ABSTRACT
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 gamma-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.
Subject(s)
Brown-Sequard Syndrome/complications , Prurigo/etiology , Pruritus/etiology , Skin/pathology , Spinal Cord Injuries/complications , Adult , Anticonvulsants/therapeutic use , Antipruritics/therapeutic use , Humans , Male , Neurologic Examination , Pregabalin , Prurigo/drug therapy , Prurigo/pathology , Pruritus/drug therapy , Skin/innervation , gamma-Aminobutyric Acid/analogs & derivatives , gamma-Aminobutyric Acid/therapeutic useABSTRACT
Orthostatic hypotension (OH) is one of the many autonomic disturbances observed in Parkinson's disease (PD). It has been debated whether an additional impairment of cerebral autoregulation (CA) in PD patients may exacerbate the consequences of OH upon brain perfusion. We assessed CA in PD patients and the potential influence of dopaminergic agents. CA was determined by means of transcranial Doppler (TCD) monitoring of the middle cerebral artery (MCA) at rest and during a thigh cuff release test inducing a systemic blood pressure (BP) drop. Fourteen patients were investigated when taking their usual dopaminergic medication and after drug discontinuation for 12 h. A control group was composed of 11 age-matched subjects (CS). In comparison with PD patients, CS presented a significantly higher increase of the mean cerebral blood flow velocities in the MCA after the BP drop. Mean velocities were increased above the initial values in all CS, whereas a flattened curve was observed in PD patients. No significant differences could be further observed between the PD patients regarding the BP, the cerebrovascular resistance, the heart rate and the pulsatility index. These results provide evidence of an impaired cerebral autoregulation in PD patients which appears independent of dopaminergic treatment.
