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(See also page 1128) This, another distinctive paraneoplastic syndrome, is also associated with the anti-Hu antibody (It should be emphasized, however, that a nondescript, mainly sensory neuropathy is a more common accompaniment of systemic cancer, and it may or may not be associated with the anti-Hu antibody) The sensory neuronopathy and neuropathy were rst described by Denny-Brown in 1948 and are notable because they served to introduce the modern-day concept of paraneoplastic neurologic disease The initial symptoms in both processes are numbness or paresthesias, sometimes painful, in a limb or in both feet There may be lancinating pains at the onset Over a period of days in some cases, but more typically over weeks, the initially focal symptoms become bilateral and may spread to all limbs and their proximal portions and then to the trunk It is this widespread and proximal distribution and the involvement of the face, scalp, and often the oral and genital mucosa that mark the process as a sensory ganglionitis and radiculitis and are highly suggestive of a paraneoplastic process As the illness progresses, all forms of sensation are greatly reduced, resulting in disabling ataxia and pseudoathetoid movements of the outstretched hands The re exes are lost, but strength is relatively preserved Autonomic dysfunction including constipation or ileus, sicca syndrome, pupillary are exia, and orthostatic hypotension is sometimes associated Also, a virtually pure form of peripheral autonomic failure has been recorded as a paraneoplastic phenomenon (paraneoplastic dysautonomia) One of our patients with sensory neuronopathy had gastric atony with fatal aspiration after vomiting, and another died of unexpected cardiac arrhythmia Very early in the illness, the electrophysiologic studies may be unexpectedly normal, but this soon gives way to a loss of all sensory potentials, sometimes with indications of a mild motor neuropathy The spinal uid often contains an elevated protein and a few lymphocytes As with paraneoplastic encephalomyelitis, most of the cases associated with small-cell lung cancer demonstrate the anti-Hu antibody As mentioned, neuropathy and encephalomyelitis often occur together The sensory neuronopathy-ganglionopathy that is related to Sjogren disease and an idiopathic variety do not have this antibody, making its presence a reliable marker for lung cancer in patients with sensory neuropathy The paraneoplastic illness is refractory to all forms of treatment and most patients die within months of onset, but there have been reports of brief remissions with plasma exchange and intravenous gamma globulin applied early in the illness Resection of the lung tumor may halt progression of the neurologic illness This disorder is discussed further in Chap 46 It should be mentioned that a sensory polyneuropathy from chemotherapeutic agents, notably the platinum-based ones and vincristine, needs to be distinguished from the anti-Hu neuropathy. birt data matrix Java Data Matrix Barcode Generator - BarcodeLib.com
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qr code crystal reports 2008 The J4L Barcodes are integrated in Eclipse Birt 4.3 or later. The components support 1D barcodes, PDF417, Datamatrix , QRCode, Azteccode and Maxicode. ssrs barcode font download * Acts through direct striatal projection neurons ** Acts through indirect striatal projection neurons LGP lateral globus pallidus (external segments) MGP medial globus pallidus (internal segments) STN subthalamic nucleus SNpr substantia nigra pars reticulata SNpc substantia nigra pars compacta transmission in the basal ganglia In contrast to the almost instantaneous actions of glutamate and its antagonist, GABA, at synapses, the monoamines have more protracted effects lasting for seconds or as long as several hours And they in uence rapid as well as slower synaptic activities Dopamine and related neurotransmitters have a slower in uence through the second messenger cyclic adenosine monophosphate (cAMP), which in turn controls the phosphorylation or dephosphorylation of numerous intraneuronal proteins These intracellular effects are summarized by Greengard The effects of certain drugs are better understood on the basis of the manner in which they alter or interfere with neurotransmitter function Several of these drugs namely reserpine, the phenothiazines, and the butyrophenones (notably haloperidol) induce prominent parkinsonian syndromes in humans Reserpine, for example, depletes the striatum and other parts of the brain of dopamine; haloperidol and the phenothiazines work by a different mechanism, probably by blocking dopamine receptors within the striatum The basic validity of the physiologic pharmacologic model outlined is supported by the observation that excess doses of L-dopa or of a direct-acting dopamine receptor agonist lead to excessive motor activity Furthermore, the therapeutic effects of the main drugs utilized in the treatment of Parkinson disease become understandable in the context of neurotransmitter function To correct the basic dopamine de ciency from a loss of nigral cells that
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