Clinical Features

  • Sergio Canavero
  • Vincenzo Bonicalzi
Chapter

Abstract

Brain central pain (BCP) has been caused by all kinds of lesions at any level along the spinothalamoparietal path, from brainstem to cortex. These include rapidly or slowly developing processes, compressive or disruptive/distractive. Minor indirect trauma can also cause BCP [1, 2]. Stroke, either ischemic or hemorrhagic, is the commonest cause of BCP. The entire spectrum of causes of stroke can lead to CP. Several instances of rare etiologies are on record. De la Cruz-Cosme et al. [3] reported on an 18-year-old man who developed sudden bilateral amaurosis with subsequent transient loss of consciousness and hypotonia followed by right frontal headache, left limbs numbness, and feeling of weakness. Left hemiparesis with ipsilateral hemihypesthesia followed (days) by development of hyperalgesia and allodynia (including hemiface) and motor impairment (thalamic hand) were observed. The final diagnosis was cryptogenic cerebral infarction associated to patent foramen ovale that led to CPSP (thalamic). One year after percutaneous closure of the foramen, recovery was complete with no more pain. Zaki et al. [4] reported on an HIV-infected 10-year-old boy, with a history of excessive sleepiness for 8 days and fever for 2 days. Constant and burning pain plus allodynia was present since 10 days, with loss of both superficial (touch, pinprick, and temperature) and deep (vibration and position sense) sensations in the left upper and lower limb. The final diagnosis was CP secondary to CytoMegaloVirus vasculitis affecting the right thalamus: antiviral therapy led to full resolution. Ruggieri et al. [5] described four children, who developed reversible CP and thalamic analgetic syndromes during measles infection. On MRI, there was evidence of deep cerebral vein thrombosis and lesions localized selectively to both capsulothalamic regions. Verma et al. [6] reported on a 17-year-old boy with a 2-month history of a sudden onset tingling sensation (paresthesia) over the left hemibody accompanied by forgetfulness and apathy. Within 7–8 days of onset, paresthesia improved. The final diagnosis was multiple small infarcts also involving the thalami due to a craniovertebral junction anomaly: surgery led to complete recovery after 1 month.

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Copyright information

© Springer International Publishing AG 2018

Authors and Affiliations

  • Sergio Canavero
    • 1
  • Vincenzo Bonicalzi
    • 2
  1. 1.HEAVEN/GEMINI International Collaborative GroupTurinItaly
  2. 2.AOUCittà della Salute e della Scienza di Torino, Department of Neurosciences, Rita Levi MontalciniUniversità di TorinoTurinItaly

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