Recovery of function

In working with PCP and polydrug abusers who have impaired everyday functioning, counselors must be ultimately concerned with the individual s ability to recover. Objective prediction of recovery of function, using NP tests, involves a baseline evaluation and at least one repeated assessment. Patterns of NP strengths and deficits in the two or more assessments may then be compared. Clinical inferences can be made, describing skills that show relative permanence of deficit (with no change on repeated measurement), or... 

Treatment. Treatment for dystonia is for the most part symptomatic, except in rare instances where known mechanisms are present and specific therapies are available. The available treatments include support and rehabilitation, pharmacotherapy and, in some cases, functional neurosurgery. Sensory retraining in humans with focal dystonias has resulted in a substantial recovery of function in some patients. 

Ticks have a bad reputation for good reasons. Not only are they carriers of a number of diseases, the saliva of some can cause paralysis. North American natives were aware of tick paralysis, but the condition was officially noted as a disease of both animals and humans in 1912. The bites of at least 60 species of ticks can cause paralysis, which often does not appear until several days after the bite. The first indication is redness and swelling around the site of the bite. This is followed by neuromuscular weakness and difficulty in walking. If the tick is not removed, speech and breathing are affected, with eventual respiratory paralysis and death. Fortunately, removal of the tick results in a quick recovery of function. The exact mechanism of paralysis is not known but it appears to come from a substance that affects the neuromuscular junction. While not related to the venom of the tick saliva, the tick can also transmit diseases such as Lyme disease, Rocky Mountain spotted fever, Q fever, typhus, and others. Table 13.1 lists some venomous arachnids. 

Sbordone, R.J., Liter, J.C., Pettier-Jennings, P. (1995) Recovery of function following severe traumatic brain injury a retrospective 10-year follow-up. Brain Inj 9, 285-99. 

Resensitization Recovery of functional response after desensitization. 

Fig. 6. Proposed hypothetical mechanisms of pre- and post-synaptic plasticity that might underlie recovery of function following partial lesions of the nigrostriatal dopamine neurones. A. Schematic illustration of two intact dopamine terminals making synaptic contact with a post-synaptic striatal neurone. B. Following partial lesion, spared terminals up-regulate to restore normal levels of postsynaptic activation by a combination of processes that include (1) increased firing, (2) increased dopamine synthesis, (3) increased dopamine release, (4) reduced dopamine uptake, (5) diffusion to deafferented synapses, and (6) supersensitivity of all post-synaptic synapses. (Redrawn from Zigmond and Sticker (1984), with permission.)...

Rosenblad C, Martinez-Serrano A, Bjorklund A (1998) Intrastriatal glial cell line-derived neurotrophic factor promotes sprouting of spared nigrostriatal dopaminergic afferents and induces recovery of function in a rat model of Parkinson s disease. Neuroscience 62 129 137. 

Schallert T, Lindner MD (1990) Rescuing neurons from trans-synaptic degeneration after brain damage helpful, harmful, or neutral in recovery of function Can J Psychol 44 216-292. 

Celluloses are similar to other linear polymeric materials in that they can possess one-dimensional order within an individual chain as well as three-dimensional order within an aggregate of chains. Increments in the levels of order occur during the isolation of native celluloses and also as a result of exposure to conditions that promote molecular mobility, such as elevated temperatures and immersion in plasticizing fluids. These increments generally result in embrittlement of the cellulosic materials. Similar effects are expected to occur upon aging of cellulosic textiles and papers over extended periods, and may be accelerated by hydrolytic cleavage of cellulosic chains. The implications of these effects for conservation practices, both with respect to recovery of function as well as in the assessment of deterioration, are reviewed. 

Normal daily secretion of hydrocortisone is 10-30 mg. The exogenous daily dose that completely suppresses the cortex is hydrocortisone 40-80 mg, or prednisolone 10-20 mg, or its equivalent of other agents. Recovery of function is quick after a few days use but when used over months recovery takes months. A steroid-suppressed adrenal continues to secrete aldosterone. 

Hirschberg DL, Yoles E, Belkin M, Schwartz M (1994) Inflammation after axonal injury has conflicting consequences for recovery of function Rescue of spared axons is impaired but regeneration is supported. J Neuroimmnnol 50 9-16. 

Murray M, Fischer I, Smeraski C, Tessler A, Giszter S (2004) Towards a definition of recovery of function. J Neurotrauma 21 405-413. 

Pronounced mitochondria swelling with loss of cristae, development of amorphous matrix densities, and breaks in the sarcolemma are seen in irreversibly injured myocytes. Increased mitochondrial size is an early indication of ischemia. In hearts with 3-15 min of ischemia, morphologic injury is reversible, yet some mitochondria remain swollen even at 20 min of reperfusion. Therefore, a majority of the mitochondria in the ischemic myocardium is expected to be edematous at 30 min of reperfusion. However, early CSIL treatment of ischemic hearts (I and 5 min) results in normal mitochondrial size, smaller than that of CSIL-treated hearts at later times (35). Cessation of mitochondrial electron transport has been observed 2 s after the onset of global ischemia in isolated rat hearts (36). The results of mitochondrial size determination are compatible with the delay in the recovery of function with later administration of CSIL. Thus, mitochondrial ultra-structural data agree with the functional and histochemical data. Preservation of cell membrane integrity after CSIL intervention results in a faster recovery of function and a reduction in infarct size. Whether this is associated with prevention of the influx of extracellular Ca that is associated with ischemia and reperfusion is not assessed in our studies. However, uncontrolled influx of Ca into the cytosol occurs after reperfusion and results in rigor (37, 38). 

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