Cases reported "Causalgia"

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11/30. Surgical relief of causalgia with an artificial nerve guide tube: Successful surgical treatment of causalgia (Complex Regional Pain syndrome Type II) by in situ tissue engineering with a polyglycolic acid-collagen tube.

    Two patients with causalgia associated with allodynia and finger contracture were treated surgically with a bioresorbable nerve guide tube made from polygycolic acid and collagen: the injured segment of the digital nerve was resected and the resulting gap (25 and 36mm) was bridged with the tube. In both cases, a neuroma was found on the injured nerve and many sprouting branches were. After reconstruction, the causalgia and allodynia disappeared and movement of the fingers recovered during the following 6 months. Functional recovery was objectively identified for 1 year and 9 months. Both patients regained full use of their finger and were free of discomfort for up to 24 and 18 months, respectively. Since the first description of causalgia in 1864, there has been no definitive treatment for this intractable burning pain. Our experience shows that at least some types of causalgia can be resolved successfully by surgery.
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keywords = nerve
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12/30. Painful neuropathy with trigeminal nerve involvement in type 2 diabetes.

    After several years of treatment for type 2 diabetes mellitus, a 69-year-old Japanese man developed an acute painful neuropathy, characterized by bilateral causalgia and dysaesthesia in his cheeks and around his eyes, typically 30 min to 3 h after meals. As his glycaemic control deteriorated, his haemoglobin (Hb) A1c level gradually increased from 7 - 8% to 10.3% and his symptoms became more severe. The pain radiated out along the distribution of the ophthalmic and maxillary divisions of the trigeminal nerve. The patient was treated with insulin therapy and his HbA1c level decreased from 10.3% to 6.8% within 7 months. Five months after initiating insulin therapy, his symptoms showed a dramatic improvement. This was a very unusual case of bilateral acute painful neuropathy that involved the ophthalmic and maxillary divisions of the trigeminal nerve, and in which aggravation of the symptoms clearly related to poor glycaemic control.
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ranking = 19.888049363173
keywords = trigeminal nerve, nerve
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13/30. Painful sciatic neuropathy following cardiac surgery.

    Ten patients developed bilateral asymmetrical lower limb sensori-motor or motor deficits associated with prominent causalgic pain after cardiac surgery. The clinical and electrophysiological abnormalities indicated bilateral proximal sciatic nerve lesions, although in several cases the distinction from a diffuse ischaemic axonopathy was difficult to make. This pattern of postcardiac surgery peripheral neurological dysfunction has not been previously described but is likely to relate either to the intra-operative posturing technique for access to the saphenous veins and/or the upright posture used to nurse patients in the immediate post-operative period and is in keeping with the previously demonstrated susceptibility of peripheral nerves to pressure palsy during cardiac surgical procedures.
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ranking = 0.28571428571429
keywords = nerve
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14/30. Bilateral burning foot pain: monitoring of pain, sensation, and autonomic function during successful treatment with sympathetic blockade.

    We describe a patient with burning pain in both feet associated with local autonomic disturbances following bilateral traumatic sciatic mononeuropathies. The diagnosis of a sympathetically maintained pain was confirmed through a prompt response to sympathetic blockade. Although a mild alcohol-nutritional neuropathy was found, the clinical findings strongly suggested a diagnosis of bilateral causalgia. Clinical evaluation and quantitative sensory testing were performed prior to and after successive unilateral lumbar sympathetic nerve blocks. After unilateral blockade, bilateral improvement was recorded in measures of pain, sudomotor function, and foot temperature. Other measures of autonomic function showed variable responses to sympathetic blockade. Quantitative sensory testing revealed a dramatic alteration in the contralateral limb's thermal sense following unilateral block. This case underscores the potential for bilateral causalgia and provides additional evidence for a central mechanism operating in this disorder. The relationship between bilateral causalgia and the "burning feet syndrome" in alcoholic neuropathy is discussed.
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ranking = 0.14285714285714
keywords = nerve
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15/30. Neuroleptic-induced "painful legs and moving toes" syndrome: successful treatment with clonazepam and baclofen.

    The syndrome of "painful legs and moving toes" is characterised by spontaneous causalgic pain in the lower extremities associated with peculiar involuntary movements of the toes and feet. It has been observed after a variety of lesions affecting the posterior nerve roots, the spinal ganglia and the peripheral nerves. The pathophysiology of the syndrome is unknown. I report a patient who developed the syndrome during treatment for schizophrenia with the antipsychotic agent molindone hydrochloride. The patient's response to the combination of clonazepam and baclofen suggests that the pathophysiology of the "painful legs and moving toes" may be linked to impairment of spinal serotonergic and GABA functions.
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ranking = 0.28571428571429
keywords = nerve
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16/30. Pain clinic #15. Treatment of sciatic nerve causalgia following pelvic fracture.

    Direct injury to the sciatic nerve may occur in patients who sustain acetabular/pelvic fractures. sciatic nerve causalgia has been noted in patients who suffer posterior wall acetabular fracture with or without ipsilateral hip dislocation. sympathetic nervous system dysfunction is considered the primary cause for this syndrome, although some investigators suggest central nervous system involvement. This report documents the treatment results of three patients suffering from sciatic nerve causalgia who were referred to the Pain Treatment Center during the past year. In each case, diagnosis was confirmed by sympathetic blockade. Treatment regimens varied and included nerve blocks, cryoanalgesia techniques, and transcutaneous electrical nerve stimulation therapy. The syndrome was relieved in these patients within four to six weeks. patients were followed for six months after initial treatment.
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ranking = 1.3195978573328
keywords = nerve, injury
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17/30. Psychophysical observations on patients with neuropathic pain relieved by a sympathetic block.

    patients with sympathetically maintained pain (SMP) were tested with noxious heat pulses, innocuous mechanical stimuli, and transcutaneous electrical nerve stimulation before and during local anesthetic sympathetic blocks that relieved their pain. The perceived intensity of the pain evoked by these stimuli was measured by the patients' responses on a visual analog scale and compared to the responses obtained when the same stimuli were applied to contralateral normal skin. In 5 of 7 patients tested, graded noxious heat stimuli (43-51 degrees C) applied to painful skin resulted in heat-pain intensity ratings that were essentially identical to the responses obtained when the same stimuli were applied to the normal side. Of the remaining two patients, one was clearly hypoalgesic for heat-pain and the other was probably hyperalgesic. The normal and subnormal heat-evoked responses obtained from abnormal skin were unchanged during completely successful sympathetic blocks. Trains of noxious heat pulses (52 degrees C) evoked summation of the second pain sensation in each of the 4 patients tested. This summation effect was normal and unaffected by a sympathetic block. Four of the patients had allodynia evoked by mechanical stimulation. In each of the 3 allodynia cases tested, transcutaneous nerve stimulation at an intensity that was at threshold for detection evoked burning pain and a coexistent sensation of tingle, indicating that both sensations were due to the activation of A beta axons. patients without touch-evoked pain reported that electrical stimuli at threshold for detection produced only the sensation of tingle. The pains evoked by touch and by threshold-strength nerve stimulation were eliminated during sympathetic block. In patients with allodynia, trains of gentle mechanical stimuli and trains of threshold-strength electrical nerve stimuli produced summation of the intensity of the burning pain sensation when the stimuli were presented at 0.3 Hz. These results add to a growing body of evidence indicating that the touch-evoked pain of some patients is due to abnormal central activity evoked by input from A beta low-threshold mechanoreceptors. The coexistence of A beta-evoked pain with normal heat-evoked pain and normal heat-pain summation suggests that the central abnormality cannot be a simple hypersensitivity of wide-dynamic-range neurons. The effect of sympathetic blockade on A beta-evoked pain and its summation suggests that the crucial sympathetic interaction may take place centrally. The results show that there is considerable heterogeneity of sensory abnormalities among patients with SMP.(ABSTRACT TRUNCATED AT 400 WORDS)
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ranking = 0.57142857142857
keywords = nerve
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18/30. The diagnosis and management of post-traumatic pain syndromes (causalgia).

    There are two major categories of post-traumatic pain syndroms: (1) causalgia; and (2) mimocausalgia states or reflex sympathetic dystrophy. vasoconstriction is usually present. Because of the pain, limitation of motion of the extremity occurs, and may result in permanent disability. There is often a great disparity between the apparent trauma and the severity of the pain. Sympathetic blocks and sympathectomy are definitive modes of therapy. In a series of 147 patients, 56% required surgical sympathectomy. The rest were treated by sympathetic blocks, physical therapy, and other medical measures. Eighty-two percent had excellent relief of pain, 11% had good relief, while 7% had no relief. Thirty-one percent of patients had residual symptoms resulting from the original injury, or from irreversible occurrences on the basis of pain and trophic changes. Emphasis is placed on early recognition and proper treatment.
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ranking = 0.033883571618538
keywords = injury
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19/30. A case of prolonged hypotension following intravenous guanethidine block.

    A 25-year-old female developed causalgia following a nerve injury in the left hand, and this was treated successfully with a series of intravenous guanethidine blocks. However, after the 13th block, systolic arterial blood pressure decreased to 60 mmHg and remained low (80 mmHg) for one week. Accumulation of guanethidine at the sympathetic nerve ending, resulting in autonomic denervation, might be the underlying mechanism of the prolonged hypotension. Treatment was conservative; however, the use of tricyclic antidepressants and sympathomimetic amines to restore the blood pressure to a normal level can be considered with appropriate caution.
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ranking = 6.2612008509558
keywords = nerve injury, nerve, injury
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20/30. Mechanisms of causalgia and related clinical conditions. The role of the central and of the sympathetic nervous systems.

    The definition of causalgia as a pain state following peripheral nerve injury has been accepted since the term was introduced by Weir Mitchell over a century ago. In the present paper, problems of nomenclature and nosology are discussed, and attention is drawn to the fact that the same clinical features can occur spontaneously, in nontraumatic nerve lesions, in the absence of a part as in phantom limb states, and in diseases confined to the central nervous system. attention is also drawn to the lack of correlation of pain with the effects mediated by catecholamines in the sympathetic nervous system and with the response to sympathetic blockade. Concerning mechanisms, a number of peripheral mechanisms have been postulated. These are reviewed, and while they might be correct when causalgia arises from peripheral nerve damage, they cannot provide adequate explanation for at least some instances of causalgia. The relevance of the neuroma as a model for chronic pain in general, and causalgia, is questioned. Also questioned is the view that causalgia is a state that depends on peripheral involvement of the sympathetic nerve supply. Certain authors in the past considered that the central nervous system (CNS) played an important part in causalgia, and current evidence supporting this view is assessed. Involvement of the CNS is suggested by the development of causalgia in diseases confined to the CNS and in phantom pain states; the unusual distribution of pain sometimes experienced; the paradoxical development of widespread pain that can occur after damage to the sympathetic nervous system; the effects of peripheral sympathetic blockade even when the cause lies centrally; and central interactions with motor, sensory and psychological phenomena. Reservations concerning the role of catecholamines in causalgia are outlined, and the possibility is considered that nonadrenergic substances may be implicated.
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ranking = 6.5469151366701
keywords = nerve injury, nerve, injury
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