By Y. Daro. American University. 2018.

The new time-limited certificate is in effect for 10 years from the date the previous certificate expires order 20 mg tadora free shipping, not from the date the recertifica- tion exam is taken buy 20 mg tadora fast delivery. THE CERTIFICATE The Board will issue a time-limited certificate to each Diplomate who successfully completes the recertification process. This certificate will be dated from the year the Diplomate’s orig- inal certificate was due to expire. Participants must submit their CME statement and pay the annual fee for the 10th year of the recertification program before the certificate will be issued. Participants earn certificates if all requirements of the recertification program are met, including: 1. Total of 500 CME credits accumulated and reported in the 10-year period prior to issuing the certificate; 3. The Board will issue the new certificate after the expiration date on the original certificate. Further details and current information for the certification and recertification programs can be obtained by writing to the ABPMR or by visiting their website. Suite 674 Rochester, MN 55902-3092 Telephone: (507) 282-1776 ABPMR E-mail: office@abpmr. INTRODUCTION DEFINITION OF STROKE Sudden focal (sometimes global) neurologic deficit secondary to occlusion or rupture of blood vessels supplying the brain Symptoms > 24 hours = stroke Symptoms < 24 hours = transient ischemic attack (TIA) Reversible ischemic neurologic deficit (RIND) = (this term is no longer used) EPIDEMIOLOGY Stroke, after heart disease and cancer, is the third leading cause of death in the United States. RISK FACTORS (Stewart, 1999) Nonmodifiable: Age—single most important risk factor for stroke worldwide; after age 55, incidence increases for both males and females Risk more than doubles each decade after age 55 Sex ( male > female) Race ( African Americans 2× > whites > Asians) Family history (Hx) of stroke 1 2 STROKE Modifiable (treatable) risk factors: Hypertension—probably the most important modifiable risk factor for both ischemic and hemorrhagic stroke; increases risk by sevenfold History of TIA/prior stroke (~ 5% of patients with TIA will develop a completed stroke within 1 month if untreated) Heart disease (Dz. A = artery; CN = cranial nerve FIGURE 1–2 The Circle of Willis is a ferocious spider that lives in the brain. Note that he has a nose, angry eyebrows, two suckers, eyes that look outward, a crew cut, antennae, a fuzzy beard, 8 legs, a belly that, according to your point of view, is either thin (basilar artery) or fat (the pons, which lies from one end of the basilar artery to the other), two feelers on his rear legs, and male genitalia. It is evident that lower-limb motor strip is in anterior cerebral artery distribution while upper-extremity motor strip is sup- plied by middle cerebral artery. Most of the lateral aspect of the hemisphere is mainly supplied by the middle cerebral artery. The anterior cerebral artery supplies the medial aspect of the hemisphere from the lamina termi- nalis to the cuneus. The posterior cerebral artery supplies the posterior inferior surface of the temporal lobe and the visual cortex. STROKE 5 FIGURE 1–5 Major vascular territories are shown in this schematic drawing of a coronal section through the cerebral hemisphere at the level of the thalamus and the internal capsule. MCA, middle cerebral artery; ACA, anterior cerebral artery; PCA, posterior cerebral artery. May have embolism from extracranial arteries affected by stenosis or ulcer Embolic: 30% of all strokes Usually occurs during waking hours Deficit is immediate Seizures may occur at onset of stroke Cortical signs more frequent Most often embolus plugs one of the branches of the middle cerebral artery. An embolus may cause severe neurologic deficits that are temporary; symptoms resolve as the embolus fragments Presence of atrial fibrillation, history of recent myocardial infarction (MI) and occurrence of emboli to other regions of the body support Dx of cerebral embolism Suggested by history and by hemorrhagic infarction on CT (seen in 30% of patients with embolism) also by large low-density zone on CT encompassing entire territory of major cerebral artery or its main divisions Most commonly due to cardiac source: mural thrombi and platelet aggregates Chronic atrial fibrillation is the most common cause. Seen with myocardial infarction, cardiac aneurysm, cardiomyopathy, atrial myxoma, valvular heart disease (rheumatic, bacterial endocarditis, calcific aortic stenosis, mitral valve prolapse), sick sinus syndrome 75% of cardiogenic emboli go to brain Lacunar infarction: 20% of all strokes Lacunes are small (less than 15 mm) infarcts seen in the putamen, pons, thalamus, caudate, and internal capsule Due to occlusive arteriolar or small artery disease (occlusion of deep penetrating branches of large vessels) Occlusion occurs in small arteries of 50—200 m in diameter Strong correlation with hypertension (up to 81%); also associated with micro-atheroma, microembolism or rarely arteritis Onset may be abrupt or gradual; up to 30% develop slowly over or up to 36 hours CT shows lesion in about 2/3 of cases (MRI may be more sensitive) Relatively pure syndromes often (motor, sensory)—discussed below Absence of higher cortical function involvement (language, praxis, non-dominant hemi- sphere syndrome, vision) Neuroanatomic Location of Ischemic Stroke (Adams, 1997) 1. Anterior Circulation INTERNAL CAROTID ARTERY (ICA): (most variable syndrome): Occlusion occurs most fre- quently in the first part of the ICA immediately beyond the carotid bifurcation. Central retinal artery ischemia is very rare because of collateral supply 8 STROKE Cerebral infarction: Presentation of complete ICA occlusion variable, from no symptoms (if good collateral circulation exists) to severe, massive infarction on ACA and MCA dis- tribution. Failure of distal perfusion of internal carotid artery may involve all or part of the middle cerebral territory and, when the anterior communicating artery is small, the ipsi- lateral anterior cerebral artery. FIGURE 1–7 Arterial anatomy of major vessels on the right side carrying blood from the heart to the brain. MIDDLE CEREBRAL ARTERY (MCA): Occlusion occurs at stem of middle cerebral or at one of the two divisions of the artery in the sylvian sulcus. 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, paraplegia, incontinence and frontal lobe/personality dysfunction Occlusion of one anterior cerebral artery distal to anterior communicating artery results in: – Contralateral weakness and sensory loss, 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, 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.

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As in adult imaging cheap tadora 20mg free shipping, con- images of the opposite limb may help confirm the trast-enhanced sequences are useful in the examina- presence of an abnormality on the symptomatic side buy tadora 20 mg amex. MR studies should be performed with the small- est coil that fits tightly around the body part being 3. In general, a flexible surface coil is better MR Imaging than an adult head or knee coil for examination of tendon and ligament lesions in the extremities of MR imaging of tendon and ligaments in children infants and small children. Immobilization of the and adolescents is performed with the same proto- limb can be achieved with a combination of tape, col of pulse sequences used in adults. Images are obtained in sequences (short TE/short TR) are used to obtain the the two orthogonal planes for the structure to be Fig. In the knee (a), the medial collateral ligament (arrow- heads) appears as a thin anisotropic band that overlies the internal aspect of the knee connecting the medial femoral condyle with the tibial epiphysis (E). Deep to the ligament the medial meniscus (arrow) appears as a hyperechoic triangular structure. In the ankle (b), the anterior talofibular ligament (arrowheads) appears as a tight hyperechoic band that joins the talus and the fibula Ultrasonography of Tendons and Ligaments 43 examined, longitudinal and axial to the tendon or 3. High-resolution matrices (512 or 1024) Overuse Injuries and thin slices (1 to 3 mm) with minimal interslice gaps are optimum. For children of 1 year of age or Overuse injuries are the consequence of exceed- younger, oral chloral hydrate (50 mg/kg) is used ing the ability of tendon insertion to recover from for sedation. When the child is older than 6 years, submaximal cyclic loading in tension, compression, sedation is unnecessary in most cases. Monitoring shear or torsion, and depend on a variety of factors, the sedated child during the examination by staff including tissue strength, joint size, and the patient’s trained in anaesthesia with equipment safe for use age and skeletal maturity. Some tendons with a curvilinear course site involved is the knee, with injury to the inser- may exhibit focal signal changes caused by tissue tions of the patellar tendon, either the anterior tibial anisotropy when their fibres run at 55° with respect apophysis (Osgood-Schlatter disease) or the lower to the magnetic field (magic-angle effect). Examin- pole of the patella (Sinding-Larsen-Johansson dis- ers should be aware of this artefact to avoid confu- ease or jumper’s knee). Osgood-Schlatter disease usually affects boys with a history of participation in sports and a rapid growth 3. Sinding-Larsen-Johansson disease is similar Tendon Abnormalities to jumper’s knee. In both diseases, standard lateral radiographs can demonstrate a fragmented appear- A variety of disorders can affect tendons in children, ance of the apophysis. High-resolution US is an although they occur less commonly than in adults. It will demonstrate degenerative, inflammatory and infectious condi- focal hypoechoic swelling of the physeal cartilage, tions. The weakest point of the muscle–tendon– hypoechoic changes in the patellar tendon from bone unit in children is not the musculotendinous tendinosis and fluid collection from infrapatellar junction or the tendon substance, as seen in adults, bursitis (Fig. In the acute phase, local but the attachment of the tendon to the non-ossified hyperaemia can be demonstrated with colour and cartilage. Similar to the signs dren, and especially in school-aged athletes, involve observed in the knee, the posterior apophysis of the the tendino-osseous junction whilst degenerative calcaneus can undergo fragmentation (Sever’s dis- changes and ruptures in the tendon substance ease) leading to chronic heel pain. Two main types of abnormality US is also suitable for noninvasive follow-up of the are observed: acute trauma that results in partial or disease. MR imaging findings include increased T2- complete detachment of the apophysis by avulsion at weighted signal at the insertion of the tendon, in the the site of tendon insertion, and chronic lesions when surrounding soft tissue and in the adjacent bone repeated microtrauma secondary to overload leads marrow. Sonography is increasingly being used to confirm the clinical suspicion. Around the pelvis, high-resolution US is able to detect apophyseal avulsion at the ischial tuberosity (hamstrings muscles), the anterior supe- 44 M. Longitudinal 12-5 MHz grey-scale (a) and colour Doppler (b) images of the patellar tendon in a 15-year-old boy with focal tenderness and chronic pain over the tibial tuberosity reveal a swollen hypoechoic distal patellar tendon (arrowheads) and bony irregularity and fragmentation of the anterior tibial surface (asterisk); P patella. In the colour Doppler image (b), local increased flow signals (arrowheads) reflect intratendinous hyperaemia. A lateral radiograph (c) dem- onstrates a fragmented irregular apophysis (arrows) rior iliac spine (sartorius muscle and tensor fascia advantages of this technique include better images lata) and anterior inferior iliac spine (rectus femo- of deep-seated tendons or difficult-to-scan regions ris muscle), the iliac crest (abdominal and gluteus (Fig. At that commonly occurs at the poles of the patella these sites, the fracture edge may extend directly (proximally, insertion of the quadriceps tendon; dis- through the physeal cartilage, into the ossifying tally, insertion of the patellar tendon), the proximal apophysis or the underlying bone. US identifies a broad with posterior acoustic shadowing from avulsed sleeve of cartilage, often associated with an osseous bone fragments and local haematoma (Fig. In doubtful or difficult cases, MR minimal displacement, high-resolution US may imaging may be a useful adjunct to US.

In a comprehensive evaluation discount tadora 20mg without a prescription, patients should be asked about their sleep—specifically proven tadora 20 mg, do they have any difficulty initiating or maintaining sleep? If the patient endorses any of these difficulties, psychologists can probe further and help determine whether there are (often easy) changes that can be made. For example, does the patient discontinue caf- feine consumption eight hours and alcohol four hours before bedtime? ASSESSMENT OF CHRONIC PAIN SUFFERERS 221 What does the patient do when he or she wakes up in the middle of the sleep cycle? Patients should be asked about what treatments they have tried in the past and are using presently. Also, are they or health care providers considering addi- tional treatments in the future, such as surgery for their pain? If there is a pending treatment, what does the patient know about the procedure(s) be- ing considered, what are the patient’s expectations about the likely results, how confident are they in the potential of this treatment? How worried are they about the treatments being considered, what do their significant oth- ers think about the treatment(s) being contemplated? Answers to these questions are useful in evaluating whether patients have already assumed a self-management role or whether they see themselves as reliant on others for all their care. When patients with persistent pain seek compensation for lost wages or are involved in litigation, these processes can add an additional layer of distress. Keeping up with paper- work, phone calls, visits to physicians and hospitals, and meetings with attorneys are often undesirable activities. They may have realistic con- cerns about the potential outcomes of the assessment. Moreover, patients involved in litigation are usually in the awkward position of having to “prove” how disabled they are as a result of an injury. The more they at- tend to their limitations, the less they attend to their improvements. Yet an important part of rehabilitation is taking note of capabilities and maximiz- ing a “wellness” role. Psychologists should ask patients about these areas in order to assess whether compensation or litigation statuses might inad- vertently be contributing to and maintaining the patients’ symptoms. The psychologist needs to be vigilant for the potential of secondary gains color- ing the patient’s presentation. This cannot, however, be taken as an indication that those involved with litigation and receiving disability compensation are dissimulating or exaggerating. Moreover, although the studies suggest that litigation and compensation are predictors of dis- ability these factors are only relative predictors. That is, not every patient who is involved with litigation or who is receiving compensation will ipso facto respond poorly to treatment or report higher levels of pain (Turk, 1997). The clinician must be cautious not to overemphasize the role of 222 TURK, MONARCH, WILLIAMS these factors in his or her evaluation of chronic pain sufferers and in treat- ment recommendations. Patients’ Responses to Their Symptoms and Responses From Signifi- cant Others. When the patient experiences an increase in pain, does he or she complain about it to significant others? From a biopsychosocial perspective, antecedents and consequences of pain symptoms and associated behaviors can potentially shape future ex- periences and behaviors. Pain psychologists use this information to formu- late hypotheses about what behavioral factors in a person’s life may serve to maintain or exacerbate the pain experience. It is helpful to gather this in- formation through interviews with patients and significant others together as well as separately. During conjoint interviews the psychologist should observe interactions between the significant others and responses by sig- nificant others to patients expressions of pain and suffering. People who feel that they have a number of successful methods for coping with pain may suffer less than those who behave and feel helpless, hopeless, and demoralized.

Although laboratory studies often involve highly controlled and specific noxious stimulation cheap tadora 20 mg on-line, real-life tissue trauma usually involves a spectrum of afferent activity buy tadora 20 mg lowest price, and the pattern of activity may be a greater determinant of the stress response than the specific receptor system involved (Lilly & Gann, 1992). Traumatic injury, for example, might involve complex signaling from the site of injury including inflammatory mediators, baroreceptor signals from blood volume changes, and hypercapnea. Diminished nociceptive transmission during stress or injury helps peo- ple and animals to cope with threat without the distraction of pain. Labo- ratory studies with rodents indicate that animals placed in restraint or subjected to cold water develop analgesia (Amir & Amit, 1979; Bodnar, Glusman, Brutus, Spiaggia, & Kelly, 1979; Kelly, Silverman, Glusman, & Bodner, 1993). Lesioning the PVN attenuates such stress-induced analge- sia (Truesdell & Bodnar, 1987). The medullary mechanisms involved in this are complex and include the response of the solitary nucleus to baroreceptor stimulation (Ghione, 1996). Stressor-induced, increased blood pressure stimulates carotid barorecep- tors, and these in turn activate the solitary nucleus, which then initiates ac- tivity in descending pathways that gate incoming nociceptive traffic at the dorsal horn of the spinal cord. This mechanism links psychophysiological response to a stressor with endogenous pain modulation. Some investigators emphasize that neuroendocrine arousal mechanisms are not limited to emergency situations, even though most research empha- sizes that such situations elicit them (Grant, Aston-Jones, & Redmond, 1988; Henry, 1986). In complex social contexts, submission, dominance, and other transactions can elicit neuroendocrine and autonomic responses, modified perhaps by learning and memory. This suggests that neuroendocrine proc- esses accompany all sorts of emotion-eliciting situations. The hypothalamic PVN supports stress-related autonomic arousal through neural as well as hormonal pathways. It sends direct projections to the sympathetic intermediolateral cell column in the thoracolumbar spinal 3. PAIN PERCEPTION AND EXPERIENCE 75 cord and the parasympathetic vagal complex, both sources of preganglionic autonomic outflow (Krukoff, 1990). In addition, it signals release of epineph- rine and norepinephrine from the adrenal medulla. ACTH (adrenocortico- trophic hormone) release, although not instantaneous, is quite rapid: It occurs within about 15 seconds (Sapolsky, 1992). These considerations impli- cate the HPA axis in the neuroendocrinologic and autonomic manifestations of emotion associated with tissue trauma. In addition to controlling neuroendocrine and autonomic nervous sys- tem reactivity, the HPA axis coordinates emotional arousal with behavior (Panksepp, 1986). As noted earlier, stimulation of the hypothalamus can elicit well-organized action patterns, including defensive threat behaviors and autonomic arousal (Jänig, 1985). The existence of demonstrable behav- ioral subroutines in animals suggests that the hypothalamus plays a key role in matching behavioral reactions and bodily adjustments to challeng- ing circumstances or biologically relevant stimuli. Moreover, stress hor- mones at high levels, especially glucocorticoids, may affect central emo- tional arousal, lowering startle thresholds and influencing cognition (Sapolsky, 1992). Saphier (1987) observed that cortisol altered the firing rate of neurons in limbic forebrain. Clearly, stress regulation is a complex, feedback-dependent, and coordinated process. The hypothalamus appears to take executive responsibility for coordinating behavioral readiness with physiological capability, awareness, and cognitive function. Chapman and Gavrin (1999) suggested that prolonged nociception may cause a sustained, maladaptive stress response in patients. Signs of this in- clude fatigue, dysphoria, myalgia, nonrestorative sleep, somatic hyper- vigilance, reduced appetite and libido, impaired physical functioning, and impaired concentration. In this way, the emotional dimension of persisting pain may, through its physiological manifestation, contribute heavily to the disability associated with chronic or unrelieved cancer pain. Central Serotonergic Pathways The serotonergic system is the most extensive monoaminergic system in the brain. It originates in the raphé nuclei of the medulla, the pons, and the mesencephalon (Grove, Coplan, & Hollander, 1997; Watson, Khachaturian, Lewis, & Akil, 1986). Descending projections from the raphé nuclei modu- late nociceptive traffic at laminae I and II in the spinal cord and also motor neurons. The raphé nuclei of the midbrain and upper pons project via the medial forebrain bundle to multiple limbic sites such as hypothalamus, sep- tum and hippocampus, cingulate cortex, and cerebral cortex, including frontal cortex. The potential role of serotonergic mechanisms in affective disorders, particularly depression and panic disorder, continues to receive a great 76 CHAPMAN deal of attention (Grove et al.

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