By B. Leif. University of Louisiana at Lafayette. 2018.
Part IV: The Limbic System The material includes History of the Brain purchase dapoxetine 90 mg without a prescription, 3-D Brain A quite detailed presentation on the various as- Anatomy generic 60mg dapoxetine free shipping, Mind Illusions, and Scanning the Brain. Epi- pects of the limbic system, with much expla- sodes include: The Baby’s Brain, The Child’s Brain, The nation and special dissections. The Secret Life of the Brain is a co-production of NOTE: It is suggested that these videotapes be pur- Thirteen/WNET New York and David Grubin Produc- chased by the library or by an institutional (or departmen- tions, © 2001 Educational Broadcasting Corporation and tal) media or instructional resource center. Information regarding the purchase of these and other videotapes may be obtained from: Health Sciences Con- sortium, 201 Silver Cedar Ct. These edited videotape presentations are on the skull and the brain as the material would be shown to students in CD-ROMS the gross anatomy laboratory. They have been prepared with the same teaching orientation as this atlas and are Numerous CDs are appearing on the market, and their particularly useful for self-study or small groups. These evaluation by the teaching faculty is critical before rec- videotapes of actual specimens are particularly useful for ommending them to learners. In addition, several of the students who have limited or no access to brain specimens. It is indeed a difﬁcult task to obtain and review 20–25 minutes. A listing of the CD-ROMs available can be viewed on the Web site Neuroanatomy and Neuropathology on INTERIOR OF THE SKULL the Internet (above) — see http://www. This program includes a detailed look at the bones of the skull, the cranial fossa, and the various foramina for the The following has been reviewed: cranial nerves and other structures. Included are views of the meninges and venous sinuses. Brainstorm: Interactive Neuroanatomy By Gary Coppa and Elizabeth Tancred, Stan- THE GROSS ANATOMY OF THE HUMAN BRAIN SERIES ford University A highly interactive and well-integrated cross- Part I: The Hemispheres linked presentation of the anatomy and some A presentation on the hemispheres, the func- functional aspects of the nervous system. Louis, MO, Part II: Diencephalon, Brainstem, and Cerebellum 63146-9934. A detailed look at the brainstem, with a focus on © 2006 by Taylor & Francis Group, LLC . ATLAS OF FUNCTIONAL NEUROA NATOMY SECOND EDITION © 2006 by Taylor & Francis Group, LLC © 2006 by Taylor & Francis Group, LLC ATLAS OF FUNCTIONAL NEUROA NATOMY SECOND EDITION Walter J. Boca Raton London New York A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc. Government works Printed in the United States of America on acid-free paper 10987654321 International Standard Book Number-10: 0-8493-3084-X (Softcover) International Standard Book Number-13: 978-0-8493-3084-1 (Softcover) Library of Congress Card Number 2005049418 This book contains information obtained from authentic and highly regarded sources. Reprinted material is quoted with permission, and sources are indicated. Reasonable efforts have been made to publish reliable data and information, but the author and the publisher cannot assume responsibility for the validity of all materials or for the consequences of their use. No part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, please access www. CCC is a not-for-profit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Library of Congress Cataloging-in-Publication Data Hendelman, Walter. Atlas of functional neuroanatomy / Walter Hendelman. To my wife and life partner, Teena and to our daughter, Lisanne and sadly now to the memory of our daughter, Devra To the many teachers and mentors and colleagues in my career as a neuroscientist, and particularly with respect and gratitude to Dr. Malcolm Carpenter To all those students, staff, and colleagues who have assisted me in this endeavor and to all the students who have inspired me in this learning partnership. As a teacher, it is my conviction that each slide or picture that is shown to students should be accompanied by an explanation; these explanations formed the basis of an atlas. Diagrams were created to help students understand the structures and pathways of the nervous system and each illustration was accompanied by explanatory text, so that the student could study both together. The pedagogical perspective has not changed over the various editions of the atlas as it expanded in content, but the illustrations have evolved markedly. They changed from simple artwork to computer-based graphics, from no color to 2-color, to the present edition in full color. The illustrations now include digital photographs, using carefully selected and dissected specimens. Most of the diagrams in the atlas were created by medical students, with artistic and/or technological ability, who could visualize the structural aspects of the nervous system. These students, who had completed the basic neuroanatomy course, collaborated with the author to create the diagrams intended to assist the next generation of students to learn the material more easily and with better understanding. I sincerely thank each of them for their effort and dedication and for their frequent, intense discussions about the material (please see the acknowledgements). They helped decide which aspects should be included in an atlas intended for use by students early in their career with limited time allotted for this course of study during their medical studies. This atlas has beneﬁted from the help of colleagues and staff in the department of which I have been a member for over 30 years, and from professional colleagues who have contributed histological and radiological enhancements, as well as advice. The previous edition of this atlas included a CD ROM containing all the images in full color.
A train of stimuli is given to a peripheral nerve stimulation in a defined frequency dapoxetine 90mg low cost. The resulting CMAP amplitudes and areas are recorded and measured buy discount dapoxetine 90 mg on line. Repetitive nerve stimulation allows a distinction between pre- and postsynaptic transmission disorders. MG is usually detected at low fre- quency 3 Hz stimulation, whereas high frequency stimulation (20 Hz) leads to an incremental response in the Lambert Eaton Myasthenic syndrome (LEMS). Although this technique is extremely useful, decremental and incremental responses can be observed in other conditions. Evoked responses, in particular somatosensory evoked responses, allow mea- Evoked responses surement of central structures like the posterior columns, and provide addition- al insight into peripheral-central conduction properties. Magnetic stimulation techniques are usually performed with a coil and can be Magnetic stimulation used to measure central conduction time as a parameter for central motor techniques function. Stimulation at the vertebral column and in proximal nerve segments allows measurement of these difficult to approach segments. In Europe, concentric needle electrodes are mainly used, while in the USA monopolar needles in combination with surface reference electrodes are used. The application of surface electrodes for the assessment of muscle function is still a matter of debate. Three different steps of evaluation of the electrical activity are usually taken: – Insertional activity is created by small movements of the needle electrode, and results in amorphous discharges with short durations. It is usually increased in neuropathic processes, but is difficult to quantify, and often labeled “irritability”. Strictly speaking, pathologic conditions like myotonia, neuromyotonia, myokymia, and complex repetitive discharges (CRDs) be- long in that category, but are usually considered spontaneous activity. The end plate region has typical short negative spikes. Potentials generated from single muscle fibers are called fibrillations and positive sharp waves. More complex discharges from the motor unit are fascicula- tions, myokymia, neuromyotonia, and the discharges of muscle-cramps and tetany. CRDs stem from electrically linked muscle fibers, firing in a synchro- nous pattern. These MUAPs have a variable duration, depending on the method of assessment (concentric needle, monopolar, or single fiber technique), and depend on the muscle and the age of the patient. At mild contraction the duration is usually in the range of 5 to 15 ms, has up to four phases, and an amplitude between 300–3000 µV. For the assessment of MUAPs, duration is more constant and reliable than amplitude. Maximum contraction produces overlapping MUAPs, called an interference pattern under normal conditions. The spectrum of pathologic abnormalities ranges from individual MUAPs firing in neurogenic conditions, to a full interference pattern with low amplitude in myopathies. Types of pathological discharges: Fasciculations resemble MUAPs in configuration, but have an irregular dis- charge pattern. They may be linked with a visible or palpable muscle twitch. They can be benign, or occur as part of a neuromuscular condition and are notably increased in ALS. CRDs (“bizarre high frequency discharges”) are caused by groups of adjacent muscle fibers discharging with ephaptic spread from one fiber to another. They are usually seen in chronic neurogenic and myopathic disease processes. They typically begin and end abruptly, and have a frequency of 5–100 Hz. The frequency does not change and contrasts with the waning and waxing pattern of myotonia. Myotonic discharges are induced by mechanical provocation (needle, percus- sion). They are independent repetitive discharges of muscle fibers at rates of 20 to 80 Hz. The amplitude and frequency wane characteristically. They occur in myotonic dystrophy, myotonia congenita, paramyotonia congenita, hyperkalemic periodic paraly- sis, acid maltase deficiency, and myotubular myopathy. Neuromyotonia are bursts of multiple spikes, discharging in high frequency (up to 300 Hz). The frequency remains constant, but the amplitude slowly decreas- es. Sometimes groups of normal appearing MUAPs are called neuromyotonia, but may also be classified as myokymia. Myokymia is a burst of motor unit potentials (resembling normal MUAPs), and appearing in groups separated by intervals of silence. Focal myokymia is often associated with radiation damage. Cramp discharges are involuntary muscle discharges, consisting of multiple MUAPs that originate from an involuntary tetanic contraction. EMG techniques Automated or semi-automated methods are available on most new EMG machines. Decomposition techniques can extract single MUAPs from an interference pattern.
Of these bleeding complications buy 60 mg dapoxetine with visa, intracranial bleeding is the most dreaded because it is commonly fatal buy dapoxetine 90 mg fast delivery. Intracranial bleeding is more commonly seen when the platelet count drops below 10,000/µl; other risk factors include advanced age and con- comitant medical illness. A 33-year-old woman is admitted to the hospital with altered mental status. Her physician calls you for consultation; he is concerned that the patient may have thrombotic thrombocytopenic purpura (TTP). He notes that she has anemia, thrombocytopenia, and a high fever and that she is disoriented. He asks your opinion regarding certain laboratory tests he has sent. Which of the following findings is NOT consistent with a diagnosis of TTP? Schistocytes and helmet cells seen on blood smear B. Neutrophilic leukocytosis Key Concept/Objective: To be able to recognize the laboratory abnormalities associated with TTP Patients with TTP typically present with the following pentad of signs and symptoms: (1) thrombocytopenia; (2) microangiopathic hemolytic anemia with schistocytes and helmet cells; (3) renal dysfunction, which is usually mild; (4) fever, which can be very high; and (5) neurologic symptoms, including seizures and a clouded sensorium. TTP is not associ- ated with a positive direct Coombs test; hemolysis is not immune mediated. This finding should make one consider autoimmune hemolytic anemias (such as those associated with Evan syndrome and SLE, both of which should be considered in the differential diagno- sis). The other findings are consistent with TTP and are helpful in establishing the diag- nosis and differentiating it from other causes of anemia and thrombocytopenia (such as disseminated intravascular coagulation). Prompt plasmapheresis should be instituted in patients with TTP. A dentist wishes to learn more about von Willebrand disease (vWD); he recently had a patient who has the disorder suffer excessive bleeding after dental work. In your discussion, you outline several key facts about vWD, including how these patients may require treatment before dental procedures and other surgeries. Results of coagulation studies are normal in patients with vWD B. Most cases are the result of impaired function of von Willebrand factor (vWF) D. An abnormal result on the ristocetin-induced platelet aggregation test is consistent with abnormal function of the patient’s vWF (type 2 vWD) E. It affects very few people Key Concept/Objective: To know some common facts about vWD vWD is the most common hereditary bleeding disorder. It may be the result of low levels of vWF (type I vWD, which accounts for 75% of cases); qualitative defects in vWF function (type II vWD), which can be determined by use of the ristocetin-induced platelet aggrega- tion test; or a severe or total deficiency of vWF (type 3 vWD, the least common form). The disorders of platelet function associated with vWD are not associated with decreases in platelet count. A 7-year-old boy with advanced pancreatic adenocarcinoma is diagnosed with Trousseau syndrome (chronic disseminated intravascular coagulation [DIC] secondary to malignancy). Approximately 2 months ago, he was found to have a deep vein thrombosis (DVT). Which of the following is seen in cases of chronic (compensated) DIC? Predisposition toward bleeding rather than thrombosis Key Concept/Objective: To be familiar with the common laboratory and clinical findings of chronic (compensated) DIC Trousseau syndrome is a chronic form of DIC. When onset of DIC is slow, as is seen in some patients with cancer, compensation can occur. In these patients, a procoagulant state exists, and the patient has a predisposition for arterial and venous thrombosis (unlike in the acute forms of DIC, in which bleeding predominates). The typical laboratory abnor- malities associated with acute DIC (thrombocytopenia, elevations in levels of coagulation factors, microangiopathic hemolytic anemia, decreased fibrinogen levels, and elevated D- dimer levels) are usually not present in patients with the chronic form; the exception to this is an elevated D-dimer level. This patient with Trousseau syndrome and DVT should receive subcutaneous heparin if its use is not contraindicated. A 38-year-old woman develops a deep vein thrombosis (DVT) in her left leg during a cross-country car trip. She is treated with heparin for 3 days, and she is started on warfarin. She is discharged from the hos- pital with an international normalized ratio (INR) of 2. Three days later, she presents with severe pain 36 BOARD REVIEW in her left hand. Examination reveals an infarction of the third digit, with severe pain, purpura, and ery- thema. She has been compliant with regard to her medication regimen. Which of the following is most consistent with this patient’s disease process? Antithrombin III (AT-III) deficiency Key Concept/Objective: To understand the diagnosis of protein C deficiency Protein C deficiency results in a loss of ability to inactivate factor VIIa and factor Va, two major cofactors that regulate the clotting cascade. Warfarin lowers protein C levels as well as the levels of all the vitamin K-dependent clotting factors. Because the half-lives of fac- tor Xa and prothrombin are longer than that of protein C, initiation of warfarin therapy can induce a paradoxical state of hypercoagulability. This patient likely has a heterozygous protein C deficiency that was uncovered when she was treated with warfarin. In patients in whom protein C deficiency is suspected, heparin and warfarin should be initiated con- comitantly.
Often generic 90 mg dapoxetine mastercard, the hepatitis has no obvious cause purchase dapoxetine 30 mg without a prescription, and tests for hepatitis A, B, and C are negative. Aplasia can also be part of a prodrome to hairy-cell leukemia, acute lym- phoblastic leukemia, or, in rare cases, acute myeloid leukemia, or it can develop in the course of myelodysplasia. Parvovirus infection is the cause of the transient aplastic crises that occur in patients who have severe hemolytic disorders. The marrow in patients with such disorders must compensate for the peripheral hemolysis by increasing its production up to sevenfold. Although parvovirus can affect all precursor cells, the red cell precursors are the most profoundly affected. Anemia causes fatigue and shortness of breath; throm- bocytopenia causes petechiae, oral blood blisters, gingival bleeding, and hematuria, depending on the level of the platelet count. By far the major problem is the recurrent bac- terial infections caused by the profound neutropenia. The diagnosis of aplastic anemia requires a marrow aspirate and biopsy, as well as a thorough history of drug exposures, infections, and especially symptoms suggesting viral illnesses and serologic test results for hepatitis, infectious mononucleosis, HIV, and parvovirus. Measurement of red cell CD59 is helpful in the diagnosis of paroxysmal nocturnal hemoglobinuria. A 43-year-old white man presents to your clinic complaining of fatigue and paresthesias. He is a vegetar- ian and does not take a multivitamin. His examination reveals pallor, an absence of hepatosplenomegaly, normal muscle strength throughout, and loss of position sensation and vibratory sensation distally. A CBC reveals anemia, with a mean corpuscular volume (MCV) of 106 fl. His WBC, platelet count, and serum chemistries are normal. He has had no toxic exposures and is taking no medications. Which of the following statements about megaloblastic anemia is false? Absorption of cobalamin in the small intestine is dependent on pro- teins produced in the mouth and stomach B. Megaloblastic erythropoiesis is characterized by defective DNA synthe- sis and arrest at the G2 phase, with impaired maturation and a buildup of cells that do not synthesize DNA and that contain anom- alous DNA C. In most patients with severe cobalamin deficiency, the neurologic examination is normal D. Cobalamin deficiency is treated with parenteral cobalamin therapy Key Concept/Objective: To understand the etiology, diagnosis, and treatment of pernicious anemia Megaloblastic erythropoiesis is characterized by defective DNA synthesis and arrest at the G2 phase, with impaired maturation and a buildup of cells that do not synthesize DNA and that contain anomalous DNA. This condition leads to asynchronous maturation between the nucleus and cytoplasm. RNA production and protein synthesis continue; thus, larger cells, or megaloblasts, are produced. In addition to macrocytic and megaloblastic anemia, the patient with cobalamin deficiency may have weakness, lethargy, or dementia, as well as atrophy of the lingual papillae and glossitis. Neuropathy is the presenting fea- ture in about 12% of patients with cobalamin (vitamin B12) deficiency without concomi- tant anemia. Patients with severe cobalamin deficiency initially complain of paresthesia. The sense of touch and temperature sensitivity may be minimally impaired. The disease may progress, involving the dorsal columns, causing ataxia and weakness. The physical examination reveals a broad- based gait, the Romberg sign, slowed reflexes, and a loss of sense of position and feeling of 5 HEMATOLOGY 7 vibration (especially when tested with a 256 Hz tuning fork). A 53-year-old woman is referred to your office by her gynecologist for management of anemia. She expe- rienced menopause at 48 years of age and has had no further vaginal bleeding. During her last office visit, her hematocrit was 29%, and her MCV was 107 fl. She admits to drinking a pint of wine daily, and she engages in occasional binge drinking on weekends. She denies any other sources of blood loss or icterus. She is apparently only mild- ly symptomatic with some fatigue. Which of the following statements regarding megaloblastic anemia caused by folic acid deficiency is false? Serum folic acid levels more accurately reflect tissue stores than do red blood cell folic acid levels B. Folic acid deficiency can be differentiated from cobalamin deficiency by measuring methylmalonic acid and homocysteine levels; both are elevated in cobalamin deficiency, but only homocysteine is elevated in folic acid deficiency C. Megaloblastic anemia caused by folic acid deficiency can be masked by concurrent iron deficiency anemia, but hypersegmented polymor- phonuclear cells (PMNs) should still be present on the peripheral smear D. Folinic acid can be used to treat patients with megaloblastosis and bone marrow suppression associated with the use of methotrexate Key Concept/Objective: To understand the diagnosis and treatment of megaloblastic anemia caused by folic acid deficiency Patients with megaloblastic anemia who do not have glossitis, a family history of perni- cious anemia, or the neurologic features described for cobalamin deficiency may have folic acid deficiency. Tests to determine folic acid deficiency vary in their accuracy.
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