By A. Silvio. Centenary College of Louisiana.
Temperature bio- feedback and relaxation training in the treatment of migraine headaches: One-year follow- up female viagra 100mg lowest price. Physical function and physical performance in patients with pain: What are the measures and what do they mean? General social support and physical activity: An analysis of the Ontario Health Survey purchase 50 mg female viagra with mastercard. Theoretical perspectives on the relation between catastrophizing and pain cheap 100mg female viagra fast delivery. One-year followup of patients with osteoarthritis of the knee who participated in a program of super- vised fitness walking and supportive patient education purchase female viagra 50mg. Health status, adherence with health recommendations, self-efficacy and social support in patients with rheumatoid arthritis. Cognitive-behavioral therapy for clinical pain control: A 15-year update and its relationship to hypnosis. International Journal of Clinical and Experimental Hyp- nosis, 45, 396–416. Combining somatic and psychosocial treatment for chronic pain patients: Per- haps 1 + 1 does = 3. A cognitive-behavioral perspective on chronic pain: Beyond the scalpel and syringe. Neglected topics in the treatment of chronic pain patients—Re- lapse, noncompliance, and adherence enhancement. Neglected topics in chronic pain treatment out- come studies: Determination of success. Behavioral treatment for chronic low back pain: A systematic review within the framework of the Cochrane Back Review Group. Fear-avoidance and its consequences in chronic musculo- skeletal pain: A state of the art. Surface electromyography in the identification of chronic low back pain patients: The development of the flexion relaxation ratio. Craig Department of Psychology, University of British Columbia Thomas Hadjistavropoulos Department of Psychology, University of Regina Controversies abound concerning the role of psychological features of pain and their use in pain management. Although pain has been clearly identi- fied as a psychological experience, one does not have to spend much time talking to people or reading the literature to discover disagreements about the nature of this experience. Contested issues include a willingness to dis- miss the importance of patient thoughts and feelings, questions about the meaning of behavioral displays of pain, debates about the role of social contexts, disagreements about how one should assess pain, and whether and how one should attempt to control painful distress. Similar disagree- ments concerning pain mechanisms and intervention approaches are found when considering anthropological, nursing, pharmacological, surgical, neurophysiological, genetic, or any other perspective on pain; however, the focus here is on psychological processes. Roots of dissension concerning models of pain and pain management are found in persistent and uncontrolled pain. Pain remains a very serious problem with highly debilitating and destructive consequences for large numbers of people. Almost everyone can anticipate episodes of poorly con- trolled acute pain in their future, and there are distressingly high numbers of patients with persistent or recurrent pain. Both signal the failures of cur- rent explanatory models and the inadequacies of current applications of treatment or palliative interventions, despite numerous advances in our un- derstanding of biological, psychological, and social mechanisms in pain and 303 304 CRAIG AND HADJISTAVROPOULOS improved pain control strategies (Wall & Melzack, 2001). There should be urgency and contention in the field until a better measure of pain control is accomplished. Indeed, it seems surprising that the inadequacies of our un- derstanding of pain and our limitations in controlling pain are not more widely understood or publicized, and that they are not greater sources of scientific, practitioner, and public unrest. Recent decades have seen concerted efforts to provide an evi- dence-based understanding of pain, and to improve utilization of these un- derstandings by practitioners. Many of the recent advances have resulted from the inspiration and leadership of John Bonica (1953; Loeser, Butler, Chapman & Turk, 2001), the integrative perspective and heuristic benefits of the gate control theory of pain (Melzack & Wall, 1965), and the organiza- tional structure and impetus generated by the founding of the International Association for the Study of Pain in 1974 (http://www. Many factors contribute to differences of opinion in our understanding of pain and pain management.
For exam- ple discount 50mg female viagra free shipping, early in life a person may learn to associate pain with others’ responses to his or her behavior (e purchase female viagra 50 mg amex. Later in life order female viagra 50mg without a prescription, the person may use pain as an unconscious defense against various bouts of emotional distress he or she experiences (much as posited by Freud) generic female viagra 50 mg otc. Although the former of these propositions was supported in part by findings from empiri- cal tests of social learning influences on pain (e. What type of person is most likely to do this or, in other words, to have a pain-prone personality? Engel (1959) suggested that those with psychiatric conditions, as described by diagnostic nomenclature of the day (e. Amendments to Engel’s model, such as Blumer and Heil- broon’s (1982) position on chronic pain as a variant of major depressive dis- order, or masked depression, added depressed affect, alexithymia, family history of depression and chronic pain, and discrete biological markers (e. The results of a large number of studies suggest that the prevalence of current psychiatric conditions is, indeed, elevated in patients with chronic pain relative to base rates in the general population (e. It is questionable, however, whether the presence of psychiatric morbidity makes one more likely to use pain as an unconscious defense mechanism and, thereby, more prone to persistent pain (see, e. With few exceptions (Adler, Zlot, Hürny, Minder, 1989), the psychody- namic formulations have not fared well against empirical scrutiny (see re- views by Gamsa, 1994; Large, 1986; Roth, 2000; Roy, 1985), and now have di- minished popularity in mainstream psychology. Notwithstanding, they did play a key role in drawing attention to the importance of psychological (and contextual) factors in the experience of pain at a time when treatment for pain was primarily directed by the biomedical model. This attention led to increased and continuing research into a wide array of psychosocial vari- ables (e. Indeed, the interest in psychological factors spawned by psychodynamic theorists served as an essential precursor to the development of contemporary biopsychosocial approaches. However, using Roth’s (2000) analogy of the double-edged sword, it is noteworthy that there are lingering and unwanted scars of this psychodynamic thrust. These include the general tendency to assume (a) that all cases of pain in the absence of identifiable physical pathology are the result of psychological factors, and (b) that these are equally relevant to all people with persistent pain. Although incorrect, these assumptions can (and still often do) have a negative impact on opinions and general treatment of people who suffer from persistent pain conditions. GATE CONTROL THEORY As noted earlier, Melzack and colleagues’ seminal papers on the gate con- trol theory of pain (Melzack & Casey, 1968; Melzack & Wall, 1965) are fre- quently cited as the first to integrate physiological and psychological mech- 40 ASMUNDSON AND WRIGHT anisms of pain within the context of a single model. It is beyond the scope of this chapter to provide a detailed synopsis of the theory; however, given its contribution to current conceptualizations of pain, a brief overview is warranted. Melzack and Wall (1965) proposed that a hypothetical gating mechanism within the dorsal horn of the spinal cord is responsible for allowing or disal- lowing the passage of ascending nociceptive information from the periph- ery to the brain. These essential elements are as follows: · The gating mechanism is influenced by the relative degree of excitatory activity in the spinal cord transmission cells, with excitation along the large-diameter, myelinated fibers closing the gate and along the small- diameter, unmyelinated fibers opening the gate. Since this original proposal we have, of course, moved beyond believing that the key to understanding pain is knowing what happens in the dorsal horn. Melzack and Casey (1968) further proposed that three different neural networks (i. They also recog- nized that processing of input could occur in parallel, at least at the sensory and affective level. This revised model allowed for “perceptual information regarding the location, magnitude, and spatiotemporal properties of the noxious stimulus, motivational tendency toward escape or attack, and cog- nitive information based on analysis of multimodal information, past experi- ence, and probability of outcome of different response strategies” (pp. Think back to the case of Jamie, who had pain associated with muscle strain in the low back. Applying the postulates of the gate control theory, Jamie’s pain experience might be understood as follows: Stimulation of nociceptors in the region of muscle strain facilitated transmission of infor- mation along ascending fibers, through an open gate, and on to Jamie’s brain. At the same time, Jamie’s brain was sending information about her current cognitions and emotional state (i. The summation of the ascending nociceptive input and descending information regarding cognition and 2.
ANTERIOR CEREBRAL ARTERY (ACA) (Figure 1–9): If occlusion is at the stem of the anterior cerebral artery proximal to its connection with the anterior communicating artery ⇒ it is usually well tolerated because adequate collateral circulation comes from the artery of the opposite side If both anterior cerebral arteries arise from one stem ⇒ major disturbances occur with infarction occurring at the medial aspects of both cerebral hemispheres resulting in aphasia trusted female viagra 50mg, paraplegia purchase female viagra 100mg visa, incontinence and frontal lobe/personality dysfunction Occlusion of one anterior cerebral artery distal to anterior communicating artery results in: – Contralateral weakness and sensory loss female viagra 100mg fast delivery, affecting mainly distal contralateral leg (foot/leg more affected than thigh) – Mild or no involvement of upper extremity 10 STROKE – Head and eyes may be deviated toward side of lesion acutely – Urinary incontinence with contralateral grasp reflex and paratonic rigidity may be present – May produce transcortical motor aphasia if left side is affected – Disturbances in gait and stance = gait apraxia FIGURE 1–9 The distribution of the anterior cerebral artery on the medial aspect of the cerebral hemisphere buy female viagra 50mg with visa, showing principal regions of cerebral localization. Posterior Circulation: Vertebrobasilar Arteries & Posterior Cerebral Arteries POSTERIOR CEREBRAL ARTERY (PCA): Occlusion of PCA can produce a variety of clinical effects because both the upper brainstem and the inferior parts of the temporal lobe and the medial parts of the occipital lobe are sup- plied by it. Particular area of occlusion varies for PCA because anatomy varies 70% of times both PCAs arise from basilar artery; connected to internal carotids through posterior communicating artery 20%–25%: one PCA comes from basilar; one PCA comes from ICA 5%-–10%: both PCA arise from carotids Clinical presentation includes: Visual field cuts (including cortical blindness when bilateral) May have prosopagnosia (can’t read faces) palinopsia (abnormal recurring visual imagery) alexia (can’t read) transcortical sensory aphasia (loss of power to comprehend written or spoken words; patient can repeat) Structures supplied by the interpeduncular branches of the PCA include the oculo- motor cranial nerve (CN 3) and trochlear (CN 4) nuclei and nerves STROKE 11 Clinical syndromes caused by the occlusion of these branches include oculomotor palsy with contralateral hemiplegia = Weber’s syndrome (discussed below) and palsies of ver- tical gaze (trochlear nerve palsy) VERTEBROBASILAR SYSTEM: Vertebral and basilar arteries: supply midbrain, pons, medulla, cerebellum, and posterior and ventral aspects of the cerebral hemispheres (through the PCAs. At the pontomedullary junction, the two vertebral arteries join to form the basilar artery, which supplies branches to the pons and midbrain. Cerebellum is supplied by posterior-inferior cerebellar artery (PICA) from vertebral arteries, and by anterior-inferior cerebellar artery (AICA) and superior cerebellar artery, from basilar artery Vertebrobasilar system involvement may present any combination of the following signs/symptoms: vertigo, nystagmus, abnormalities of motor function often bilateral. Lateral Medullary (Wallenberg’s) Syndrome This syndrome is one of the most striking in neurology. Signs and symptoms include the following: – Ipsilateral side Horner’s syndrome (ptosis, anhydrosis, and miosis) decrease in pain and temperature sensation on the ipsilateral face cerebellar signs such as ataxia on ipsilateral extremities (patient falls to side of lesion) – Contralateral side Decreased pain and temperature on contralateral body – Dysphagia, dysarthria, hoarseness, paralysis of vocal cord – Vertigo; nausea and vomiting – Hiccups – Nystagmus, diplopia Note: No facial or extremity muscle weakness seen in this syndrome 12 STROKE II. Benedikt’s Syndrome (Red Nucleus/Tegmentum of Midbrain): Obstruction of interpeduncular branches of basilar or posterior cerebral artery or both Ipsilateral III nerve paralysis with mydriasis, contralateral hypesthesia (medial lemniscus), contralateral hyperkinesia (ataxia, tremor, chorea, athetosis) due to damage to red nucleus III. Syndromes of the ParamedianArea (Medial Brainstem): Paramedian area contains: Motor nuclei of CNs Cortico-spinal tract Medial lemniscus Cortico-bulbar tract Signs/symptoms include: contralateral hemiparalysis ipsilateral CN paralysis Location (grossly) of cranial nerve nuclei on brainstem * NOTE: nucleus of CN 1 and CN 2 located in forebrain. Spinal division of CN 11 arises from ventral horn of cervical segments C1–C6. TABLE 1–2 Syndromes of the Paramedian Area (Medial Brainstem) Medial Medullary Syndrome Weber Syndrome Millard-Gubler Syndrome “Another Lesion” Ipsilateral CN 3 palsy Ipsilateral CN 6 paralysis Ipsilateral CN 12 palsy (often CN 7 also involved) Contralateral hemiplegia Contralateral hemiplegia Contralateral hemiplegia (extension into medial lemniscus is Foville’s Syndrome with gaze palsy to side of lesion). Weber Syndrome (Base of midbrain): Obstruction of interpeduncular branches of posterior cerebral artery or posterior choroidal artery or both. Ipsilateral CN 3 cranial nerve paralysis, contralateral hemiplegia, contralateral Parkinson’s signs, contralateral dystaxia (mild degree of ataxia). Millard-Gubler Syndrome (Base of pons): Obstruction of circumferential branches of basilar artery. Ipsilateral facial (CN 7) and abducens (CN 6) palsy, contralateral hemiplegia, analgesia, hypoesthesia. Basilar Artery Occlusion Syndrome Occlusion may arise in several ways: atherosclerotic plaque in the basilar artery itself (usually lower third) occlusion of both vertebral arteries occlusion of one vertebral artery when it is the only one of adequate size Note: Thrombosis usually only obstructs a branch of basilar artery rather than the trunk Emboli, if they get through the vertebral arteries, usually lodge in one of the posterior cerebral arteries or at the upper bifurcation of the basilar artery May cause internuclear ophthalmoplegia, conjugate horizontal gaze palsy, ocular bobbing. Locked-in syndrome: tetraparesis with patients only able to move eyes vertically or blink; patient remains fully conscious secondary to sparing of the reticular activating system; caused by bilateral lesions of the ventral pons (basilar artery occlusion). Some degree of paresis accompanies nearly all cases of basilar artery occlusion. Neuroanatomic Location of Lacunar Infarction Syndromes TABLE 1–4 Lacunar Syndrome Anatomical Location 1. Pure motor hemiplegia Posterior limb of internal capsule –Weakness involves face, arm, and leg; no sensory Corona radiata deficits, aphasia or parietal signs Pons 2. Pure sensory stroke Thalamus (ventro-lateral) Parietal white matter Thalamocortical projections 3. Dysarthria—clumsy hand syndrome Basis pontis Internal capsule (anterior limb) 4. Ataxia and leg paralysis Pons Midbrain Internal capsule Cerebellum Parietal white matter Coronal Radiata 6. Hemichorea-hemiballismus Head of the caudate Thalamus Subthalamic nucleus HEMORRHAGIC STROKES (see Table 1–1) 15% of all strokes may be secondary to hypertension, ruptured aneurysm, arteriovenous mal- formation (AVM), blood dyscrasias/bleeding disorders, anticoagulants, bleeding into tumors, angiopathies. Hypertensive Intracerebral Hemorrhage Linked to chronic HTN (> one-third occur in normotensives) Sudden onset of headache, and/or loss of consciousness Vomiting at onset in 22%–44% Seizures occur in 10% of cases (first few days after onset) Nuchal rigidity common Sites: putamen, thalamus, pons, cerebellum; some from white matter Frequently extends to ventricular subarachnoid space Preceded by formation of “false” aneurysms (microaneurysms) of Charcot & Bouchard = arterial wall dilations 2˚ to HTN Locations 1. Putamen: Most common; hemiplegia 2˚ to compression of adjacent internal capsule. Vomiting in ~ 50%; headache frequent but not invariable Large hemorrhage: Stupor/coma + hemiplegia with deterioration in hours.
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