He also explained that it is analogous to hunger, the will to power, and so on insisting that it is a fundamental instinct that is innate in all humans.Freud developed the idea of a series of developmental phases in which the libido fixates on different erogenous zones—first in the oral stage (exemplified by an infants pleasure in nursing), then in the anal stage (exemplified by a toddlers pleasure in controlling his or her bowels), then in the phallic stage, through a latency stage in which the libido is dormant, to its reemergence at puberty in the genital stage. (Karl Abraham would later add subdivisions in both oral and anal stages. )Freud pointed out that these libidinal drives can conflict with the conventions of civilised behavior, represented in the psyche by the superego. It is this need to conform to society and control the libido that leads to tension and disturbance in the individual, prompting the use of ego defenses to dissipate the psychic energy of these unmet and mostly unconscious needs into other forms. Excessive use of ego defenses results in neurosis. A primary goal of psychoanalysis is to bring the drives of the id into consciousness, allowing them to be met directly and thus reducing the patients reliance on ego defenses.Freud viewed libido as passing through a series of developmental stages within the individual. Failure to adequately adapt to the demands of these different stages could result in libidinal energy becoming dammed up or fixated in these stages, producing certain pathological character traits in adulthood.
Adie syndrome, also known as Holmes-Adie syndrome, is a neurological disorder characterized by a tonically dilated pupil that reacts slowly to light but shows a more definite response to accommodation (i.e., light-near dissociation). It is frequently seen in females with absent knee or ankle jerks and impaired sweating. The syndrome is caused by damage to the postganglionic fibers of the parasympathetic innervation of the eye, usually by a viral or bacterial infection that causes inflammation, and affects the pupil of the eye and the autonomic nervous system. It is named after the British neurologists William John Adie and Gordon Morgan Holmes, who independently described the same disease in 1931. Signs and symptoms
Adie syndrome presents with three hallmark symptoms, namely at least one abnormally dilated pupil (mydriasis) which does not constrict in response to light, loss of deep tendon reflexes, and abnormalities of sweating. Other signs may include hyperopia due to accommodative paresis, photophobia and difficulty reading. Some individuals with Adie syndrome may also have cardiovascular abnormalities. Pathophysiology
Pupillary symptoms of Holmes–Adie syndrome are thought to be the result of a viral or bacterial infection that causes inflammation and damage to neurons in the ciliary ganglion, located in the posterior orbit, that provides parasympathetic control of eye constriction. Additionally, patients with Holmes-Adie Syndrome can also experience problems with autonomic control of the body. This second set of symptoms is caused by damage to the dorsal root ganglia of the spinal cord. Adies pupil is supersensitive to ACh so a muscarinic agonist (e.g.