Cases reported "Hyperalgesia"

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1/45. 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. ( info)

2/45. 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. ( info)

3/45. Treatment of central post-stroke pain with oral ketamine.

    Case report of 68 year old female with central post-stroke pain successfully treated with oral ketamine. The patient's pain was refractory to conventional pain treatments and she had persistent right hemi-body neuropathic pain with allodynia and hyperalgesia. An intravenous ketamine trial, followed by oral ketamine with titration to 50mg three times a day was beneficial in decreasing allodynia and hyperalgesia, as well as improving functional capabilities. Known side effects including dysphoria, hallucinations, and paranoid feelings were attenuated with benzodiazepines. ( info)

4/45. 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. ( info)

5/45. chest pain. Differentiating GIT from cardiac causes.

    BACKGROUND: chest pain is a common presenting symptom in general practice. Although a cardiac cause is not the commonest origin, a high index of suspicion is needed. When the diagnosis is not clear, a cardiac cause should be considered until proven otherwise. A gastrointestinal origin of chest pain is not infrequent and may be due to oesophageal, gastric or biliary disease. Oesophageal causes are most common and include reflux, hypersensitivity or dysmotility. OBJECTIVE: This paper reviews the main gastrointestinal causes that may present with acute chest pain. DISCUSSION: Clinical history taking is the key to decision making and guides the choice of prompt or routine investigation or a therapeutic trial. When reflux is suspected as the cause, a therapeutic trial of high dose antisecretory therapy is appropriate. Investigations may be helpful when typical reflux symptoms are not present or there is a poor response to this approach. Investigations may include endoscopy, ambulatory pH monitoring, barium swallow or oesophageal manometry. ( info)

6/45. 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. ( info)

7/45. Disruption of thermal perception in a multiple sclerosis patient with central pain.

    OBJECTIVE: To investigate integrative thermal perception in a patient with multiple sclerosis. DESIGN: Quantitative thermosensory testing was used to evaluate pain and other sensations produced by heat, cold, and the thermal grill pain illusion. PATIENT: The authors report on a 43-year-old patient with central pain manifest most strongly in her left arm and hand, contralateral to an upper cervical spinothalamic lesion due to multiple sclerosis. OUTCOME MEASURES AND RESULTS: Quantitative thermosensory testing showed that the patient had heat hypalgesia (no pain with stimuli of 45-50 degrees C) and cold allodynia (pain with innocuous cool temperatures, 25-10 degrees C). Whereas healthy subjects rated 20 degrees and 40 degrees C as nonpainful, but the thermal grill (intermixed 20 and 40 degrees C stimuli) as painful, the patient rated the thermal grill as less painful than 20 degrees C. CONCLUSIONS: The absence of thermal grill-evoked pain is consistent with the hypothesis that in some cases of central pain the loss of the thermosensory pathway results in disruption of the normal cold inhibition of burning pain. ( info)

8/45. Analgesic effects of ketamine ointment in patients with complex regional pain syndrome type 1.

    OBJECTIVE: ketamine hydrochloride (KET), an agent used for general anesthesia, has local anesthetic effects and N-methyl-D-aspartate (NMDA) receptor antagonist action. Because recent studies emphasized the role of peripherally distributed NMDA receptors in processing the nociceptive information, we investigated whether peripheral application of the ointment containing KET is able to attenuate the symptoms of local neuropathic pain. case reports: We applied ointment containing KET (0.25%-1.5%) to the affected area on limbs in 5 patients with complex regional pain syndrome type I (CRPS I) and in 2 patients with type II (CRPS II). One to 2 weeks later, we observed improvement of the report of pain intensity, measured by the visual analog scale, in 4 patients with acute early dystrophic stage of CRPS I. Swelling of the affected limbs subsided as well. No apparent changes were noticed in 1 patient with chronic atrophic stage of CRPS I and in both patients with CRPS II. CONCLUSION: Topical application of KET appears to be beneficial for the patients with acute early dystrophic stage of CRPS I because of either its local anesthetic effect or NMDA receptor antagonist action. patients with chronic atrophic stage of CRPS I and CRPS II patients do not appear to respond to this treatment. ( info)

9/45. hyperalgesia: an emerging iatrogenic syndrome.

    Clinical reports suggest that opioids, intended to abolish pain, can unexpectedly produce hyperalgesia. This paradoxical effect may be mechanistically related to tolerance induced by increasing doses of opioids. Two case reports illustrate a syndrome characterized by increasing pain pursued by escalating opioid doses, which results in a worsening of the clinical picture. Several experimental data may help explain the course of this challenging clinical condition. In escalating opioid doses rapidly, a risk of opioid-induced hyperalgesia should be recognized, as higher doses of opioids may stimulate rather than inhibit the central nervous system by different mechanisms. Alternative procedures should be taken into consideration to break this cycle, should it occur. More data are needed to detect this condition, as currently no diagnostic information on specific markers, clinical or biochemical, exists. ( info)

10/45. 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. ( info)
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