By G. Hernando. University of Idaho.
Small lesions within the decussation of the pyramids may result ﬁbers that project to the spinal cord buy discount avanafil 100 mg on line. Glutaminergic corticospinal ﬁbers in a bilateral paresis of the upper extremities (lesion in rostral portions) and terminals are found in all spinal levels but are especially concen- or a bilateral paresis of the lower extremities (lesion in caudal portions) trated in cervical and lumbosacral enlargements 50 mg avanafil amex. This correlates with based on the crossing patterns of ﬁbers within the decussation. Some corticospinal dromes), or midbrain (the Weber syndrome) all produce alternating ﬁbers may branch and terminate at multiple spinal levels. These present as a contralateral hemiplegia of the tor neurons are inﬂuenced by corticospinal ﬁbers either directly or in- upper and lower extremities, coupled with an ipsilateral paralysis of directly via interneurons. Acetylcholine and calcitonin gene-related the tongue (medulla), facial muscles or lateral rectus muscle (pons), peptides are present in these large motor cells and in their endings in and most eye movements (midbrain). Lesions in the internal capsule (lacu- Clinical Correlations: Myasthenia gravis, a disease characterized nar strokes) produce contralateral hemiparesis sometimes coupled with by moderate to profound weakness of skeletal muscles, is caused by various cranial nerve signs due to corticonuclear (corticobulbar) ﬁber circulating antibodies that react with postsynaptic nicotinic acetyl- involvement. Bilateral weakness, indicative of corticospinal involve- choline receptors. Progressive muscle fatigability throughout the day ment, is also present in amyotrophic lateral sclerosis. Abbreviations ACSp Anterior corticospinal tract LCSp Lateral corticospinal tract Somatotopy of CSp Fibers ALS Anterolateral system ML Medial lemniscus A Position of ﬁbers coursing to APGy Anterior paracentral gyrus MLF Medial longitudinal fasciculus upper extremity regions of BP Basilar pons PO Principal olivary nucleus spinal cord CC Crus cerebri PrCGy Precentral gyrus L Position of ﬁbers coursing to CNu Corticonuclear (corticobulbar) Py Pyramid lower extremity regions of ﬁbers RB Restiform body spinal cord CSp Corticospinal ﬁbers RNu Red nucleus T Position of ﬁbers coursing to IC Internal capsule SN Substantia nigra thoracic regions of spinal cord Review of Blood Supply to Corticospinal Fibers STRUCTURES ARTERIES Posterior Limb of IC lateral striate branches of middle cerebral (see Figure 5–38) Crus Cerebri in paramedian and short circumferential Midbrain branches of basilar and posterior communicating (see Figure 5–27) CSp in BP paramedian branches of basilar (see Figure 5–21) Py in Medulla anterior spinal (see Figure 5–14) LCSp in Spinal Cord penetrating branches of arterial vasocorona (leg ﬁbers), branches of central artery (arm ﬁbers) (See Figure 5–6) Motor Pathways 191 Corticospinal Tracts Thigh Somatomotor cortex Leg APGy Foot Somatotopy of CSp Post. These ﬁbers inﬂuence—ei- lesioned side and away from the side of the hemiplegia. In addition to ther directly or through neurons in the immediately adjacent reticular a contralateral hemiplegia, common cranial nerve ﬁndings in capsular le- formation—the motor nuclei of oculomotor, trochlear, trigeminal, ab- sions may include 1) deviation of the tongue toward the side of the ducens, facial, glossopharyngeal and vagus (both via nucleus ambiguus), weakness and away from the side of the lesion when protruded and 2) spinal accessory, and hypoglossal nerves. This reﬂects the fact that corticonuclear (cortico- eas 6 and 8 in caudal portions of the middle frontal gyrus), the precen- bulbar) ﬁbers to genioglossus motor neurons and to facial motor neu- tral gyrus (somatomotor cortex, area 4), and some originate from the rons serving the lower face are primarily crossed. Fibers from area 4 occupy the genu of ticonuclear ﬁbers to the nucleus ambiguus may result in weakness of the internal capsule, but those from the frontal eye ﬁelds (areas 8,6) may palatal muscles contralateral to the lesion; the uvula will deviate to- traverse caudal portions of the anterior limb, and some (from areas wards the ipsilateral (lesioned) side on attempted phonation. In addi- 3,1,2), may occupy the most rostral portions of the posterior limb. In contrast to from area 4 terminate in, or adjacent to, cranial nerve motor nuclei ex- the alternating hemiplegia seen in some brainstem lesions, hemisphere cluding those of III, IV, and VI. In addition, it is important to note the following: 1) vertical gaze palsies (midbrain), 2) the Parinaud syn- that descending cortical ﬁbers (many arising in areas 3, 1, 2) project to drome—paralysis of upward gaze (tumors in area of pineal), 3) internu- sensory relay nuclei of some cranial nerves and to other sensory relay clear ophthalmoplegia (lesion in MLF between motor nuclei of III and nuclei in the brainstem, such as those of the posterior column system. VI), 4) horizontal gaze palsies (lesion in PPRF), or 5) the one-and-a-half Neurotransmitters: Glutamate ( ) is found in many corticofu- syndrome. In the latter case, the lesion is adjacent to the midline and in- gal axons that directly innervate cranial nerve motor nuclei and in volves the abducens nucleus and adjacent PPRF, internuclear ﬁbers those ﬁbers that terminate near (indirect), but not in, the various mo- from the ipsilateral abducens that are crossing to enter the contralat- tor nuclei. The cerebral artery occlusion) or the internal capsule (as in lacunar strokes result is a loss of ipsilateral abduction (lateral rectus) and adduction or occlusion of lenticulostriate branches of M1) give rise to a con- (medial rectus, the “one”) and a contralateral loss of adduction (medial tralateral hemiplegia of the arm and leg (corticospinal ﬁber involve- rectus, the “half ”); the only remaining horizontal movement is con- ment) coupled with certain cranial nerve signs. Strictly cortical lesions tralateral abduction via the intact abducens motor neurons. Abbreviations AbdNu Abducens nucleus OcNu Oculomotor nucleus AccNu Accessory nucleus (spinal accessory nu. Many of brainstem and spinal cord, and the general distribution of tectospinal reticulospinal ﬁbers inﬂuence the activity of lower motor neurons. Tectospinal ﬁbers originate from deeper lay- Clinical Correlations: Isolated lesions of only tectospinal and ers of the superior colliculus, cross in the posterior (dorsal) tegmental reticulospinal ﬁbers are essentially never seen. Tectospinal ﬁbers pro- decussation, and distribute to cervical cord levels. Several regions of ject to upper cervical levels where they inﬂuence reﬂex movement of cerebral cortex (e. Such movements may be diminished or slowed in tum, but the most highly organized corticotectal projections arise from patients with damage to these ﬁbers. Pontoreticulospinal ﬁbers (medial reticulospinal) ulospinal) ﬁbers are excitatory to extensor motor neurons and to neu- tend to be uncrossed, while those from the medulla (bulboreticu- rons innervating axial musculature; some of these ﬁbers may also in- lospinal or lateral reticulospinal) are bilateral but with a pronounced hibit ﬂexor motor neurons.
The second task is clearly phosphate and speeds its transport from mitochondria to more difficult buy discount avanafil 50mg, even though the external work done (i buy 100mg avanafil amex. The ventricles not only develop creased by increasing heart rate, the energy expended in the the pressure required to move the blood, but must maintain internal work of isovolumetric contraction increases propor- the pressure during systole. By contrast, if cardiac output is increased by in- the external work alone as calculated from arterial pressure creasing stroke volume, there is a much smaller increase in and stroke volume. This means that increasing cardiac output by is raised by increasing stroke volume but not mean arterial increasing heart rate is more energetically costly than the pressure, the oxygen consumption of the heart increases same increase by means of stroke volume. Alternatively, if arterial pressure is increased, the oxygen consumption per beat goes up much more. Altered myocardial contractility has signif- words, pressure work by the heart is far more expensive in icant energetic consequences because of differential effects terms of oxygen consumption than volume work. However, in- otropic agents can also cause the heart to do the same Afterload. The discussion of pressure work versus volume stroke work at a smaller end-diastolic volume, reducing work emphasizes the importance of afterload as a determi- both afterload and internal work. During exercise, in- nant of energy use and oxygen consumption by the heart. Thus, an in- contribution of ventricular radius to afterload and avoids crease in ventricular radius, as can occur with heart failure, the inefficiency of an increase in end-diastolic volume. The Double Product Is Used Clinically to Estimate the Energy Requirements of Cardiac Work Heart Rate. Thus far, we have considered only the ener- getic events associated with a single cardiac contraction. A useful index of the cardiac oxygen consumption is the The energy consumed per unit time is equal to the energy product of aortic pressure and heart rate—the double consumed in a single heartbeat multiplied by the heart rate. This index includes one of the determinants of ex- It follows that the production of energy from oxidative ternal work (pressure) and the determinant of energy use as phosphorylation per unit time must be sufficient to match a function of time, heart rate. The double product does not the energy consumed in a single heartbeat multiplied by include the effect of changes in stroke volume on energy the heart rate. Much of the internal work of the heart occurs during account effect of changes in radius of the ventricle on en- isovolumetric contraction, when force is being developed ergy consumption. The extra energy required by patholog- but no external work is being done. If cardiac output is in- ically dilated hearts is not reflected in the double product. CHAPTER 14 The Cardiac Pump 251 REVIEW QUESTIONS DIRECTIONS: Each of the numbered (B) Left atrial pressure is always less drug A than for drug B items or incomplete statements in this than left ventricular pressure (E) Cardiac efficiency is higher with section is followed by answers or by (C) Aortic pressure reaches its lowest drug B than with drug A completions of the statement. Using the data below, which is ONE lettered answer or completion that is (D) The ventricles eject blood during correct? The figure below shows pressure- greater than end-diastolic volume Volume in ventricle at end of systole: volume loops for two situations. Point Y in the figure below is the 60 mL compared with loop A, loop B control point. Which point Heart rate: 70 beats/min demonstrates corresponds to a combination of Mean arterial blood pressure: increased contractility and increased 90 mm Hg 150 ventricular filling? Oxygen consumption: 4 L/min 50 100 150 End-diastolic volume Arterial oxygen 19 mL/100 mL Volume (mL) content: blood (A) Point A Mixed venous oxygen 3 mL/100 mL (A) Increased preload (B) Point B content: blood (B) Decreased preload (C) Point C Heart rate: 180 beats/min (C) Increased contractility (D) Point D (A) Cardiac output is 12 L/min (D) Increased afterload (E) Point E (B) Cardiac output is 25 L/min (E) Decreased afterload 5. During the cardiac cycle, volume and no change in systolic (D) Stroke volume is 100 mL (A) The aortic and mitral valves are aortic blood pressure. Starting with the (E) Stroke volume cannot be calculated never open at the same time same baseline, drug B causes a 33% without data on end-diastolic and end- (B) The first heart sound is caused by increase in systolic and mean aortic systolic volume the rapid ejection of blood from the blood pressure and no change in stroke 8. Neither drug changes heart decrease in stroke volume, compared (C) The mitral valve is open rate. During the cardiac cycle, consumption of the heart more than 200 beats/min (A) The second heart sound is associated drug B (E) Stimulation of sympathetic nerves with opening of the aortic valve (D) The “double product” is greater for to the heart SUGGESTED READING Ed. Philadelphia: Lippincott Williams & Lilly, LS: Pathophysiology of Heart Dis- Davidson CJ, Bonow RO. Systemic vascular resistance is most influenced by the ra- mean arterial pressure. The venous side of the systemic circulation contains a minants of pulse pressure. The purpose of this chapter is consider these equation, variables in detail, in preparation for discussions of blood flow to specific regions of the body as well as the regulation – – – – – – – Pa Pd (Ps Pd)/3 or Pa (2Pd Ps)/3 (1) of the circulation.
Review a textbook and the recent literature on the subject matter; then give it to your attorney to review discount 50mg avanafil with visa. You must understand that your efforts in educating your attorney about the medical aspects of the case will be worthwhile purchase 50mg avanafil with amex. You can be certain that the plaintiff attorney is doing the same research. Chapter 3 / Risk Reduction 39 However, no one knows your case like you do. Make certain that the basic medical information that the plain- tiff attorney certainly will have has been provided to your attorney. From the plaintiff attorney’s perspective, when doctors work closely with their attorneys, are not in denial about a lawsuit, and discharge their responsibilities to their patients, the chances of winning are diminished. ONCE YOUR DEPOSITION IS SCHEDULED, THE PLAINTIFF ATTORNEY IS LOOKING FOR SPECIFIC THINGS The order of the information the plaintiff attorney seeks is as impor- tant as their content. Thus, it is important for you to react to people in an accommodating manner. The effort you make in relating to those around you during the deposition and during the trial will be key to whether you are successful in the litigation. If you do not respect your attorney, ask your insurance carrier for another one. Do not show your contempt or lack of respect for the justice system through your lack of respect for your attorney. Plaintiff attorneys are allowed to ask you questions during a deposi- tion. If you are courteous and respectful when asked questions, the plaintiff attorney will conclude that you will behave that way in trial as well. To show respect and be the kind of caring doctor that jurors will love is not how a plaintiff attorney wants you to behave. Study the medical aspects of the case and then teach them to your attorney. You may think you will remember the facts of the case simply by having experienced them, but you will be surprised at the details you have forgotten. However, you still must understand that this is the least important thing the plaintiff attorney is looking for when he or she assesses your ability to fight a potential suit. The most important thing is you and the impression you will makeon a jury. If you are honest and straightforward with your patients when there is a complication and you are honest and straightforward to a jury, you have maximized your risk reduction. The attorney for the injured person must assess his or her ability to win in trial. That attorney is risking his or her time and money to pursue a case for which a fee will only be recovered if he or she wins. The assessment takes place before the attorney ever meets you and is based on what you have written in your medical records. The attorney looks to see if you are honest and forthcoming, which is not something he or she wants to see in a potential defendant. If you share your concerns with the patient when there is a complication, that openness will be a very effec- tive deterrent to a plaintiff lawyer. You may feel you are raising a red flag by documenting that something is wrong. However, you may be keeping your patient from going to an attorney for answers, and you will be showing what a wonderful doctor (and witness) you will be if there is a lawsuit. Your goal is to minimize the chances of your patient seeking legal aid to get answers. Your goal is also to be successful if all that occurred was a complication rather than a deviation from the standard of medi- cal care. Hopefully, this chapter helps you understand some simple ways of accomplishing these goals. Chapter 4 / Physician As a Witness 41 4 The Physician As a Witness Joel A. Mattison, MD, FACS SUMMARY This chapter is a personal reflection on the role of the physician as an expert witness in medical malpractice litigation. It looks at both the individual experience and professional obligations of the expert from both the medical and the legal perspectives.