LOCALIZATION IN CLINICAL NEUROLOGY 6TH EDITION PDF

Develop and perfect your neurological localization skills with the gold standard text in the field. Anatomical localization skills based in physical examination are essential for any clinician caring for patients with neurologic disease processes. Improve your diagnostic accuracy and avoid unnecessary testing with this outstanding roadmap to neurologic diagnosis. Key Features: Comprehensive coverage addresses all brain regions, as well as cranial, spinal, and peripheral nerves.

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Localization derives from the Latin term locus or site. Localization is the diagnostic exercise of determining from the signs most often or symptoms of the patient what site of the nervous system has been a ected by a disease process. Important injury to the nervous system results in abnormal function, be it behavioral, motor, or sensory.

Characteristics of the dysfunction often pave the way for a topographic from the Greek term topos or place diagnosis. Localization and topographic diagnosis refer to the same thing: the determination of where in the nervous system the damage has occurred. Even in the age of sophisticated neurophysiology, neuroimaging, and molecular biology, the clinical diagnosis should precede the use of these other techniques if their full diagnostic potential is to be realized.

Clinical localization has particular relevance to the adequate use of ancillary procedures. As an example, congenital brain cysts, strikingly visible on imaging procedures, are often wrongly blamed for a variety of neurologic disorders, while the actual disease remains overlooked and untreated. The thoughtful use of ancillary procedures in neurology, guided by clinical localization, minimizes discomfort for patients and the waste of resources. A Brief History of Localization: Aphasia as an Example The history of localization is the history of early neurology, concerned with topographic diagnosis that would eventually lead to therapy.

In few areas of neurology was the development of localization as interesting and so much at the center of famous controversies as it was in the case of aphasia. In fact, the oldest known document on neurologic localization concerns aphasia. It was recorded in an Egyptian papyrus from the Age of the Pyramids about — BC , where an Egyptian surgeon described the behavior of an aphasic individual: If thou examinest a man having a wound in his temple, penetrating to the bone, and perforating his temporal bone; … if thou ask of him concerning his malady and he speak not to thee; while copious tears fall from both his eyes, so that he thrusts his hand often to his face so that he may wipe both his eyes with the back of his hand … Edwin Smith surgical papyrus, Case 20, BC [12].

From the time of Hippocrates, in ancient Greece, it was documented that injury to the left part of the brain resulted in weakness of the right side of the body. However, paired organs in the body were thought to have identical functions. In the midth century, Paul Broca — revolutionized the then current understanding of the functional organization of paired organs by describing lateralization of language to the left hemisphere [5,13].

In his paper, he wrote: Now, this function of the intellectual order, which controls the dynamic element as well as the mechanical element of articulation, seems to be the nearly constant privilege of the left hemisphere convolutions, since lesions that result in aphemia are almost always localized in that hemisphere … That is tantamount to saying that we are left-brained with regard to language.

Just as we control movements in writing, drawing, embroidering, etc, with the left hemisphere, so we speak with the left hemisphere. Broca de ned the inferior frontal gyrus as the area that, when injured, would lead to aphemia [13].

He also noted the variation in the expression of diverse lesions in the inferior frontal gyrus, characteristic of the plasticity found in cortical organization: During the course of our study of brains of patients with aphemia, many times before, we had determined that the lesion of the third left frontal convolution was not always in direct relation to the intensity and the impairment of language.

For example, we had observed that speech was completely wiped out as a result of a lesion with the size of 8 to 10 mm, whereas, in other cases, lesions that were tenfold more extensive had only partly impaired the capacity for articulate speech. Already in , Carl Wernicke — wrote: The whole area of convolution encircling the Sylvian ssure, in association with the cortex of the insula, serves as a speech center. After describing a year-old woman with the sudden onset of confused speech, Wernicke goes on to describe the pathologic findings: The branch of the artery of the left Sylvian ssure, running down into the inferior sulcus of Burdach, was occluded by a thrombus tightly adherent to the wall.

Current techniques, such as functional brain mapping, promise to clarify further the localization of mechanisms underlying neurologic dysfunction.

Recent neurophysiological and neuroimaging ndings, obtained with the use of diffusion tensor imaging and other functional magnetic resonance imaging MRI techniques, are challenging this notion [6].

Clinical Diagnosis and Lesion Localization Clinical diagnosis in neurology requires several steps: 1. Recognition of impaired function 2. Identification of what site of the nervous system has been affected, that is, localization 3. Definition of the most likely etiology, often resulting in a differential diagnostic list 4. In the original, the label on the superior temporal gyrus was simply a, but from the context, it should have been a 1. C is the central ssure; around the Sylvian ssure S extends the rst primitive convolution.

Within this convolution, ai is the central end of the acoustic nerve, a its site of entry into the medulla oblongata; b designates the representation of movements governing sound production, and is connected with the preceding through the association bers ai b running in the cortex of the insula. Each of these steps is important. The rst one, recognition of impaired function, depends on a good history and neurologic examination.

Only by storing the range of normal neurologic functions in their mind can physicians recognize an abnormal neurologic function. Inexperience or carelessness in examining a patient often results in overlooking a neurologic de cit and therefore missing a diagnosis. For instance, mild chorea may appear to the inexperienced as normal dgetiness. The slow eye movements of a pontocerebellar disorder may pass completely unrecognized by someone who looks only for a full excursion of the eyes.

Abnormal neurologic ndings come in the form of abnormal behavior, impaired posture or gait, di culty with movements of the face or extremities, and, nally, sensory disturbances, including pain. Pain exempli es well several of the di culties physicians face when confronting possible neurologic dysfunction.

First, is the dysfunction real? Is the pain really there or is the patient trying to deceive? We have witnessed the plight of a paraplegic patient who had been repeatedly asked by health care personnel to stop pretending not to be able to move his legs. Second, to what extent is the dysfunction pathologic, that is, indicative of injury serious enough to warrant a formal diagnostic workup?

Many aches and pains do not re ect serious disease. Third, is the dysfunction neurologic in origin? Is the pain due to injury of the a ected body part or neurologic dysfunction? Is the dysfunction a manifestation of a disease of the nervous system rather than of the organ mediating the function? Is the patient unable to walk because of arthritis or because the motor system is a ected?

All these questions nd an answer when the physician recognizes patterns that belie neurologic impairment, for instance, in the case of pain, a characteristic radicular nature and distribution. In other cases, the neurologic examination may reveal other manifestations of unquestionable neurologic dysfunction. Knowledge of localization tells us that the pain derives from injury of the median nerve at the point where the pain increases on percussion.

What is needed to localize the lesion, in this case as in any other, is a good working knowledge of neuroanatomy. Neuroanatomy is a key to localization. In this book, a synopsis of the anatomy of each structure of the nervous system precedes the discussion on localization of lesions of that structure. Damage to the structure alters the function mediated by this structure.

For example, an injury to the oculomotor nerve results in mydriasis in the eye supplied by this nerve. Neuroanatomy provides the road map for localization. Localizing is identifying the site of injury on the neuroanatomic map. As with any other map, we need either an address, with street name and number, or the intersection between two well-de ned streets or roads.

Injury expresses itself through neurologic dysfunction, be it behavioral, motor, or sensory. If we know what kind of dysfunction can result from injury of the di erent parts of the nervous system, we will be able to identify the source of the injury. Some types of dysfunction directly give us the address we are looking for. A combination of resting tremor, bradykinesia, and rigidity tells us that the substantia nigra of the patient has been injured. At other times, we use the approach of looking for the intersection between two streets.

From some signs we deduce that a particular pathway must be a.

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Localization in Clinical Neurology – 5th Edition

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