1/8. hyperalgesia with reduced laser evoked potentials in neuropathic pain.Nociceptive evoked potentials to laser stimuli (LEPs) are able to detect lesions of pain and temperature pathways at peripheral, spinal and supraspinal levels. It is commonly accepted that LEP attenuation correlates with the loss of pain and temperature sensations, while pathological heat-pain hypersensitivity has been associated with increased LEP amplitude. Here we present two patients in whom increased pain sensation (hyperalgesia) to laser stimuli was, on the contrary, associated to delayed, desynchronized and attenuated LEPs. Both patients experienced increased unpleasantness and affective reactions to laser, associated to poor ability to localize the stimulus. In both cases the results may be explained by an overactivation of the 'medial pain system', in one patient due to deafferentation of cortical sensory areas by a capsular lesion, and in the other to imbalance between A-delta and C fiber excitation due to peripheral nerve injury. Our results suggest that LEPs, as currently recorded, reflect the activity of a 'lateral' pain system subserved by rapidly conducting fibers. They may therefore, assess the sensory and cognitive dimensions of pain, but may not index adequately the affective-emotional aspects of pain sensation conveyed by the 'medial' pain system. The dissociation between pain sensation and cortical EPs deserve to be added to the current semiology of LEPs, as the presence of abnormal pain to laser on the background of reduced LEPs substantiates the neuropathic nature of the pain.- - - - - - - - - - ranking = 1keywords = spinal (Clic here for more details about this article) |
2/8. The development of cutaneous allodynia during a migraine attack clinical evidence for the sequential recruitment of spinal and supraspinal nociceptive neurons in migraine.Recently, we showed that most migraine patients exhibit cutaneous allodynia inside and outside their pain-referred areas when examined during a fully developed migraine attack. In this report, we studied the way in which cutaneous allodynia develops by measuring the pain thresholds in the head and forearms bilaterally at several time points during a migraine attack in a 42-year-old male. Prior to the headache, he experienced visual, sensory, motor and speech aura. During the headache, he experienced photo-, phono- and odour-phobia, nausea and vomiting, worsening of the headache by coughing or moving his head, and cutaneous pain when shaving, combing his hair or touching his scalp. Comparisons between his pain thresholds in the absence of migraine and at 1, 2 and 4 h after the onset of migraine revealed the following. (i) After 1 h, mechanical and cold allodynia started to develop in the ipsilateral head but not in any other site. (ii) After 2 h, this allodynia increased on the ipsilateral head and spread to the contralateral head and ipsilateral forearm. (iii) After 4 h, heat allodynia was also detected while mechanical and cold allodynia continued to increase. These clinical observations suggest the following sequence of events along the trigeminovascular pain pathway of this patient. (i) A few minutes after the initial activation of his peripheral nociceptors, they became sensitized; this sensitization can mediate the symptoms of intracranial hypersensitivity. (ii) The barrage of impulses that came from the peripheral nociceptors activated second-order neurons and initiated their sensitization; this sensitization can mediate the development of cutaneous allodynia on the ipsilateral head. (iii) The barrage of impulses that came from the sensitized second-order neurons activated and eventually sensitized third-order neurons; this sensitization can mediate the development of cutaneous allodynia on the contralateral head and ipsilateral forearm at the 2-h point, over 1 h after the appearance of allodynia on the ipsilateral head. This interpretation calls for an early use of anti-migraine drugs that target peripheral nociceptors, before the development of central sensitization. If central sensitization develops, the therapeutic rationale is to suppress it. Because currently available drugs that aim to suppress central sensitization are ineffective, this study stresses the need to develop them for the treatment of migraine.- - - - - - - - - - ranking = 4keywords = spinal (Clic here for more details about this article) |
3/8. Direct clinical evidence for spinal hyperalgesia in a patient with irritable bowel syndrome.OBJECTIVE: Our objective was to evaluate GI motor and sensory function and spinal cord testing in a patient with severe irritable bowel syndrome. methods: A patient is described who underwent an extensive assessment of GI motor and sensory function including transit studies, colonic and rectal barostat studies, sensory and manometric studies of the small bowel, and colon and anorectal physiology testing. The patient also underwent testing with spinal cord stimulation and spinal drug delivery as part of a pain management assessment. RESULTS: The viscerosomatic referral pain pattern resulting from rectal distention was consistent with spinal hyperalgesia. The patient underwent testing for spinal cord stimulation and spinal drug delivery. CONCLUSION: This novel finding provides direct clinical evidence for the presence of spinal hyperalgesia in a patient with irritable bowel syndrome, consistent with the existing indirect clinical evidence and animal data.- - - - - - - - - - ranking = 5.5keywords = spinal (Clic here for more details about this article) |
4/8. Long-term treatment with ketamine in a 12-year-old girl with severe neuropathic pain caused by a cervical spinal tumor.A 12-year-old girl presented with head and neck pain, myoclonic movements, and decreased strength in all extremities caused by a cervical spinal tumor (glioblastoma multiforme). A partial resection of the tumor was performed. Three weeks later, she had superficial pain distributed in all dermatomes below her cervical medullary lesion. touch (e.g., gentle hugs from relatives) and movements elicited paroxysm of intense pain. The pain was not relieved by increased doses of morphine. A test dose of ketamine (7.5 mg intravenous) provided an abrupt decrease in pain intensity, and continuous infusions of subcutaneous morphine and intravenous ketamine were started. benzodiazepines were administered to avoid psychotomimetic effects from ketamine and to diminish myoclonic movements. The doses of analgesics and benzodiazepines were increasingly titrated (subcutaneous morphine 163-750 mg/24 hr, intravenous ketamine 36-410 mg/24 hr, subcutaneous midazolam 5-20 mg/24 hr, and intravenous diazepam 11.5-122.5 mg/24 hr) until her death 67 days after start of ketamine. She remained awake until the last day before her death. For the last 29 days of life, the pain treatment regimen was successfully continued in her home (400-km distance from the hospital). In conclusion, this case demonstrates that ketamine treatment may be effective in children with severe neuropathic pain not responsive to other analgesics. This patient also demonstrates the feasibility of long-term ketamine treatment in pediatric oncology and that such treatment can be administered in a home care setting.- - - - - - - - - - ranking = 2.5keywords = spinal (Clic here for more details about this article) |
5/8. Treatment of chronic neuropathic pain after traumatic central cervical cord lesion with gabapentin.central cord syndrome may be associated with severe pain, resistant to conventional pain therapy regimens. chronic pain may be a persistent problem in rehabilitation of spinal cord injuries. These pain syndromes are long lasting and challenging to treat. Gabapentin has been shown to be useful in treatment of different conditions which may be caused by increased neuronal excitability. This report describes a case where central cord syndrome and its chronic neuropathic pain associated with allodynia was successfully treated with gabapentin.- - - - - - - - - - ranking = 0.5keywords = spinal (Clic here for more details about this article) |
6/8. Insights into the pathophysiology of neuropathic pain through functional brain imaging.We present here an example case of neuropathic pain with heat allodynia as a major symptom to illustrate how the functional imaging of pain may provide new insights into the pathophysiology of painful sensory disorders. Tissue injury of almost any kind, but especially peripheral or central neural tissue injury, can lead to long-lasting spinal and supraspinal re-organization that includes the forebrain. These forebrain changes may be adaptive and facilitate functional recovery, or they may be maladaptive, preventing or prolonging the painful condition, and interfering with treatment. In an experimental model of heat allodynia, we used functional brain imaging to show that: (1) the forebrain activity during heat allodynia is different from that during normal heat pain, and (2) during heat allodynia, specific cortical areas, specifically the dorsolateral prefrontal cortex, can attenuate specific components of the pain experience, such as affect, by reducing the functional connectivity of subcortical pathways. The forebrain of patients with chronic neuropathic pain may undergo pathologically induced changes that can impair the clinical response to all forms of treatment. Functional imaging, including PET, fMRI, and neurophysiological techniques, should help identify brain mechanisms that are critical targets for more effective and more specific treatments for chronic, neuropathic pain.- - - - - - - - - - ranking = 1keywords = spinal (Clic here for more details about this article) |
7/8. horner syndrome with causalgia.A previously healthy man presented with burning pain in the chest wall and arm; there was horner syndrome on the same side. After extensive investigation, the disorder was attributed to a foraminal osteophyte involving the left T1 spinal root.- - - - - - - - - - ranking = 0.5keywords = spinal (Clic here for more details about this article) |
8/8. Chronic opioid therapy as alternative treatment for post-herpetic neuralgia.neurosurgical procedures such as the dorsal root entry zone operation, ganglionectomy, and spinal-cord stimulation have been offered to patients with intractable post-herpetic neuralgia (PHN). Poor efficacy or high morbidity have limited the overall usefulness of these procedures. We recently conducted a preliminary open-label study with long-acting oral opioids. The mean pretreatment pain score, on a scale of 0 to 10 (0 = no pain) was 9.0 /- 0.3 (mean /- SEM, N = 20). At two months of treatment the average pain score was 4.0 /- 0.4 (p < 0.001, paired t test), and at six months the average pain score was 3.8 /- 0.2 (p < 0.001, N = 16). These observations warrant a controlled opioid trial for patients affected by PHN.- - - - - - - - - - ranking = 0.5keywords = spinal (Clic here for more details about this article) |