Focal pruritus may have a neurological cause. According to the underlying mechanism, two categories of central itch have been distinguished, neuropathic and neurogenic pruritus. We here describe a patient with Brown-Séquard syndrome related to unilateral damage of the spinal cord. The patient progressively developed neuropathic pruritus with chronic prurigo lesions showing strictly hemicorporal distribution. The patient was given pregabalin, an analogue of the neurotransmitter γ-aminobutyric acid,with significant improvement. Our observation of chronic prurigo with hemicorporal involvement is unique. It underscores the importance of a detailed neurological examination in case of persistent localized itch and further supports the idea that chronic prurigo reflects a neurological problem in a subset of affected patients. Antiepileptic drugs should be considered not only for neuropathic pain, but also for neuropathic itch.
Background:In several studies, antiretroviral drugs (principally zidovudine) have been used with success in the treatment of myelopathy associated with human Tlymphotrophic virus 1 (HTLV-1) (tropical spastic paraparesis-HTLV-1-associated myelopathy). The retrovirus HTLV-1 has been implicated as a causative agent of Sjö gren syndrome (SS) in clinical reports and murine experiments. Moreover, a recognized complication of primary SS is a myelopathy, which has been shown in case reports to respond to immunosuppressive treatment.Objective: To describe a patient with a rapidly progressive, extensive myelopathy with evidence of HTLV-1 infection and SS (probably secondary to HTLV-1) in whom we achieved spectacular therapeutic success using combined immunosuppressive and antiviral therapy.
not only showed impairment of the anterior horn neurons but also involvement of the descending spinal pathways suggestive of incomplete transverse myelitis. This presumption was supported by the clinical finding of brisk tendon reflexes and a central conduction delay demonstrated by motor evoked potentials. Respiratory muscles were not affected. An additional polyradiculitis cannot be differentiated from an anterior horn lesion by clinical symptoms or electrophysiologically. One argument in favour of a polyradiculitis was the clearly increased total protein in our patient. MRI did not disclose any spinal cord lesion. A low incidence of cerebral or spinal MRI lesions in TBE infection has also been reported elsewhere. 1 Thus MRI is of limited value in the diagnosis of TBE. 1 This may be explained by the rapid resolution of early T2 hyperintensities. Resolution of MRI lesions despite the limited clinical improvement after 6 weeks has been described by Beer et al. 6 This seems to be in contrast with lesions in brain parenchyma in which a good correlation between clinical improvement and restitution of T2 abnormalities has been found. 2 This unusual case shows that even in patients presenting with incomplete transverse myelitis without signs of meningitis or meningoencephalitis, a TBE virus infection should be considered as a differential diagnosis.
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