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In transgenic mice hair loss in men 50th buy 1 mg finasteride otc, (1838) hair loss in men 90th cheap generic finasteride uk, in his atlas Structure and Function of Neoplasms hair loss in men 2 discount finasteride uk, first enunciated the appealing idea that tumors might originate in embryonic cells left in the brain during devel opment. This idea was elaborated upon by Cohnheim (1878), who postulated that the source of tumors was an anomaly of the embryonic anlage. Ribbert, in 1904, extended this hypothesis by postulating that the potential for differentiation of these stem cells would favor blasto matous growth. Although it is not a popular notion today, Bailey and Cushing attached the suffix blastoma to indicate all tumors com posed of primitive-looking cells, such as glioblastoma and medulloblastoma. One prominent theory was that most tumors arise from neoplastic transformation of mature adult cells (dedifferentiation). A normal astro cyte, oligodendrocyte, microgliocyte, or ependymocyte is transformed into a neoplastic cell and, as it multiplies, the daughter cells become variably anaplastic, more so as the degree of malignancy increases. What has emerged from these studies is the view that the biogenesis and progression of brain tumors are a consequence of defects in the control of the cell cycle. Some molecular defects predispose to tumor genesis; others underlie subsequent progression and accelerated malignant transformation and yet others may confer sensitivity or resistance to chemotherapeutic agents. This model presupposes the acquisition of mul tiple genetic defects over time since, with the exception of special inherited conditions such as neurofibromatosis, ataxia telangectasia, and a few others, these are not germ line mutations but are acquired as somatic events in the course of tumor evolution. In cases that have an inherited and transmissible germ line defect there may be additional events that also cause somatic genetic mutations. Typically, inher ited mutations affect only one of two copies of a tumor suppressor gene that, by itself, does not cause cancer. These ideas are consistent with the observation that many of the gene defects that predispose to cancer are dominantly inher ited. More recently, single nucleotide polymorphisms have been identified that in combination predispose to certain childhood tumors such as neuroblastoma, or to the more aggressive forms of various tumors. If this is indeed the case, it may be that the apparent dedifferentiation of tumor cells is an artifact of their histo logic appearance and not a fundamental property. Medulloblastomas, polar spongioblasto mas, optic nerve gliomas, and pinealomas occur mainly before the age of 20 years, and meningiomas and glio blastomas are most frequent in the sixth decade of life. A number of mutations, only some inherited, also figure greatly in the genesis of certain tumors, particularly retinoblastomas, neurofibromas, and hemangioblasto mas. The gliomas associated with neurofibromatosis and tuberous sclerosis and the cerebellar hemangioblastomas of von Hippel-Lindau are the best examples of a genetic determinant. The rare familial disorders of multiple endo crine neoplasia and multiple hamartomas are associated with an increased incidence of anterior pituitary tumors and meningiomas, respectively. Other early changes include overexpres sion of genes that control growth factors or their receptors as noted below. After the tumor develops, progression to a more malignant grade of astrocytoma or to a glioblastoma may be triggered by defects in the p16-retinoblastoma gene signaling pathway, loss of chromosome 10 (seen in approximately 90 percent of high-grade gliomas), or over expression of the epidermal growth factor gene. In fact, it is striking that analysis of the patterns of these defects in some tumors correlates with the staging and aggressive characteristics of these tumors. Knowledge of the molecular signatures of certain tumors may have considerable clinical value. For example, oligodendrogliomas that have combined deletions in chromosomes 1p and 19q respond well to chemother apy and this property increases survival (Reifenberger and Louis; Louis et al, 2002). Much of the modern genetic understanding of brain tumors is derived from the technical gene microarrays.
The lesions in these cases consisted of surface contusions (48 percent) hair loss in men 50s clothing 5 mg finasteride amex, lacerations of the cerebral cortex (28 percent) hair loss quinine buy finasteride 1mg cheap, subarachnoid hem orrhage (72 percent) hair loss shampoo reviews purchase finasteride 5mg free shipping, subdural hematoma (15 percent), extradural hemorrhage (20 percent), and skull fractures (72 percent). As these figures indicate, several pathologic entities were found in the same patient. There is that relatively small, distressing group of severely brain-injured patients in whom the vital signs become normal but who never regain full consciousness. Such a patient, especially if a child, may still emerge from coma after 6 to 12 weeks or longer and make a relatively good, although usually incomplete, recovery. Some of those who survive for long periods open their eyes and move their heads and eyes from side to side but betray no evidence of seeing or recognizing even the closest members of their families. They do not speak and are capable of only primi tive postural or reflex withdrawal movements. Fourteen percent of the patients in the Traumatic Coma Data Bank remained in this state. Hemiplegia or quadri plegia with varying degrees of decerebrate or decorticate posturing are usually present. Life is terminated after sev eral months or years by some medical complication but some of our patients have survived for decades. Adams has examined the brains of 14 patients who remained in coma and in vegetative states from 1 to 14 years. Among patients who survived and remained vegetative until death, Adams and colleagues (2000) found that 80 percent had thalamic damage and 71 percent had findings of diffuse axonal injury. Moreover, trauma of extracranial organs and this sues is frequent and obviously contributes to the fatal outcome. Recent functional studies have shown that a limited proportion of patients who are in a vegetative or minimally conscious state can be trained to purposefully engage parts of the cerebrum. In generalizing about this category of head injury, the effects of contusion, hemorrhage, and brain swelling often become evident within 18 to 36 h after the injury and then may progress for several days. If a patient survives this period, his chances of dying from complica tions of these effects are greatly reduced. The mortality rate of those who reach the hospital in coma is approxi mately 20 percent, and most of the deaths occur in the first 12 to 24 h as a result of direct injury to the brain in combination with other nonneurologic injuries. Of those alive at 24 h, the overall mortality falls to 7 to 8 percent; after 48 h, only 1 to 2 percent of patients succumb. There is some evidence that transfer of such patients to an intensive care unit, where personnel experienced in the handling of head injury can monitor them, improves the chances for survival (see further on). One modest advance in the medical treatment of traumatic unresponsiveness has come from a randomized trial by Giacino and colleagues. Amantadine accelerated slightly the emergence from the vegetative or minimally conscious state; it was given for 4 weeks between the fourth and twelfth weeks after injury, 100 mg twice per day and increasing to 200 mg twice per day. The effects were less evident by 6 weeks but this seems like a prom ising approach. In cases of longer standing, deep brain stimulation of thalamic nuclei has been explored intermit tently in past decades and has had some notable successes. They each have characteristic clinical and imaging features but they may be admixed and the contribution of each to the clinical state must be assessed before deciding on a course of action. The injury, even when it fractures the skull, may not have produced coma initially, or it may be part of a devastating craniocerebral injury.
The orbits are involved in 20 percent of patients and lesions here simulate the clinical and radiologic appearance of orbital pseudotumor hair loss 3 months after giving birth order finasteride american express, cellulitis hair loss joan rivers purchase finasteride pills in toronto, or lymphoma hair loss in men enhancement order finasteride with paypal. There is a fibrinoid necrosis of their walls and an infiltra tion by neutrophils and histiocytes. The sedimentation rate is elevated, as are the rheumatoid and antiglobulin factors. A degree of therapeutic success in this formerly fatal disease has been achieved by the use of cyclo phosphamide, chlorambucil, rituximab, or azathioprine. Other neurologic manifestations are related to hyper tension, which frequently accompanies the disease and may precipitate cerebral hemorrhage; to endocarditis, which may give rise to cerebral embolism; to thrombotic thrombocytopenic purpura, which commonly complicates the terminal phase of the disease (Devinsky et al); and to treatment with corticosteroids, which may precipitate or accentuate muscle weakness, seizures, and psychosis. A similar set of neurologic problems arises in relation to the antiphospholipid antibody syndrome, 1 to 2 mg / kg per 90 to 95 percent of the cases. In acute cases, rapidly acting steroids-prednisone, 50 to 75 mg/d-is usually given in conjunction with the immunosuppressant drug(s). It is not entirely clear to us what proportion of the cerebro vascular features of lupus might be explained on the basis of the coagulation disorder or Libman-Sacks endocarditis. Arteritis Sym pto matic of U n d e rl y i n g Syste m i c D i sease and Sym path o m i m et i c D r u g I n g esti o n Drug-induced vasculitis, typical o f the ingestion of sym pathomimetic compounds, is difficult to distinguish from a more common state of focal vasospasm that may also be induced by these same agents, as discussed earlier under "Diffuse and Focal Cerebral Vasospasm, Call-Fleming Syndrome, Postpartum Cerebral Vasculopathy. The nature of this process is indeterminate but may be related to the deposition of circulating immune complexes in the walls of cerebral vessels. Seizures and death may occur as a result of a syndrome of delirium and extreme hyper thermia. More pertinent to this chapter are the strokes that arise during and just after cocaine use. Here, as emphasized by Levine and colleagues (1991), a clear distinction should be made between the complications of cocaine hydrochloride (the usual form of ingestible cocaine) and the alkaloid form, or "crack cocaine. The strokes with crack cocaine, however, are more often ischemic, typically involving the territory of a large vessel. Some ambiguity attends the vasculopathy induced by crack cocaine, cocaine hydrochloride, and the amphetamines, particularly the first of these. There are undoubted instances of a true cerebral inflammatory vasculitis, per haps of a hypersensitivity type such as those reported with biopsy verification by Krendel and colleagues, by Merkel and associates, and by others. What is confusing about these cases is the normal angiographic appearance in many instances and large vessel occlusions in others, in contrast to the pathologic changes, which are concen trated in small cortical vessels. Many cases seem to be of an entirely different type, displaying long segments of vascular attenuation in the angiogram and no evidence of an inflammatory process in biopsy or autopsy mate rial. A similar apparently vasospastic disorder is emerging from the use of high-potenClJ can nabi noids. Whether there is an increased incidence of arterio venous malformation and cerebral aneurysm in patients who have cerebral hemorrhages after ingestion of cocaine, as suggested in several articles, is uncertain but this, in any case, suggests that sympathomimetic drugs can pre cipitate hemorrhage from an underlying developmental vascular lesion (Fessler et al). Crack cocaine may also cause a choreiform disor der ("crack dancing"), not unlike that associated with antiphospholipid antibody but generalized rather than focal (see further on); usually there are small infarctions in the basal ganglia, but an immune mechanism has also been suggested. Another entirely different type of small vessel arteri this occurs as a hypersensitivity phenomenon. Often it is associated with an allergic skin lesion (Stevens-Johnson vasculopathy or a leukocytoclastic vasculitis). The clinical picture does not resemble that of polyarteritis nodosa, but the central or peripheral nervous system is affected in rare instances. The special case of intravascular lymphoma, which closely simulates a cerebral vasculitis, is discussed in Chap.
Visual field defects often remain hair loss mirena purchase finasteride 1 mg visa, but some improvement in vision can be anticipated hair loss cure vampire discount finasteride 5mg mastercard. Pituitary Apoplexy 1his syndrome hair loss cure 7th finasteride 5mg lowest price, described origi nally by Brougham, Heusner, and Adams, occurs as a result of infarction of an adenoma that has outgrown its blood supply. Pituitary apoplexy may threaten life unless the acute addisonian state is treated by hydrocortisone. If there is no improve ment after 24 to 48 h, or if vision is markedly affected, transsphenoidal decompression of the sella is indicated. Factors that may precipitate the necrosis or hemorrhage of a pituitary tumor are anticoagulation, pituitary func tion testing, radiation, bromocriptine treatment, and head trauma; most cases, however, occur spontaneously. Ischemic necrosis of the pituitary, without the presence of a tumor followed by hypopituitarism, occurs under a variety of circumstances, the most common being in the partum or postpartum period (Sheehan syndrome). M e n i n g i o m a of the S p h e n o i d R i d g e this tumor, mentioned earlier in the chapter, i s situated over the lesser wing of the sphenoid bone. Fully 75 percent of such tumors occur in women, and the average age at onset is 50 years. Most prominent among the symptoms are a slowly devel oping unilateral exophthalmos, slight bulging of the bone in the temporal region, and radiologic evidence of thick ening or erosion of the lesser wing of the sphenoid bone. Variants of the clinical syndrome include anosmia; oculo motor palsies; painful ophthalmoplegia (sphenoidal fissure and Tolosa-Hunt syndromes; see Table 47-2); blindness and optic atrophy in one eye, sometimes with papilledema of the other eye (Foster Kennedy syndrome); mental changes; seizures ("uncinate fits"); and increased intracranial pres sure. Sarcomas arising from skull bones, metastatic carcinoma, orbitoethmoidal osteoma, benign giant cell bone cyst, tumors of the optic nerve, and angiomas of the orbit must be considered in the differential diagnosis. The tumor is resectable without further injury to the optic nerve if the bone has not been invaded. M e n i n g i o m a of the O l fa ct o ry G roove this tumor originates in arachnoidal cells along the crib riform plate. The diagnosis depends on the finding of ipsilateral or bilateral anosmia or ipsilateral or bilateral blindness-often with optic atrophy and mental changes. The tumors may reach enormous size before coming to the attention of the physician but as many are small and found incidentally with cerebral imaging. The unilateral visual disturbance may consist of a slowly developing central scotoma. Abulia, confusion, forgetfulness, and inappropriate jocularity (witzelsucht) are the usual psychic disturbances from compression of the inferior frontal lobes (see Chap. M e n i n g i o m a of the Tu b e rc u l u m S e l l a Cushing was the first to delineate the syndrome caused by this tumor. The pre senting symptoms were visual failure-a slowly advanc ing bitemporal hemianopia with a sella of normal size. Often the field defects are asymmetrical, indicating a combined chiasmal-optic nerve involvement. If removal is incomplete or the tumor recurs or undergoes malignant changes, radiation therapy of one type or another is indicated. The outlook is then guarded; several of our patients succumbed within a few years. G l i o m a of the B ra i n ste m Astrocytomas of the brainstem are relatively slow-grow ing tumors that infiltrate tracts and nuclei.
Some patients hair loss in men zombie buy generic finasteride 5mg online, particularly those with inferofrontal lesions hair loss cure by 2015 order finasteride overnight delivery, feel com pelled to make silly jokes that are inappropriate to the situation hair loss naturally home remedies cheap generic finasteride uk, witzelsucht or moria; they are socially uninhib ited and lack awareness of their behavior. The patient is no longer the sensitive, compassionate, effective human being that he once was, having lost his usual ways of reacting with affection and consideration to family and friends. In more advanced instances, there is an almost complete disregard for social conventions and an interest only in immediate personal gratification. The patient at the same time seems to lose an appreciation of the moti vations and thought processes of other sapient persons ("theory of mind"); this results in the inability to incor porate these factors into his responses. These changes, observed characteristically in lobotomized patients, came to be recognized as too great a price to pay for the loss of anxiety, pain, depression, and "tortured self-concern," hence the procedure became obsolete. In general, the greatest cognitive-intellectual defi cits relate to lesions in the dorsolateral parts of the prefrontal lobes and that the greatest personality, mood, and behavioral changes stem from lesions of the medial orbital parts, although the two disorders often merge with one another. Benson (and Kleist and others before him) related the syndrome of apathy and lack of initia tive to lesions in the dorsolateral frontal cortex, and a facetious, unguarded, and socially inappropriate state (see below) to orbital and medial frontal lesions. Some studies of penetrating brain injuries have reported an inconsistent but interesting relationship between left dorsal frontal lesions and anger with hostility, and right side orbitofrontal lesions, with anxiety and depression. Again, in clinical work, few lesions have this degree of localizability, making conclusions about emotional states somewhat uncertain. Although the frontal lobes are the subject of a vast literature and endless speculation (see reviews of Stuss and Benson and of Damasio), a unified concept of their function has not emerged, probably because they are so large and include several heterogeneous systems. There is no doubt that the mind is greatly altered by disease of the prefrontal parts of the frontal lobes, but often it is difficult to say exactly how it is changed. Perhaps at present it is best to regard the frontal lobes as the part of the brain that quickly and effectively orients and drives the individual, with all the percepts and concepts formed from past life experiences, toward action that is projected into the future. Psychologic tests of frontal lobe function these are of particular value in establishing the presence of frontal lobe disease and are generally constructed to detect the ability to persist in a task and the opposite, to switch mental focus on demand. They include the Wisconsin card-sorting test, the Stroop color-naming test, sequencing of pictures, "trail making" (a two-part test in which the patient draws lines, first connecting randomly arrayed numbers on a paper in order and then connecting numbers and letters that correspond in order), the verbal equivalent of trail making, and the "go-no-go" test, both of which are used regularly in the mental status examination (see below), and the three step hand posture test of Luria. The alphabet-number verbal trailmaking test requires the patient to give each letter of the alphabet followed by the corresponding number (A-1, B-2, C-3, etc. In the Luria test and its vari ants, the patient is, for example, asked to imitate, then reproduce, a sequence of three hand gestures, typically making a closed fist, holding the open hand on its side, and then opening an outstretched palm. Patients with frontal lesions on either or both sides have difficulty per forming the test in correct sequence, often perseverating, balking, or making unwanted gestures. Luria suggested testing this with the sequence of arm thrusting forward, clenching the fist, and forming a ring with the first two fingers-derivatives of this test are now used. He also pointed out (1969) that the natural kinetic "melody," or smoothness of transition from one hand position to the next is disrupted and there is a tendency to perseverate. More complex mental acts that may be easily tested and betray frontal lobe disease but are less specific, in that they are also dis ordered by lesions in other brain regions, include serial subtraction ("working memory"), interpretation of prov erbs, tests of rapid motor response, and others. Contralateral spastic hemiplegia Contralateral gaze paresis Apathy and loss of initiative or its opposite, slight elevation of mood, increased talkativeness, tendency to joke inappropriately D. The temporal lobe includes the superior, middle, and inferior temporal, lateral occipitotemporal, fusiform, lin gual, parahippocampal, and hippocampal convolutions and the transverse gyri of Heschl. The last of these con stitutes the primary auditory receptive area and is located within the sylvian fissure. It has a tonotopic arrangement: fibers carrying high tones terminate in the medial portion of the gyrus and those carrying low tones, in the lateral and more rostral portions (Merzenich and Brugge). The planum temporale (area 22), an integral part of the audi tory cortex, lies immediately posterior to the Heschl con volutions, on the superior surface of the temporal lobe.
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