Cases reported "Sensation Disorders"

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1/14. Chronic axonal sensory and autonomic polyneuropathy without motor involvement: a new 'chronic inflammatory neuropathy?'.

    We report the case of a woman with axonal sensory and autonomic neuropathy lasting several months who improved in association with steroid administration. During the course of her disease and in the follow-up, the patient underwent repeated cerebrospinal fluid (CSF) examinations, neurophysiological somatic, autonomic nervous system studies and sural nerve biopsy. Clinical and laboratory assessments demonstrated the occurrence of a monophasic, chronic sensory and autonomic neuropathy. A sural nerve biopsy suggested an axonopathy. After a progressive worsening of symptoms lasting about 6 months, steroid treatment was started and within 6 months a complete recovery, with normalization of the CSF findings, was observed. Although the 'chronic inflammatory neuropathies' are still debated entities, the features of this chronic, exclusively sensory and autonomic neuropathy are new, and the occurrence of a high protein level in the CSF, together with the favorable outcome associated with steroid treatment, suggests that our case might be another variant in this debated area.
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2/14. Acute mercury vapour poisoning in a shipyard worker--a case report.

    Acute mercury vapour poisoning is a serious, potentially fatal but fortunately rarely encountered problem. It is most commonly due to industrial accidents. The vapour is a direct respiratory tract irritant as well as a cell poison, exerting its greatest effects in the lungs, nervous system, kidneys and liver. We present a case of mercury vapour poisoning in a shipyard workers presenting as an acute chemical pneumonitis, which resolved with aggressive supportive therapy. Further investigations later revealed transient mild neuropsychiatric symptoms, and residual peripheral neuropathy. No chelation therapy was instituted. The detailed investigative work that led to the discovery of the source of mercury is also presented. This case alerts us to the potential hazard to shipyard workers who may work in ships previously carrying oil contaminated with mercury. There have been no previous reports of mercury poisoning in shipyard workers. A high index of suspicion leading to early diagnosis and institution of appropriate supportive measures in suspected cases can be life-saving.
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3/14. Subacute sensory neuropathy associated with Epstein-Barr virus.

    A 35-year-old man experienced severe sensory loss, pseudoathetosis, and areflexia during recovery from a severe viral illness. Sensory nerve action potentials were absent, motor conduction velocities were mildly slowed, and blink reflexes were normal. magnetic resonance imaging (MRI) revealed abnormal signal within the central and dorsal aspects of the thoracic cord. Acute and convalescent Epstein-Barr virus (EBV) titers suggested EBV as the etiology. Subacute sensory neuropathy, with peripheral and central nervous system involvement, is a rare complication of EBV infection.
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ranking = 1.8017155503137
keywords = nervous system, central nervous system
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4/14. shock-like sensations during venlafaxine withdrawal.

    Electric shock-like sensations may occur after cessation of treatment with serotonin selective reuptake inhibitors but are reported in the literature only rarely with discontinuation of venlafaxine. Two patients experienced severe shock-like sensations during venlafaxine withdrawal. For both patients symptoms occurred with lowering of the dosage and persisted for 5 days after complete discontinuation of the drug. These sensations may represent significant alteration of neuronal activity in the central nervous system.
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ranking = 1.8017155503137
keywords = nervous system, central nervous system
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5/14. dialysis disequilibrium: another reversible posterior leukoencephalopathy syndrome?

    dialysis disequilibrium syndrome is a disorder of the central nervous system in patients on dialysis. The underlying etiology is thought to be primarily due to cerebral edema; however, neuroradiologic findings have not been described previously. We describe a patient who presented with new onset headaches and status epilepticus after beginning hemodialysis. Her neuroimaging studies revealed white matter changes in the posterior parietal and occipital lobes similar to those seen in patients with reversible posterior leukoencephalopathy syndrome (RPLS). This case suggests that dialysis disequilibrium syndrome and RPLS may represent a spectrum of disorders in which the underlying mechanism is vasogenic edema.
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ranking = 1.8017155503137
keywords = nervous system, central nervous system
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6/14. Extradural spinal cord compression by rheumatoid nodule.

    Rheumatoid disease is a systemic disorder affecting multiple organs. It is known to affect the nervous system in a variety of ways, but its presentation with spinal cord compression by a rheumatoid nodule is rare. We report two cases presenting with cord compression by a rheumatoid nodule who underwent surgical decompression with good recovery.
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7/14. Primary AL (kappa-light chain) amyloidosis manifesting as peripheral neuropathy in a young male without increase in serum and urine immunoglobulin load: a diagnostic challenge.

    Primary systemic or AL amyloidosis is a multisystem disorder characterized by diffuse extracellular infiltration of a fibrillar protein of monoclonal light chain origin (AL). Majority of the patients have monoclonal immunoglobulin in serum and/or urine and some have clonal proliferation of plasma cells in their bone marrow. This disease has the widest spectrum of organ involvement, most commonly affecting the kidneys, heart and liver. Involvement of peripheral nervous system is not infrequent and may be the presenting feature of the disease process. Thus, recognition of peripheral neuropathy and affecting the kidney as an early symptom of AL amyloidosis may widen the scope for therapeutic intervention. We describe here a rare case of primary amyloidosis (AL) kappa-light chain presenting with clinical features of peripheral neuropathy and affecting the kidney and heart at an early age of 18 years, hitherto unreported in literature. The case was further interesting as it was not associated with increased serum/urine immunoglobulins or plasma cells in bone marrow. Diagnosis was confirmed using immuno-electron microscopy on sural nerve biopsy.
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8/14. 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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ranking = 1.8017155503137
keywords = nervous system, central nervous system
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9/14. Painful neuropathy: C-nociceptor activity may not be necessary to maintain central mechanisms accounting for dynamic mechanical allodynia.

    OBJECTIVE: In neuropathic pain states, dynamic mechanical allodynia is mediated by large diameter A beta-fibers. We test whether ongoing peripheral C-nociceptor input is necessary to maintain central changes hypothetically responsible for A beta-mediated allodynia. CASE REPORT: A patient with long-standing diabetes mellitus demonstrated generalized signs of painless diabetic small fiber polyneuropathy. Following mechanical trauma, the patient additionally developed a typical neuropathic pain syndrome at the arm. Despite substantial impairment of cutaneous small fiber function, he complained of severe dynamic mechanical allodynia confined to a forearm skin area. methods AND RESULTS: Marstock test revealed a considerably increased cold perception threshold within the allodynic area and on the contralateral side. The patient could not perceive any warm sensation on either side. histamine iontophoresis was not followed by any itch or pain sensations within the allodynic area or contralaterally. Nociceptive C-fiber axon reflex reactions were substantially impaired within the allodynic skin or contralaterally. Standard neurophysiological testing and quantitative vibrametry showed only mild impairment of large diameter sensory and motor fiber function at the arms. Cardiovascular reflex tests showed almost no heart rate variation indicating impairment of vagal small fiber function. CONCLUSIONS: (a) Cutaneous nociceptive C-fibers do not signal dynamic mechanical allodynia. This symptom may hypothetically be due to secondary changes in the central nervous system processing that might strengthen the synaptic ties between A beta-fibers and central nociceptive pathways, or due to peripheral multiplication of primary afferent low threshold mechanoreceptor input. (b) Ongoing nociceptive C-fiber input is not necessary to maintain either hypothetical mechanism. (c) Hypothetical secondary central hyperexcitability might work autonomously without any nociceptive C-fiber input for a long time or even indefinitely in some neuropathic patients.
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ranking = 1.8017155503137
keywords = nervous system, central nervous system
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10/14. motor neuron disease with multi-system involvement presenting as tetraparesis, ophthalmoplegia and sensori-autonomic dysfunction.

    We carried out a postmortem examination on two Japanese patients, 64- and 80-year-old men whose survival was prolonged with an artificial respirator. They had no family history of neuropsychiatric disorders and were suspected, clinically, as having a motor neuron disease that differed from amyotrophic lateral sclerosis (ALS). As well as upper and lower motor neuron impairment, they showed a variety of symptoms, such as sensory disturbances, hypohidrosis, impotence, ophthalmoparesis and/or atonic neurogenic bladder, and their protein content in cerebrospinal fluid was elevated markedly. Pathological examination revealed the following extensive nervous system involvement: (1) the upper and lower voluntary motor systems, including the IIIrd, IVth and VIth cranial nerve nuclei: (2) the reticular formation and its major afferent pathways; (3) the vestibulospinal and tectospinal systems; (4) the spinocerebellar system and the exteroceptive somatic afferent pathways; (5) the dentatorubral and pallidoluysian systems; and (6) the substantia nigra, locus ceruleus and intermediolateral and Onufrowicz's nuclei. Neither Bunina bodies, Lewy body-like hyaline inclusions nor ubiquitin immunoreactive skein-like structures were observed. The distribution of the lesions was quite different from that in patients with ALS and the other known related diseases. Recently, seven autopsied cases with clinical and histopathological similarities to our patients have been reported in japan. Our conclusion is that our two and these seven patients should be classified as having a new motor neuron disease entity, which can be is differentiated from ALS.
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