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Monday, January 10, 2022

Anatomy of the Basal Ganglia and Related Structures

Anatomy of the Basal Ganglia and Related Structures

Anatomy of the Basal Ganglia and Related Structures

BASAL NUCLEI (GANGLIA)
BASAL NUCLEI (GANGLIA)


OVERVIEW OF MOVEMENT DISORDERS

For the past 30 years, movement disorders have encompassed the study of a group of conditions characterized by poverty of movement, the akinetic-rigid syndromes, and those with excessive movements, the hyperkinetic movement disorders (tremor, dystonia, myoclonus, chorea/ballism, tics, and others). This traditional view, in which disorders of basal ganglia resulted in the aforementioned syndromes, has now expanded to include the ataxias and disorders of gait and posture. Advances in surgical techniques and imaging studies have broadened the clinical horizon and catchments of the movement disorders specialist. With the increasing indications for botulinum toxin therapy, spasticity and others disorders are now managed by many movement disorders neurologists.

Ventilatory Patterns and the Apnea Test

Ventilatory Patterns and the Apnea Test

Ventilatory Patterns and the Apnea Test

Ventilatory Patterns and the Apnea Test


Central Pattern Generator for Breathing. In health, the anatomic origin of the cyclic pattern of breathing is the brainstem. Sectioning the brainstem above the pons leaves breathing unaffected when the vagus nerve (cranial nerve X) carrying afferent information from the lungs is intact. Vagotomy results in a reduction in the breathing frequency and an increase in tidal volume. Transection below the medulla results in complete cessation of breathing. Sectioning above the central medulla results in rhythmic but irregular breathing, with vagotomy slowing the irregular pattern. Transection at the level of the upper pons leads to a slowing of respiration and an increase in tidal volume. If both vagus nerves are cut, the result is the cessation of breathing at full inspiration (called apneusis), or inspiratory spasms interrupted by intermittent expirations (called apneustic breathing). The central pattern generator for breathing is located within the medullary center.

Brain Death

Brain Death

Brain Death

Brain Death


Severe hypoxic-ischemic encephalopathy may result in brain swelling of such severity that all blood flow into the cranium is blocked, thereby worsening the ischemia to a terminal stage. Brain death is a clinical diagnosis based on the absence of neurologic function in the context of a diagnosis that has resulted in irreversible coma. In the United States, it indicates death of the entire brain; in the United Kingdom, it refers to death of the brainstem. Coma and apnea must coexist. A complete neurologic examination that includes the elements outlined in Plates 6-4 and 6-9 is mandatory to determine brain death, with all components appropriately documented. The current recommendation in adults is that a single evaluation suffices for the diagnosis of brain death. In children, two assessments should be performed, with the duration of interval between tests varying with age.

Vegetative State and Minimally Conscious State

Vegetative State and Minimally Conscious State

Vegetative State and Minimally Conscious State

Vegetative State and Minimally Conscious State


Survivors of some severe circulatory event, who are initially comatose, may pass through a spectrum of clinical conditions before partially or fully recovering consciousness. If, after having been in a coma, the patient opens the eyes but remains unable to initiate voluntary motor activity, this behavior marks the transition to what is called the vegetative state (VS). The further transition to minimally conscious state (MCS) is characterized by reproducible evidence of simple voluntary behavior. Emergence from MCS is signaled by the return of functional communication or object use. Further developments lead to outcomes ranging from severe disability to a good recovery. If, however, the patient remains in the VS for more than 1 month after the occurrence of brain damage, this condition is called the persistent vegetative state (PVS). This state is not necessarily irreversible. Reversibility is much less likely in patients in the permanent vegetative state, that is, in VS lasting more than 3 months after hypoxic-ischemic damage or 1 year after traumatic brain injury.

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage


At a national level, out-of-hospital cardiac arrests are an all-too-frequent occurrence. One quarter of individuals experiencing such an arrest will receive emergency cardiopulmonary resuscitation. However, fewer than 20% of these events will lead to survival at hospital discharge even with the combined efforts of emergency and hospital critical care services. Of those who do survive, many will have profound neurologic injury and disability.

Atrial Enlargement

Atrial Enlargement

Atrial Enlargement

Atrial Enlargement


Enlargement of the right atrium, as compared to the left, occurs in patients with cor pulmonale, pulmonary hypertension, and tricuspid or pulmonary stenosis. As a result, the first atrial electric movement predominates, and the electric axis of the P wave generally is toward the foot and to the front. As a consequence, the P waves are small in lead I but are tall in leads II, III, and aVF, often exceeding the upper limit of normal (2.5 mm) for lead II. The vector loop is down, forward, and large. Moderately tall P waves are present in leads V1 and V2.

Axis Deviation in Normal Electrocardiogram

Axis Deviation in Normal Electrocardiogram

Axis Deviation in Normal Electrocardiogram

Axis Deviation in Normal Electrocardiogram


In the normal individual the mean electric axis of the P wave, QRS complex, and T wave often reflects the anatomic position of the heart in the chest; an abnormal axis can result from heart disease. Plate 2-19 illustrates normal variations in the vectorcardiographic loop. The QRS and T loops in the frontal plane vary between −30 and +110 degrees and in the horizontal plane between +30 and −30 degrees, measured from the left arm.

Cardiac Depolarization and Repolarization and Mean Instantaneous Vectors

Cardiac Depolarization and Repolarization and Mean Instantaneous Vectors

Cardiac Depolarization and Repolarization and Mean Instantaneous Vectors

PROGRESSION OF DEPOLARIZATION
PROGRESSION OF DEPOLARIZATION


PROGRESSION OF DEPOLARIZATION

Atrial Depolarization and Mean Vectors

The cardiac impulse originates in the sinus node and starts the process of atrial depolarization by lowering the resistance of the cell membrane, allowing neutralization or reversal of certain dipoles. This leaves an electric-wave front, an accession wave, which is preceded by positive forces and followed by negative ones. Normally, this wave is initiated at the sinoauricular (S-A) node (see Plate 2-17). Early during atrial depolarization, however, the wave spreads toward the foot and A-V node. Toward the end of atrial depolarization, the accession wave is directed toward the left atrium and left arm. The early atrial depolarization wave may be represented as a vector, the length of which indicates the magnitude (strength) of the voltage generated by the accession wave. The late atrial depolarization voltage is represented by a second vector, the length of which is a measure of the voltage generated at this time.

Electrocardiogram

Electrocardiogram

Electrocardiogram

Electrocardiogram


An electrocardiogram is a graphic representation of voltage variations plotted against time. The variations result from the depolarization and repolarization of the cardiac muscle, which produces electric fields that reach the surface of the body where electrodes are located. An electrocardiographic machine is a galvanometer that records voltage variations, usually on paper tape. The first such machine was developed by Wilhelm Einthoven in 1906. It consisted of a silver-plated quartz string situated in a fixed magnetic field. Voltage variations from the body passed through the string, and the interaction of the electric fields between the magnet and the string resulted in the string’s movement, which was photographed. The modern ECG machine is similar to these early models, but microelectronics and computer interfaces have been incorporated, making them more useful and powerful. Although more convenient to use, these newer machines are no more accu- rate than the original ECG built by Einthoven.

Specialized Conduction System

Specialized Conduction System

Specialized Conduction System

PHYSIOLOGY OF SPECIALIZED CONDUCTION SYSTEM
PHYSIOLOGY OF SPECIALIZED CONDUCTION SYSTEM


PHYSIOLOGY OF SPECIALIZED CONDUCTION SYSTEM

Under normal conditions, heart activation results from an impulse originating in a cell or cell group (the pace-maker) and from the propagation of this impulse to all fibers of the atria and ventricles. Arrival of the electrical signal at the contractile fibers of the heart initiates contraction. Regular rhythmic activity requires the presence of specialized automatic fibers. Coordinated contraction of the atria and ventricles requires a system that distributes the electrical impulse to the muscle fibers of these chambers in the proper sequence and at the proper time. Both these functions are performed by specialized groups of cardiac fibers.

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