Cases reported "Hyperesthesia"

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1/17. Idiopathic small-fiber sensory neuropathy in childhood: A diagnosis based on objective findings on punch skin biopsy specimens.

    Idiopathic small-fiber sensory neuropathy (SFSN) has not previously been reported in children. Although affected patients complain of neuropathic pain, this condition is often difficult to diagnose because of the few objective physical signs and normal nerve conduction studies. We report a girl with idiopathic SFSN in whom the results of a sural nerve biopsy were normal, but punch skin biopsy revealed reduced intraepidermal nerve fiber density and established the diagnosis. Idiopathic SFSN should be considered in the differential diagnosis of children who have burning limb pain with no routine electrophysiologic or pathologic abnormalities.
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2/17. Superficial nerve damage of thumb of laparoscopic surgeon.

    We report a case of digital nerve (superficial branch of the radial nerve) compression injury in the thumb caused by repeated compression at the proximal phalanx level by a finger grip of a laparoscopic instrument during laparoscopic surgery.
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3/17. Neuropathic complications of mandibular implant surgery: review and case presentations.

    Injuries to trigeminal nerves during endosseous implant placement in the posterior mandible appear to occur acutely in approximately 5-15 of cases, with permanent neurosensory disorder resulting in approximately 8%. Nerve lateralization holds even higher risks from epineurial damage or ischaemic stretching. Neuropathy from implant compression and drill punctures can result in neuroma formation of all types, and in some cases precipitate centralized pain syndrome. Two patterns of clinical neuropathy are seen to result; hypoaesthesias with impaired sensory function, often seen with phantom pain, and hyperaesthesias with minimal sensory impairment but presence of much-evoked pain phenomena. The clinician must differentiate, through careful patient questioning and stimulus-response testing, those patients who are undergoing satisfactory spontaneous nerve recovery from those who are developing dysfunctional or dysaesthetic syndromes. Acute nerve injuries are treated with fixture and nerve decompression and combined with supportive anti-inflammatory, narcotic and anti-convulsant therapy. Surgical exploration, neuroma resection and microsurgical repair, with or without nerve grafting, are indicated when unsatisfactory spontaneous sensory return has been demonstrated, and in the presence of function impairment and intractable pain.
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4/17. platypus envenomation--a painful learning experience.

    OBJECTIVE: To describe in detail for the first time, the clinical course and medical management of a significant human envenomation by the Australian platypus (Ornithorhynchus anatinus). CLINICAL FEATURES: A 57-year-old man was envenomated via two spur wounds to the right hand from each hind leg of a male platypus. Pain was immediate, sustained, and devastating; traditional first aid analgesic methods were ineffective. INTERVENTION AND OUTCOME: On admission to hospital, narcotics administered intravenously, both intermittently and by infusion, provided inadequate analgesia. A right wrist block was dramatically effective. After the blockade narcotic analgesic support was required for several days. The patient spent six days in hospital, and the envenomated area remained painful, swollen and with little movement for three weeks. Significant functional impairment of the hand persisted for three months, the cause of which is uncertain. CONCLUSIONS: male platypus venom remains largely unstudied. It produces savage local pain and marked local swelling, but no apparent tissue ischaemia. No antivenom is available; in its absence the only effective analgesia appears to be regional nerve blockade, when the envenomation site and available skills permit. Immobilisation assists.
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5/17. lateral sinus thrombosis associated with zoster sine herpete.

    herpes zoster results from reactivation of the varicella zoster virus (VZV). zoster sine herpete (ZSH) is an uncommon manifestation of VZV infection and presents with similar symptoms but without the vesicular rash. We describe an unusual case of lateral sinus thrombosis (LST) that developed during the clinical course of ZSH in the C2 distribution. A 55-year-old woman presented with a 3-day history of left temporal and postauricular pain, nausea, vomiting, and mild photophobia. She denied otalgia, otorrhea, and hearing loss. Examination revealed hyperesthesia in the left C2 nerve root distribution without evidence of herpetic rash. A computed tomography scan showed minimal fluid in the left mastoid cavity (not mastoiditis) and thrombus within the left lateral and sigmoid dural sinus. magnetic resonance imaging and magnetic resonance angiogram confirmed these findings. Laboratory studies revealed elevated neurotrophic immunoglobulin g levels to VZV. Hypercoagulable studies were normal. She was subsequently treated with Neurontin, acyclovir, and anticoagulation. Her symptoms improved, and she was discharged 3 days later. LST is generally a complication of middle ear infection. Nonseptic LST, however, may result from dehydration, oral contraceptive use, coagulopathy, or thyroid disease. This unusual case raises the suspicion that thrombosis resulted from VZV associated thrombophlebitis in the ipsilateral cerebral venous sinuses along the second cervical nerve root distribution. A high index of suspicion is necessary in such cases so that a different treatment course can be identified and antiviral medication initiated promptly.
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6/17. Thermal and tactile sensory deficits and allodynia in a nerve-injured patient: a multimodal psychophysical and functional magnetic resonance imaging study.

    OBJECTIVE: A case study was conducted to examine a patient with chronic neuropathic pain of the right foot following peripheral nerve injury and characterize associated sensory abnormalities. methods: Multimodal psychophysical examination of the patient's affected and nonaffected foot included thermal sensibility, dynamic touch, and directional sensibility. In addition, we used functional magnetic resonance imaging to study cortical representation of brush-evoked allodynia. RESULTS: Detailed psychophysical examination revealed substantial deficits in warm, cool, and tactile perception on the injured foot. These findings indicated severe dysfunction of perceptual processes mediated by A beta, A delta, and C fibers. Despite reduced tactile perception, light touch evoked a deep burning pain in the foot. Functional magnetic resonance imaging during brushing of the patient's injured foot showed that tactile allodynia led to activation of several cortical regions including secondary somatosensory cortex, anterior and posterior insular cortex, and anterior cingulate cortex. Brushing of the patient's nonaffected foot led to fewer activated regions. DISCUSSION: The profound sensory disturbances suggest a possible deafferentation type of tactile allodynia mediated by changes within the central nervous system, such as a disruption of normal tactile or thermal inhibition of nociception. The functional magnetic resonance imaging data suggest that tactile allodynia is represented in similar brain regions as experimental pain.
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7/17. Intradural-extramedullary cavernous hemangioma of the left motor root C7--case report and update of the literature.

    OBJECTIVE: Intradural-extramedullary cavernomas of the spine are rare lesions with only 21 published cases to date. Due to their rareness and special characteristics diagnosis often is difficult. We report on an additional case of an intradural-extramedullary cavernoma of the spine. PATIENT: A 56-year-old male presented with left shoulder pain and acute onset of pain affecting the whole spinal column two weeks prior to admission. There were no motor deficits, but a hypesthesia corresponding to the right distal C8-dermatome. MRI revealed an intradural-extramedullary, expansive lesion at the level of C6 with a hyperintense appearance in both T (1)- and T (2)-weighted images. Neither a hemosiderin rim nor contrast enhancement was visible. RESULTS: During surgery a hematoma and a reddish, berry-like tumor adherent to the left motor root C7 were removed. There were no new neurological deficits, and shoulder and back pain resolved within a few weeks after surgery. Histopathologically a cavernous hemangioma was diagnosed. CONCLUSIONS: The patient's symptoms were caused both by direct nerve compression and by spinal hemorrhage, most likely spinal SAH. As there was no characteristic hemosiderin rim and due to the hyperintense appearance in T (1)- and T (2)-weighted MR scans, a radiological diagnosis of hemorrhage and classification of the lesion was difficult. Despite their rareness, in patients with signs of spontaneous, spinal SAH and/or nerve compression syndromes cavernous hemangiomas have to be considered as a potential cause.
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8/17. Symptoms of notalgia paresthetica may be explained by increased dermal innervation.

    Notalgia paresthetica is a sensory neuropathy characterized by infrascapular pruritus, burning pain, hyperalgesia, or tenderness. To assess whether the symptoms may be caused by alterations in the cutaneous innervation, skin from the affected area of patients (n = 5) was compared with controls (n = 10) comprising the contralateral unaffected area from the same patients and site-matched biopsies of normals, using immunohistochemistry. frozen sections were immunostained with antisera to the neuropeptides substance p, calcitonin gene-related peptide, vasoactive intestinal polypeptide, and neuropeptide with tyrosine, and to the general neural marker PGP 9.5 and the glial marker S-100 to show the overall innervation and glial cells, respectively. No discernible change in the distribution of neuropeptide-immunoreactive axons was found, but all of the specimens from the affected areas had a significant increase in the number of intradermal PGP 9.5-immunoreactive nerve fibers compared with unaffected areas from the same patients and normal controls. Epidermal dendritic cells immunoreactive for S-100, possibly langerhans cells, were substantially increased. It is concluded that there is an increase in the sensory epidermal innervation in the affected skin areas in notalgia paresthetica, which could contribute to the symptoms, and that neural immunohistochemistry of skin biopsies could be helpful in the diagnosis of the disease.
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9/17. Notalgia paraesthetica--report of three cases and their treatment.

    Notalgia paraesthetica is a rare entity which involves the posterior primary rami of thoracic nerves T2-T6. patients present with a localized discomfort or pruritus on the back. The condition runs a benign course and usually resolves spontaneously. However, whilst present the symptoms can be relentless and disturbing to patients. We report three patients with notalgia paraesthetica, all of whom were helped symptomatically by the topical application of the local anaesthetic cream, EMLA (2.5% lignocaine and 2.5% prilocaine).
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10/17. Chronic hyperalgesia and skin warming caused by sensitized C nociceptors.

    A patient suffering from an acquired painful syndrome, due to injury to primary somatic afferent units, was studied. Clinical features included chronic spontaneous burning pain in one hand, abnormal painful response to nonnoxious cutaneous stimuli, and deviation of temperature and dystrophic changes in symptomatic skin. Diagnostic stellate ganglion blocks did not improve spontaneous or stimulus-induced pains, and observation of sympathetic efferent neural activity and vasomotor effector responses revealed no abnormality, failing to support an autonomic contribution to the pathogenesis of the pains. A quantitative psychophysical assessment documented exaggerated magnitude of pain in response to noxious stimuli in symptomatic skin, together with abnormal painful quality and prolongation of sensation induced by nonnoxious tactile or warm stimuli. Such mechanical and thermal hyperalgesia persisted during A fibre blocks, suggesting transmission by primary afferents with unmyelinated C fibres and implying sensitization of C polymodal nociceptors. Direct microneurographic recordings of single, identified C polymodal nociceptors from symptomatic skin confirmed the presence of units with pathologically enhanced receptor responses: lowered threshold and very prolonged afterdischarges. While bypassing skin receptors, strongly intraneural microstimulation in fascicles supplying symptomatic or control skin evoked equivalent magnitudes and temporal profiles of pain from both sides. Thus secondary CNS dysfunction need not be postulated to explain the painful syndrome. skin grafted onto the affected region partially recovered tactile and thermal sensation (but not pain) without expressing the painful syndrome. This supports the overall conclusion that in this patient A fibres are not involved as primary carriers of input decoded as pain. Sensitization of C polymodal nociceptors is consistent with the features of hyperalgesia in this patient: pain evoked by nonnoxious stimuli, exaggerated pain magnitude, and abnormally prolonged aftersensation of pain. This is the first documentation of chronic sensitization of human C polymodal nociceptors as a symptom of disease. In the context of sensitized C nociceptors and in the absence of sympathetic vasoconstrictor deficit, the abnormally elevated temperature in symptomatic skin is interpreted as due to antidromic vasodilatation triggered by neurosecretion from hyperactive nociceptors.(ABSTRACT TRUNCATED AT 400 WORDS)
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