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chologic factors, some of which have already been discussed, and, more recently, to certain physiologic and biochemical derangements; but none of these factors provides a completely satisfactory explanation of the primary disorder The psychodynamic theories that attempt to provide a uni ed explanation of these diverse neurotic states have been reviewed by Nemiah The symptoms of an anxiety attack resemble those of fear in many ways, though nearly always the former symptoms are longer in duration and less distinct The most important difference, however, is that the cause of fear is known to the patient, whereas that of anxiety is not On the physiologic and biochemical side, it has been observed that anger provokes an excessive secretion of norepinephrine, whereas fear is accompanied by increased secretion of epinephrine Actually, fear activates the autonomic nervous system, and the increase in epinephrine is more than counterbalanced by a parasympathetic discharge Attention has been focused on overactivity of the locus ceruleus and upper brainstem nuclei as the possible anatomic substratum of anxiety (Judd et al) Other studies have implicated serotoninergic centers Evidently, the responsiveness of the autonomic nervous system in these patients remains heightened, and a number of stimuli (cold, pain, muscular effort) may produce abnormal responses in pulse, respiration, oxygen consumption, and work performance Another interesting abnormality ( rst noted by Cohen et al) is that the blood lactic acid levels in response to exercise are higher than normal The presence of these derangements does not necessarily mean that they are causal; they are as likely secondary to other factors such as poor physical condition and apprehension associated with the syndrome Nevertheless, some investigators have found that infusions of lactic acid can trigger panic attacks in persons with anxiety neurosis (Liebowitz et al) Subsequently, a number of other theories of causation have been proposed based on the reported provocation of panic attacks by a number of different substances carbon dioxide, yohimbine, gamma aminobutyric acid (GABA), isoproterenol, and others None provides a comprehensive biological explanation Studies correlating cerebral function and blood ow indicate that when panic is induced by an intravenous injection of sodium lactate, there is an immediate increase in blood ow to the cortex of both temporal lobes In states of fear, the tips of the temporal lobes and the amygdaloid nuclei are known to become activated In the relaxed period between panic attacks, the right limbic system and the parahippocampal gyrus are abnormally active in some studies As with the aforementioned biochemical models, these seem to be more re ections of brain activity in response to the psychic experience than they are explanations Nevertheless, parts of the limbic system are presumably involved in a germinal way in the production and perpetuation of anxiety and its related states The most extreme but not inconceivable interpretation of anxiety is the James-Lange theory of emotion, which attributes the psychologic experience entirely to the accompanying physical symptoms Of potential importance is the nding of a connection between anxiety traits and certain genetic polymorphisms such as one of the serotonin transporter gene on chromosome 17 (Lesch et al) It is estimated that allelic differences on the chromosome contributes perhaps 10 percent to the overall neurotic tendency, and there is an implication that numerous additional genes may participate in a similar way Others have not found this particular association or have found it only in patients with generalized anxiety but not those with panic attacks Therefore the precise relationship of this and other genetic abnormalities to neurosis cannot be stated at this moment but a heritable component is undoubted.

Leg Hip Trunk Neck Head Shoulder Arm Elbow Forearm Wrist Fin H ge Litand rs M Rin tle id g Th Inde dle um x E b Fa Nos ye ce e

Paresthesias, tingling, buzzing Burning, heat, cold Prickling pain Pseudocramp Band tightness Lancinating pain Hyperalgesia

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Once the BIOS has finished the POST, it looks for the presence of an OS on the hard drive If the BIOS does not find a special OS pointer in the drive s master boot record, it assumes that no OS exists If you haven t yet installed an OS, you must do so at that point If an OS exists but cannot be accessed, try using the SYS command at a DOS prompt to make the drive bootable That is, reboot the computer from the floppy drive (This command is described in more detail in 10) Use the command SYS C: This command replaces the pointer in the master boot record, and the computer might be able to boot properly Unfortunately, most cases of a missing OS stem from the corruption or loss of essential OS files If this is the case, you need to reload the OS When data becomes corrupted, it might be a sign that the disk is about to fail You should consider running Scandisk to resolve these problems You might also want to consider replacing the hard disk before it fails completely Before you do this, boot from a floppy disk, then try to access and save any salvageable information from the hard drive

Large bers (in nerve or posterior columns) Small bers Combined small- and large- ber A type of paresthesia, probably related to large- ber dysfunction Lemniscal system of cord Small- ber neuropathy and radiculopathy Partial peripheral nerve damage

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