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a prolonged reaction time and bradykinesia with a prolonged time of execution, but he concedes that if bradykinesia is severe, it may result in akinesia This is apparently not the result of slowness in formulating the plan of movement; that is to say, there is no bradypraxia For a time, bradykinesia was attributed to the frequently associated rigidity, which could reasonably hamper all movements; but the incorrectness of this explanation became apparent when it was discovered that an appropriately placed stereotactic lesion in a patient with Parkinson disease may abolish rigidity while leaving the akinesia unaltered Thus it appears that apart from their contribution to the maintenance of posture, the basal ganglia provide an essential element for the performance of the large variety of voluntary and semiautomatic actions required for the full repertoire of natural human motility Hallett and Khoshbin, in an analysis of ballistic (rapid) movements in the parkinsonian patient, found that the normal triphasic sequence of agonist-antagonist-agonist activation, as described in the next chapter, is intact but lacks the energy (number of activated motor units) to complete the movement Several smaller triphasic sequences are then needed, which slows the movement The patient experiences these phenomena as not only a slowness but also a type of weakness That cells in the basal ganglia participate in the initiation of movement is also evident from the fact that the ring rates in these neurons increase before movement is detected clinically In terms of pathologic anatomy and physiology, bradykinesia may be caused by any process or drug that interrupts some component of the cortico-striato-pallido-thalamic circuit Clinical examples include reduced dopaminergic input from the substantia nigra to the striatum, as in Parkinson disease; dopamine receptor blockade by neuroleptic drugs; extensive degeneration of striatal neurons, as in striatonigral degeneration and the rigid form of Huntington chorea; and destruction of the medial pallidum, as in Wilson and Hallervorden-Spatz diseases As illustrated in Fig 4-4B, which gives a schematic representation of the hypokinetic state of Parkinson s disease, changes in the cortico-striato-pallido-thalamic circuit (in this case mainly the direct striatopallidal pathway) can be interpreted in terms of altered neurochemical and resultant physiologic connectivity within the basal ganglia The reciprocal situation, enhanced motor activity, is summarized in the analogous diagram for Huntington disease (Figure 4-4C), in which a reduction in the activity of the indirect striatopallidal pathway leads to enhanced excitatory motor drive in the thalamo-cortical motor pathway A number of other disorders of voluntary movement may also be observed in patients with diseases of the basal ganglia A persistent voluntary contraction of hand muscles, as in holding a pencil, may fail to be inhibited, so that there is interference with the next willed movement This has been termed tonic innervation, or blocking and may be brought out by asking the patient to repetitively open and close a st Attempts to perform an alternating sequence of movements may be blocked at one point, or there may be a tendency for the voluntary movement to adopt the frequency of the coexistent tremor Muscles fatigue more readily on repeated activity In still other cases, performance of a simple movement (eg, touching nger to nose, forcefully striking an object with the sted hand) is rendered impossible by the simultaneous contraction of agonist and antagonist muscles not only of the arm and hand but also of the neck, trunk, and even the legs ( intention spasm ).

The simplest method for calculating a DV01 is to average the absolute price changes of a particular treasury security for a 1-basispoint (bp) increase and decrease in yield to maturity In a simple example we use the 30 year bond trading at 122 08 or $122,25000 which is a 6 percent coupon bond with 15 years remaining until maturity This is roughly the CTD bond at this time with the price based on the current US Treasury bond futures contract A change in price of $100 will equate to 1 bp up or down in yield To get the absolute DV01, you would need to do 1bp up and 1bp down and divide the total by 2 to have a true DV01 Let s assume, for example purposes, that this bond represents the xed income risk to interest rates in your portfolio In reality you would need to nd the DV01 for each income asset and nd the appropriate maturity issue or ratio of cheapest to deliver (CTD) treasury issues to account for the maturity differential between your assets and the CTD futures As yield rises 1 bp, the risk to the price of the asset is $100 If you had $1 million in these securities each basis point would be $1,000 loss of value So a standard interestrate hike in short-term rates of 25 basis points that is carried through into the long maturity market could affect the portfolio value by $25,000 Long-term interest rates rising by 200 points could cost this bond holder $200,000 When current Fed rates are at 25 basis points to zero and long-term mortgage rates are in the 4 percent range, the risk of a 200 point hike is substantial

With the exception of that small proportion of cases (about 10 percent) in which infection is introduced from the outside (compound fractures of the skull, intracranial operation, bullet wounds), brain abscess is always secondary to a purulent focus elsewhere in the body Approximately 40 percent of all brain abscesses are related to disease of the paranasal sinuses, middle ear, and mastoid cells Of those originating in the ear, about one-third lie in the anterolateral part of the cerebellar hemisphere; the remainder occur in the middle and inferior parts of the temporal lobe The sinuses most frequently implicated are the frontal and sphenoid, and the abscesses derived from them are in the frontal and temporal lobes, respectively Purulent pulmonary infections (abscess, bronchiectasis) account for a considerable number of brain abscesses Pathogenesis Otogenic and rhinogenic abscesses reach the nervous system in one of two ways One is by direct extension, in which the bone of the middle ear or nasal sinuses becomes the seat of an osteomyelitis, with subsequent in ammation and penetration of the dura and leptomeninges by infected material and the creation of a suppurative tract into the brain Alternatively (or concomitantly), infection may spread along the veins Also, thrombophlebitis of the pial veins and dural sinuses, by infarcting brain tissue, renders the latter more vulnerable to invasion by infectious material The close anatomic relationship of the lateral (transverse) sinus to the cerebellum explains the frequency with which this portion of the brain is infected via the venous route The spread

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TABLE 8-3 Steps in the Migration of BEx Workbooks (continued)