intracranial pressure because its leading
cause in late life is ischemic optic neuropathy.
 HUTCHINSON’S PUPIL = Unilateral fixed dilated pupil
◦ Compression of III N.
◦ Ipsilateral to lesion  more common
◦ Contralateral to lesion  FL
Brain Inj. 2009 July ; 23(7): 597–601.

16. CRANIAL NERVES
 DIVISIONAL III N PALSY
 In keeping with the topographic arrangement of the fascicles
within the nerve,
 Focal : Ant Cavernous Sinus, or Sup Orbital Fissure
 False :
◦ with intrinsic brainstem disease (e.g. stroke), or
◦ with pathology in the subarachnoid space where the nerve rootlets
emerge from the brainstem (e.g. malignant infiltration).

18. CRANIAL NERVES
 INTERNUCLEAR OPHTHALMOPLEGIA
 Focal: Demyelination in Medial Longitudinal Fasciculus
 False :
◦ Myasthenia gravis,
◦ Guillain– Barré syndrome, and Miller Fisher syndrome
◦ Dermatomyositis
◦ SDH  transtentorial herniation  brainstem compression
◦ Cerebellar masses,

19. CRANIAL NERVES
 TRIGEMINAL NERVE
 Hypofunction: Trigeminal Sensory Neuropathy, e.g. in IIH,
unilateral > bilateral
 Hyperfunction: Trigeminal Neuralgia, e.g. with chronic calcified
SDH causing rotational displacement of the pons.
 Contralat posterior fossa tumor  Trigeminal Hypofunction 
Surgical removal of tumor  Trigeminal Neuralgia
 Neuralgia is a lesser degree of dysfunction than neuropathy.

20. CRANIAL NERVES
 SIXTH CRANIAL NERVE
◦ Sixth nerve palsy is the M.C. false-localizing sign of raised ICP.
◦
◦ The deficit is remote from the site of the process producing
intracranial hypertension, hence false localizing.
◦ Included in diagnostic criteria for IIH (Other C.N. is VII).
◦ In one series of 101 cases of IIH, 14 cases were noted, 11
unilateral and 3 bilateral.

21. CRANIAL NERVES
 SEVENTH CRANIAL NERVE
◦ LMN type of facial weakness is described in IIH,
◦ Sometimes B/L to produce facial diplegia.
◦ Hemifacial spasm – Contralateral posterior fossa lesions.
 EIGHTH CRANIAL NERVE
◦ Occasional Complication of IIH

22. CRANIAL NERVES
 Contralat Acoustic Neuroma  V, VI, VII nerve palsies
 Contralat Laterally placed posterior fossa meningioma 
V, IX, X nerve palsies

23. KERNOHAN-WOLTMAN NOTCH PHENOMENON
 Supratentorial Lesion 
 Transtentorial Herniation of Temporal Lobe 
 Compression of Cerebral Peduncle against Tentorial Edge
◦ Focal : Ipsilateral CP  Contralateral Hemiparesis
◦ False : Contralateral CP  Ipsilateral Hemiparesis
 Assoc. Ipsilateral III N Palsy usually present.
 Mechanism: Downward pressure  compression of the
contralateral incisura of the crus cerebri by the tentorial edge.
 Incisura of crus cerebri = Kernohan-Woltman Notch
 Imaging of Kernohan’s Notch now possible by MRI.
Brain Inj. 2009 July ; 23(7): 597–601.

25. CERVICOMEDULLARY JUNCTION
 Aberrant Vertebral Artery  Ipsilateral Medullary
Compression  Hemidiaphragmatic Paralysis
 Paresthesia in the hands, intrinsic hand muscle wasting,
distal upper limb areflexia, with or without long tract
signs (suggestive of a lower cervical myelopathy) may
occur with lesions at the foramen magnum or upper
cervical cord (‘remote atrophy’).

26. SPINAL CORD
 Patients with cervical spondylosis
◦ Painful stiff neck and diffuse nonpulsatile headache that resolves in a few hours of
waking.
◦ Lesion is most commonly at C5/6 and/or C6/7, and have corresponding focal signs
reflecting root dysfunction.
◦ However, Wasting and weakness of the small muscles of the hands (esp. abduction
of the little finger) is often present. This sign localizes to lower segmental levels
but there may be no observable anatomical change at those levels and it is
labeled as a false localizer.
 Compressive lower cervical or upper thoracic myelopathy may produce
spastic paraplegia with a mid-thoracic sensory level (or ‘girdle
sensation’).
 Lumbar spinal disease may be simulated by more rostral pathology.
Urinary retention, leg weakness, and lumbar sensory findings may be the
presenting features of high thoracic cord compression, with clinico-
radiological discrepancy of as much as 11 segments.

27. SPINAL CORD
 Three principal mechanisms have been invoked: arterial, venous, and
mechanical.
 Arterial hypothesis : tumour / disc compromises descending anterior spinal
artery blood supply to lower cervical cord  focal ischemia.
◦ Midline ventral portion of cervical cord was markedly compressed in those with false
localising sensory level, s/o ischemia in the watershed zone of the anterior spinal artery,
affecting the medial portion of the laminations of the spinothalamic tract, as the causative
mechanism for discrepancy
 Venous hypothesis : low pressure venous system is inherently more vulnerable
to compression than arterial  tissue stasis and hypoxia  neurological
dysfunction.
 Mechanical hypothesis : Extrinsic compression + anchoring of spinal cord by the
dentate ligaments  Mechanical stress  Neurological dysfunction.

28. RADICULOPATHY
 False-localizing radiculopathy
◦ may occur in IIH and cerebral venous sinus thrombosis,
◦ manifesting as acral paresthesias, backache and radicular pain,
and
◦ less often with motor deficits, which on occasion may be
sufficiently extensive to mimic GBS.
◦ Mechanism: Root compression due to elevated CSF Pressure.

29. CEREBELLAR SYNDROME
 Damage to Fronto-ponto-cerebellar pathway, e.g. as a
result of ACA territory infarction,  incoordination of the
contralateral limbs, mimicking cerebellar dysfunction.
 Posterior fossa tumors  ataxia as “false localizing” sign-
pt has headache and papilledema

30. PSEUDOATHETOSIS
 Abnormal writhing movements of the fingers,
 Worse on eye closure
 Caused by failure of proprioception along its pathway
from peripheral nerve to parietal cortex.
 It may be mistaken for choreoathetosis, which is
relatively constant irrespective of whether the eyes are
open or closed.

31. OBTURATOR NEUROPATHY
 Obturator Neuropathy: Pelvic Malignancies-
 Many patients appear to have hip flexor weakness as a
false localizing sign.
 May be explained by pain, but it is more likely due to
mechanical disadvantage of the hip flexors in the
presence of weak thigh adductors.

32. PSEUDOSYRINGOMYELIA
 Selective loss of pain and temperature sensation with
relative preservation of vibration and position sense
 Seen in amyloid polyneuropathy and Tangier disease,
both causes of Small Fibre Sensory Neuropathy.

33. IMPORTANCE
 Pose a clinical challenge – cannot be relied upon for
localisation.
 Awareness of situations in which they are most likely to
occur is necessary to heighten clinical suspicion.
 May indicate life-threatening pathology.