1/11. 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.- - - - - - - - - - ranking = 1keywords = sensory neuropathy, neuropathy (Clic here for more details about this article) |
2/11. Use of antecedent control to improve the outcome of rehabilitation for a client with frontal lobe injury and intolerance for auditory and tactile stimuli.KM, a single 23-year-old male, sustained a severe traumatic brain injury in a motor vehicle accident. Aggressive and uncooperative behaviour, resulting from the client's cognitive deficits and hypersensitivity to stimuli, made him unmanageable in a subacute rehabilitation setting. Minimizing sources of agitation reduced the client's outbursts and facilitated the completion of functional tasks, such as bathing and dressing. Modifying his environment also increased the client's participation in social and leisure activities. These changes improved the outcome of the client's rehabilitation.- - - - - - - - - - ranking = 0.00026470872885424keywords = motor (Clic here for more details about this article) |
3/11. 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.- - - - - - - - - - ranking = 0.011878873051788keywords = neuropathy (Clic here for more details about this article) |
4/11. Organophosphate-induced delayed neuropathy: case report.Organophosphate induced delayed neuropathy (OPIDN) is an uncommon clinical condition. It occurs in association with the ingestion of great amounts of organophosphate after the stimulation of cholinergic receptor. The clinical picture is characterized by a distal paresis in lower limbs associated with sensitive symptoms. Electrodiagnostic studies show a motor axonal neuropathy. Involvement of the central nervous system may occur. We describe a 39 years-old female patient who developed hyperesthesia associated with lower limbs paresis, fourteen days after she had ingested a dichlorvos-based insecticide. Electrophysiological study was characterized by an axonal polyneuropathy pattern. Pyramidal tract dysfunction was observed later in upper limbs. Considering that both peripheral and central nervous systems are involved we believe that the more appropriated term would be organophosphate induced delayed neuropathy (OPIDN) instead of organophosphate induced delayed polyneuropathy (OPIDP).- - - - - - - - - - ranking = 0.10717456619495keywords = neuropathy, motor (Clic here for more details about this article) |
5/11. 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.- - - - - - - - - - ranking = 0.0015882523731255keywords = motor (Clic here for more details about this article) |
6/11. 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.- - - - - - - - - - ranking = 0.2keywords = sensory neuropathy, neuropathy (Clic here for more details about this article) |
7/11. 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)- - - - - - - - - - ranking = 0.00026470872885424keywords = motor (Clic here for more details about this article) |
8/11. Characteristics of pyridoxine overdose neuropathy syndrome.A newly recognised neurotoxic syndrome due to pyridoxine (B6) overdose is described. It is the largest series of B6 intoxication hitherto reported. A raised serum B6 level was present in 172 women of whom 60% had neurological symptoms, which disappeared when B6 was withdrawn and reappeared in 4 cases when B6 was restarted. The mean dose of B6 in the 103 women with neurological symptoms was 117 /- 92 mgs, compared with 116.2 /- 66 mgs in the control group. There was a significant difference (P less than 0.01) in the average duration of ingestion of B6 in the neurotoxic group of 2.9 /- 1.9 years compared with 1.6 /- 2.1 years in controls. The symptoms were paraesthesia, hyperaesthesia, bone pains, muscle weakness, numbness and fasciculation, most marked on the extremities and predominantly bilateral unless there was a history of previous trauma to the limb. These women were taking a lower dose of B6 than previously described (1,2), which may account for the complete recovery within 6 months of stopping B6.- - - - - - - - - - ranking = 0.047515492207154keywords = neuropathy (Clic here for more details about this article) |
9/11. Impaired blood pressure response to norepinephrine in a case of insulin-dependent diabetes mellitus--improvement with a beta-adrenergic antagonist.A case of juvenile-onset insulin-dependent diabetes mellitus in a 30-year-old male patient is reported. He was admitted to the hospital because of severe diabetic neuropathy, predominantly in the lower extremities. Signs of autonomic neuropathy were not evident but the patient had severe orthostatic hypotension. Circulating catecholamine concentrations were normal; however, the blood pressure response to infused norepinephrine was reduced ten-fold compared to a group of normals. An improvement of the blood pressure response to sympathomimetic drugs was accomplished during the simultaneous administration of propranolol, a beta-receptor blocking agent. The present data suggest a possible defect of the adrenergic receptor system in response to sympathomimetic drugs while the release of catecholamines and the function of the parasympathetic nervous system appears to be intact. Treatment with beta-blocking agents such as propranolol as an adjunct to sympathomimetics seems to be a promising approach which might deserve further consideration in similar cases.- - - - - - - - - - ranking = 0.023757746103577keywords = neuropathy (Clic here for more details about this article) |
10/11. Obturator neuropathy after forceps delivery.A 31-year-old woman developed a disabling obturator neuropathy as a result of a difficult delivery. This was successfully diagnosed and treated by obturator nerve blocks with anesthetic and steroid at the obturator foramen.- - - - - - - - - - ranking = 0.059394365258942keywords = neuropathy (Clic here for more details about this article) |
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