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We read with interest the review by Larner1 on false localising signs. Among the various false localising signs described in patients with intracranial hypertension (ICHT), radiculopathy is an important manifestation which is probably under recognised. Many authors have documented subtle features of radiculopathy in patients with isolated intracranial hypertension (IIH). The usual manifestations of radiculopathy in these cases were acral paraesthesias,2 and backache and radicular pain.3,4 Rarely, motor deficits due to radiculopathy caused by ICHT have been described.5,6
Obeid et al reported two patients with extensive radiculopathy due to ICHT5; one individual had IIH and the other had cerebral sinus venous thrombosis. Both persons had papilloedema, marked visual impairment, and flaccid areflexic quadriparesis with normal MRI of brain, brainstem, and cervical spinal cord. The electrophysiological findings were consistent with radiculopathy. Both individuals initially received intravenous immunoglobulin for Guillain–Barré syndrome, without benefit, but they responded well to lumboperitoneal shunting. We also encountered two such cases with angiographically proven cerebral venous sinus thrombosis.6
The most likely mechanism at the basis of radiculopathy appears to be similar to that of other cranial neuropathies in ICHT—that is, mechanical compression of nerve roots, due to elevated CSF pressure distending the subarachnoid space. Documented enlargement of spinal subarachnoid space and distended root pouches in a patient with radicular pain and areflexia due to IIH supports this view.3 Radiculopathy secondary to ICHT has been reported almost exclusively in patients with IIH or cerebral venous sinus thrombosis.
Other causes of ICHT may not induce a diffuse increase in pressure in both intracranial and intraspinal compartments, and are unlikely to manifest as radiculopathy. The constellation of flaccid-areflexic quadriplegia and papilloedema may be misdiagnosed as Guillain–Barré syndrome with papilloedema.5 Careful analysis of the evolution of symptoms, estimation of CSF pressure, and appropriate vascular imaging should help to correctly identify the cause of ICHT.
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