Associate Professor, Western University of Health Sciences
Also erectile dysfunction vacuum pumps australia cheap tadalafil 10mg with amex, in 1920 bradford erectile dysfunction diabetes service cheap tadalafil 2.5 mg on-line, Cannon reported that stimulation of the sympathetic trunk released an epinephrine-like substance impotence at 70 discount tadalafil 2.5 mg overnight delivery, which increased the heart rate and blood pressure erectile dysfunction with age statistics purchase tadalafil 5mg line. As stated ear lier, the integration of these two systems is achieved pri marily in the hypothalamus. In addition, the endocrine glands are influenced by circulating catecholamines, and some of them are innervated by adrenergic fibers. Both the autonomic and endocrine systems influence the muscular, cutaneous, and mesenteric (splanchnic) vascular beds, heart rate, and stroke volume of the heart. Together, these actions serve to maintain normal blood pressure and allow reflex maintenance of blood pressure with changes in body position. Two types of baroreceptors function as the afferent component of this reflex arc by sensing pres sure gradients across the walls of large blood vessels. Those in the carotid sinus and aortic arch are sensitive to reductions in pulse pressure (the difference between sys tolic and diastolic blood pressure), while those in the right heart chambers and pulmonary vessels respond more to alterations in blood volume. The carotid sinus barorecep tors are rapidly responsive and capable of detecting beat to-beat changes, in contrast to the aortic arch nerves, which have a longer response time and discriminate only the larger and more prolonged alterations in pressure. In response to increased stimulation of these receptors, vagal efferent activity is reduced, resulting in reflex cardioacceleration. Thus, vagal activity results in reduction in heart rate and in the contractile force of the myocardium (negative inot ropy). The main sympathetic outflow from these thoracic segments is via the greater splanchnic nerve to the celiac ganglion, the postganglionic nerves of which project to the capacitance vessels of the gut. The splanchnic capacitance veins act as a reservoir for as much as 20 percent of the total blood volume, and interruption of the splanchnic nerves results in severe postural hypotension. After a high-carbohydrate meal there is a marked hyperemia of the gut and com pensatory peripheral vasoconstriction in the muscles and skin. It has also been noted that the mesenteric vascular bed is responsive to the orthostatic redistribution of blood volume but not to mental stress. The opposite response to the one described earlier, namely bradycardia and hypotension, results when vagal tone is enhanced and sympathetic tone reduced. This response can be triggered by baroreceptors, or it may arise from cerebral stimuli such as fear or sight of blood in susceptible individuals as well as from extreme pain, particularly arising in the viscera. Two slower-acting humoral mechanisms regulate blood volume and complement the control of systemic vascular resistance. Pressure-sensitive renal juxtaglomer ular cells release renin, which stimulates production of angiotensin and influences aldosterone production, both of which affect an increase of blood volume. Of lesser influence in the control of blood pressure is antidiuretic hormone, discussed in the next chapter; but the effects of this peptide become more important when autonomic failure forces a dependence on secondary mechanisms for the maintenance of blood pressure. In addition to its presence in autonomic ganglia, nitric oxide has been found to have an important local role in maintaining vas cular tone, mainly by way of attenuating the response to sympathetic stimulation. Reg u latio n of Bladder Fu nctio n the familiar functions o f the bladder and lower uri nary tract-the storage and intermittent evacuation of urine-are served by three structural components: the bladder itself, the main component of which is the large detrusor (transitional type) muscle; a functional internal sphincter composed of similar muscle; and the striated external sphincter or urogenital diaphragm. The sphinc ters assure continence; in the male, the internal sphincter also prevents the reflux of semen from the urethra during ejaculation. For micturition to occur, the sphincters must relax, allowing the detrusor to expel urine from the blad der into the urethra. This is accomplished by a complex mechanism involving mainly the parasympathetic ner vous system (the sacral peripheral nerves derived from the second, third, and fourth sacral segments of the spi nal cord and their somatic sensorimotor fibers) and, to a lesser extent, sympathetic fibers derived from the thorax. The vaguely localizable brainstem "micturition centers," with their spinal and suprasegmental connections, may contribute. The detrusor muscle receives motor innervation from nerve cells in the intermediolateral columns of gray mat ter, mainly from the third and also from the second and fourth sacral segments of the spinal cord (the "detrusor center"). These neurons give rise to preganglionic fibers that synapse in parasympathetic ganglia within the blad der wall. Short postganglionic fibers end on muscarinic acetylcholine receptors of the muscle fibers. There are also beta-adrenergic receptors in the dome of the blad der, which are activated by sympathetic fibers that arise in the intermediolateral nerve cells of TlO, Tll, and T12 segments. These preganglionic fibers pass via inferior splanchnic nerves to the inferior mesenteric ganglia. The internal sphincter and base of the bladder (trigone), consisting of smooth muscle, are also innervated to some extent by the sympathetic fibers of the hypogastric nerves; their receptors are mainly of alpha-adrenergic type, which makes it possible to thera peutically manipulate the function of the sphincter with adrenergically active drugs as well as the more com monly used cholinergic ones (see further on). The external urethral and anal sphincters are com posed of striated muscle fibers. Their innervation, via the pudendal nerves, is derived from a densely packed group of somatomotor neurons (nucleus of Onuf) in the anterolateral horns of sacral segments 2, 3, and 4. The pudendal nerves also contain afferent fibers coursing from the urethra and the external sphincter to the sacral segments of the spinal cord. These fibers convey impulses for reflex activities and, through con nections with higher centers, for sensation. Some of these fibers probably course through the hypogastric plexus, as indicated by the fact that patients with complete trans verse lesions of the cord as high as T12 may report vague sensations of urethral discomfort. The bladder is sensi tive to pain and pressure; these senses are transmitted to higher centers along the sensory pathways described in Chaps. Unlike skeletal striated muscle, the detrusor, because of its postganglionic system, is capable of some contrac tions, although imperfect, after complete destruction of the sacral segments of the spinal cord. Isolation of the sacral cord centers (transverse lesions of the cord above the sacral levels) and their peripheral nerves permits contractions of the detrusor muscle, but they still do not empty the bladder completely; patients with such lesions usually develop dyssynergia of the detrusor and external sphincter muscles (see later), indicating that coordina tion of these muscles must occur at supraspinal levels (Blaivas). With acute transverse lesions of the upper cord, the function of sacral segments is abolished for several weeks in the same way as the motor neurons of skeletal muscles (the state of spinal shock).
Creutzfeldt-Jakob D isease (Su bacute Spongiform Encephalopathy) these terms refer to a distinctive cerebral disease in which a rapidly or subacutely progressive and profound dementia is associated with diffuse myoclonic jerks and a variety of other neurologic abnormalities erectile dysfunction in diabetes type 1 purchase tadalafil 10 mg line, mainly visual or cerebellar erectile dysfunction treatment karachi generic 20 mg tadalafil with visa. Less severe changes in a patchy distribution are found in cases with a briefer clinical course erectile dysfunction vacuum pump demonstration discount 2.5mg tadalafil overnight delivery. One of the more interesting aspects of the develop ment of the prion concept has been the hypothesis that many conditions erectile dysfunction medicine reviews generic tadalafil 5mg on-line, most in the category of degenerative neurologic disease and characterized by the accumulation of specific proteins such as amyloid, tau, synuclein, and ubiquitin may have a similar mechanism in sequential, contiguous conformational change in protein aggregation. E p i d e m i o l o g y and Path o g e n es i s the disease appears in all parts o f the world an d in all seasons, with an annual incidence of 1 to 2 cases per million of population. The incidence is higher in Israelis of Libyan origin, in immigrants to France from North Africa, and perhaps in Slovakia. The incidence of spon giform encephalopathy is somewhat higher in urban than in rural areas, but a consistent temporal or spatial clustering of cases has not been observed, at least in the United States. A small proportion of all series is familial varying from 5 percent reported by Cathala and associ ates to 15 percent of 1,435 cases analyzed by Masters and coworkers (1979). The occurrence of familial cases that are not in the same household probably indicates a genetic susceptibility to infection, although the possibil ity of common early exposure to the transmissible agent cannot be excluded. Of some interest is the finding by Zanusso and colleagues of the infectious prion protein in the nasal mucosa of all nine patients studied with the sporadic disease. This suggests a route for entry into the nervous system of the aberrant prion and also a potential diagnostic test. The mini-epidemic began in 1986, with putative trans mission of the disease to some 24 humans. The mode of transmission, presumed to be the ingestion of infected meat, is reminiscent of the propaga tion of kuru in New Guinea by ceremonial ingestion of brain tissue from infected individuals that opened the era of understanding of prion disease. Prion (spongiform) encephalopathy or all types has now been firmly associated with the conversion of a normal cellular protein, PrPc to an abnormal isoform, PrPsc. The transformation involves a change in the physical conformation of the protein in which its heli cal proportion diminishes and the proportion of the f3 pleated sheet increases (see reviews by Prusiner). The current understanding is that the "infectivity" of prions and their propagation in brain tissue result from the sus ceptibility of the native PrP to alter its shape as a result of physical exposure to the abnormal protein, a so-called conformational disease. Conformationally altered prions have a tendency to aggregate, and this may be the mode of cellular destruction that leads to neuronal disease. In contrast, familial cases of prion disease are thought to be the result of one of several gene aberrations residing in the region that code for PrPc. As the isoforrns of the prions that causes the spo radic disease have been characterized, clinical patterns have emerged as more or less typical of certain protein configurations and their underlying genotypes. Several competing classification systems have been devised that are based on both the presence of methionine (M) or valine (V) at codon 129 of the prion protein and on which of two physicochemical properties it displays (termed types 1 or 2; see Parchi et al). However, classification is complicated by the fact that some brain samples show more than one type of protein. There has also been controversy regarding the relationship of the genotype to the sensitivity of diagnostic tests discussed below. In the large series of pathologically verified cases reported by Brown and coworkers, prodromal symptoms-consisting of fatigue, depression, weight loss, and disorders of sleep and appetite lasting for several weeks-were observed in about one-third of the patients. The early stages of the neurologic disease are char acterized by a great variety of clinical manifestations, but the most frequent are changes in behavior, emotional response, and intellectual function, often followed by ataxia and abnormalities of vision, such as distortions of the shape and alignment of objects or impairment of visual acuity. Typically, the early phase of the disease is dominated by symptoms of confusion, with hallucina tions, delusions, and agitation. In other instances, cer ebellar ataxia (Brownell-Oppenheimer variant) or visual disturbances (Heidenhain variant) precede the mental changes and may be the most prominent features for several months. Headache, vertigo, and sensory symp toms are complaints in some patients but become quickly obscured by dementia and muteness. As a rule, the disease progresses rapidly, so that obvious deterioration is seen from week to week and even day to day. Sooner or later, in almost all cases, myoclonic contractions of various muscle groups appear, perhaps unilaterally at first but later becoming general ized. Or, infrequently, the myoclonus may not appear for weeks or months after the initial mental changes. In a few patients, a startle response, that is elicitable for a brief period of time, is the only manifestation of myoc lonus. In general, the myoclonic jerks are evocable by sudden sensory stimuli of all sorts, a startle response (to noise, bright light, touch) but they occur spontaneously as well. Twitches of individual fingers are typical but it should be emphasized that well-formed seizures are not a component of the illness. These changes gradually give way to a mute state, stupor, and coma, but the myoclonic contractions may continue to the end. Signs of degen eration of the pyramidal tracts or anterior horn cells, palsies of convergence and upgaze, and extrapyramidal signs occur in a small number of patients as the disease advances. The disease is invariably fatal, usually in a few months and almost always less than a year from the onset. In approximately 10 percent of patients, the ill ness begins with almost stroke-like suddenness and runs its course rapidly, in a matter of a few weeks. At the other extreme, a small number of patients have report edly survived for 2 to 10 years, but these reports should be accepted with caution; in some of them, the illness appears to have been superimposed on Alzheimer or Parkinson disease or some other chronic condition that predated the prion illness. The high-voltage sharp waves, which give the appearance of periodicity (they have been called pseudo periodic), are synchronous with the myoclonus, but may persist in its absence. Long contiguous segments of the cortex, as well as vari ous parts of the basal ganglia, show these alterations in a pattern that is characteristic and mistakable only perhaps for the appearance of diffuse cerebral anoxia. According to Shiga and colleagues, these changes occur in 90 percent of cases (cortex more often than caudate or lenticular nuclei and sometimes both), making them potentially the most sensitive test for the disease but the proportion has been lower in our patients.
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Of the latter erectile dysfunction and diabetes type 1 discount tadalafil 2.5 mg on line, 61 experienced feelings of fear and anxiety erectile dysfunction treatment diabetes purchase tadalafil 5mg visa, and 21 experienced depression impotence prostate buy tadalafil in india. These clinical data call to mind the effects that had been noted by Penfield and Jasper when they stimulated the upper erectile dysfunction doctor in jacksonville fl cheap tadalafil, anterior, and inferior parts of the temporal lobe and cingulate gyrus during sur gical procedures; frequently, the patient described feelings of strangeness, uneasiness, and fear. In most instances, consciousness was variably impaired at the same time, and some patients had hallucinatory experiences as well. In these cortical stimulations, neuronal circuits sub serving fear are coextensive with those of anger; both are thought to lie in the medial part of the temporal lobe and amygdala, as discussed earlier. Both in animals and in humans, electrical stimulation in this region can arouse each emotion, but the circuitry subserving fear appears to be located lateral to that of anger and rage. Destruction of the central part of the amygdaloid nuclear complex abolishes fear reactions. These nuclei are connected to the lateral hypothalamus and midbrain tegmentum, regions from which Monroe and Heath, as well as Nashold and associates, have been able to evoke feelings of fear and anxiety by electrical stimulation. Depression is less frequent as an ictal emotion, although it occurs often enough as an interictal phenomenon (Benson et al). Of interest is the observation that lesions of the dominant hemisphere are more likely than nondominant ones to be attended by an immediate pervasive depres sion of mood, disproportionate to the degree of severity of physical disability (Robinson et al). We are inclined to the view that the onset of depression after a stroke is a reaction to disability, i. Odd mixtures of depression and anxiety are often associated with temporal lobe tumors and less often with tumors of the hypothalamus and third ventricle (see review by Alpers), and they sometimes occur at the onset of a degenerative disease, such as multiple system atrophy. Elation and euphoria are less well documented as lim bic phenomena, nor has this elevation in mood in some patients with multiple sclerosis ever been adequately explained. Feelings of pleasure and satisfaction as well as "stirring sensations" are unusual, but well-described emo tional experiences in patients with temporal lobe seizures, and this type of affective response, like that of fear, has been elicited by stimulating several different parts of the U n i n h i b ited La u g hter and C ry i n g and E m oti o n a l La b i l ity As indicated earlier, one may confidently assume that the syndrome of forced or spasmodic laughing and crying signifies cerebral disease, and, more specifically, bilateral disease of the corticobulbar tracts (see Table 25-2). Usually the motor and reflex changes of spastic bulbar (pseudo bulbar) palsy (described in the discussion of "Spastic [Pseudobulbar] Dysarthria" in Chap. Extreme emotional lability also indicates bilateral cerebral disease, although only the signs of unilateral disease may be apparent clinically. The most common pathologic bases for these clinical states are lacunar infarction or other cerebrovascular lesions, diffuse hypoxic-hypotensive encephalopathy, amyo trophic lateral sclerosis, and multiple sclerosis, as already indicated; but in a number of less-common processes, such as progressive supranuclear palsy and Wilson dis ease, it may be quite a prominent feature. P l a c i d ity and Apathy these may be the earliest and most important signs of cerebral disease. Clinically, placidity and apathy must be distinguished from the akinesia or bradykinesia of Parkinson disease and the reduced mental activity of depressive illness. Here, Alzheimer disease, normal pressure hydrocephalus, and frontal-corpus callosum tumors are the most common pathologic states underlying apathy and placidity, but these disturbances may compli cate a variety of other frontal and temporal lesions, such as those occurring with demyelinating disease or as an aftermath of ruptured anterior communicating aneurysm. O ut b u rsts of R a g e and V i o l e nce Most often such an outburst is but another episode in a lifelong sequence of sociopathic behaviors (see Chap. If an outburst of rage accompanies a seizure, the rage should be viewed as the consequence of the disruptive effect of seizure activity on temporal lobe function; how ever, as indicated earlier, an outburst of uncontrolled rage and violence is only rarely a manifestation of temporal lobe epilepsy. Lesser degrees of poorly directed com bative behavior as part of ictal or postictal automatism are more common. Rarely, rage and aggressivity are expressive of an acute neurologic disease that involves the mediotemporal and orbitofrontal regions, such as a glioma. We have several times observed such states in the course of a dementing disease and in a stable individual as a transient expression of an obscure encephalopathy. Rage reactions with continuous violent activity must be distinguished from mania, in which there is flight of ideation to the point of incoherence, euphoric or irritable mood, and incessant psychomotor activity; from E xt re m e F r i g ht and Ag itati o n Here the central problem must b e clarified by deter mining whether the patient is delirious (clouding of consciousness, psychomotor overactivity, and hallucina tions), deluded (schizophrenia), manic (overactive, flight of ideas), or experiencing an isolated panic attack (pal pitation, trembling, feeling of suffocation). In an adult without a characterologic trait of anxiety, an acute panic attack may signify the onset of a depressive illness or schizophrenia. B iza rre I deati on Deve l o p i n g Ove r Wee ks or M o nths Although these symptoms are usually caused by a psy chosis (schizophrenia or bipolar disease), one should consider a tumor, immune or paraneoplastic encepha litis, or other lesion of the temporal lobe, particularly when accompanied by temporal lobe seizures, aphasic symptoms, rotatory vertigo (rare), and quadrantic visual field defects. Such states have also been described in hypothalamic disease, suggested by somnolence, diabe tes insipidus, visual field defects, and in hydrocephalus (see Chap. Ceccaldi M, Poncet M, Milandre L, Rouyer C: Temporary forced laughter after unilateral strokes. Narabayashi H, Nacao Y, Yoshida M, Nagahata M: Stereotaxic amygdalectomy for behavior disorders. Terzian H, Daile G: Syndrome of Kliiver-Bucy reproduced in man by bilateral removal of the temporal lobes. The human internal environment is regulated in large measure by the integrated activity of the autonomic ner vous system and endocrine glands. Their visceral and homeostatic functions, essential to life and survival, are involuntary. Why the forces of evolution favored this sep aration from volition is an interesting question. Claude Bernard expressed this idea in sardonic terms when he wrote, "nature thought it prudent to remove these impor tant phenomena from the caprice of an ignorant will. However, many general neurologic diseases involve the autonomic nervous system to a varying extent, giving rise to symp toms such as syncope, sphincteric dysfunction, pupillary abnormalities, erectile dysfunction, diaphoresis, cardiac dysrhythmias, and disorders of thermoregulation. Finally, in addition to their central role in visceral innervation, autonomic parts of the neuraxis and parts of the endo crine system are engaged in all emotional experience and its display; as discussed in Chap. Although continuous throughout life, it is not alto gether automatic, being partly under volitional control. Current views of the central and peripheral control of breathing, and the ways in which it is altered by certain diseases are of considerable interest to neurologists, if for no other reason than respiratory failure is common in neurologic conditions such as coma, cervical spinal cord injury, and a large number of acute and chronic neuro muscular diseases. Many of these same comments pertain to the function of swallowing, which is largely automatic and continues at regular intervals even in sleep but is also initiated voluntarily.
Approximately 3 erectile dysfunction naturopathic treatment order tadalafil toronto,000 new cases of acoustic neuroma are diagnosed each year in the United States (incidence rate of 1 per 100 erectile dysfunction drugs on nhs 2.5mg tadalafil with amex,000 per year) erectile dysfunction facts discount tadalafil express. The tumor occurs occa sionally as part of von Recklinghausen neurofibroma tosis erectile dysfunction young adults treatment order generic tadalafil online, in which case it takes one of two forms. Rarely, if ever, do bilateral acoustic neuromas occur in this form of the disease. Schwannomas are distinguished from neurofibromas (composed of both Schwarm cells and fibroblasts) found in peripheral nerves of type 1 von Recklinghausen disease. A small percentage of neurofibromas become malignant, a phenomenon that is highly unusual in schwannomas. The examination of small tumors reveals that they practically always arise from the vestibular rather than the cochlear division of the eighth nerve, just within the internal auditory canal. As the eighth nerve schwannoma grows, it extends into the pos terior fossa to occupy the angle between the cerebellum and pons (cerebellopontine angle). In this lateral position, it is so situated as to compress the seventh, fifth, and less often the ninth and tenth cranial nerves, which are impli cated in various combinations. A larger a typical vestibular schwannoma with rim enhancement, causing compression of the left middle cerebellar peduncle. The earliest symptom reported by the 46 patients in the decades-old but instructive series of Ojemann and coworkers was loss of hearing (33 of 46 patients); headache (4 patients); disturbed sense of balance (3 patients); unsteadiness of gait (3 patients); and facial pain, tinnitus, and facial weakness, each in a single case. Some patients sought medical advice soon after the appearance of the initial symptom, some later, after other symptoms had occurred. One-third of the patients were troubled by vertigo associated with nausea, vomiting, and pressure in the ear. The vertiginous symptoms differed from those of Meniere disease in that discrete attacks separated by periods of normalcy were rare. The vertigo coincided more or less with hearing loss and tinnitus (most often a unilateral high-pitched ringing, sometimes a machinery like roaring or hissing sound, like that of a steam kettle). Some of our patients ignored their deafness for many months or years; often the first indication of the tumor in such patients is a shift to the unaccustomed ear (usually right to left) in the use of the telephone. Others neglected these symptoms to a point where they presented with impaired mentation, imbalance, and sphincteric inconti nence because of brainstem compression and secondary hydrocephalus. The neurologic findings at the time of examination in the series mentioned above were as follows: eighth nerve involvement (auditory and vestibular; 45 of 46 patients), facial weakness including disturbance of taste (26 patients), sensory loss over the face (26 patients), gait abnormality (19 patients), and unilateral ataxia of the limbs (9 patients). Inequality of reflexes and eleventh and twelfth-nerve palsies were present in only a few patients. Signs of increased intracranial pressure appear late and have been present in fewer than 25 percent of our patients. These findings are comparable to those reported by House and Hitselberger and by Harner and Laws. With the shift in recent years to fairly routine investiga tion of unilateral hearing loss by cerebral imaging, it is common to find these tumors at a far earlier stage, if as an incidental finding on cerebral imaging, well before the tumor becomes symptomatic. Audiologic and vestibular evaluation includes the various tests described in Chap. In combination, they permit localization of the deafness and vestibular disturbance to the cochlear and vestibular nerves rather than to their end organs. Treatment the preferred treatment in most symp tomatic cases has been surgical excision. Neurosurgeons who have had a lot of experience with these tumors favor a microsurgical suboccipital transmeatal approach (Martuza and Ojemann). If no attempt is to be made to save hearing, small tumors can be removed safely by the translabyrinthine approach. An alternative to surgery is focused radiation, which controls the growth of many of the smaller tumors. In a large series of patients treated with radiosurgery, facial motor and sensory functions were preserved in 75 percent of cases and, after 28 months of observation, no new neurologic deficits were detected (Kondziolka et al). This approach is favored in older patients with few symptoms but is being adopted increasingly for others. The rates of hearing loss and facial numbness and weakness are comparable or lower than with surgery, but the follow-up period in most series is less than 5 years (Flickinger et al). Focused radiation with the gamma Knife or proton beam also appears to be preferable to surgery in cases of recur rent tumor. There is no consensus on the management of an inci dentally identified tumors but it is reasonable to follow these with audiograms and serial imaging. Some sources suggest that half of lesion smaller than 2 em in diameter will not progress, or do so slowly enough that hearing and balance are not impaired. However, lesions larger than this size are associated with more surgical complica tions and make sparing of hearing less likely. Ot h e r Tu m o rs of the Ce rebe l l o p o nti n e A n g l e Neu rinoma o r schwannoma of the trigeminal (gasserian) ganglion or neighboring cranial nerves and meningioma of the cerebellopon tine angle may, in some instances, be indistinguishable from a vestibular schwannoma. Fifth cranial nerve tumors should always be considered if deafness, tinnitus, and lack of response to caloric stimulation ("dead labyrinth") are not the initial symp toms of a cerebellopontine angle syndrome. A true cholesteatoma (epidermoid cyst) is a relatively rare tumor that is most often located in the cerebellopontine angle where it may simulate an acoustic neuroma but usu ally causes more severe facial weakness. Other disorders that enter into the differential diagnosis are glomus jugulare tumor (see later), meta static cancer, neoplastic meningitis (especially lym phomatous), syphilitic meningitis, arachnoid cyst, and epidural plasmacytoma of the petrous bone. Occasionally, a tumor that originates in the pons or in the fourth ven tricle (ependymoma, astrocytoma, papilloma, medullo blastoma) or a nasopharyngeal carcinoma may present as a cerebellopontine angle syndrome. In the differential diagnosis of the several craniopha ryngioma syndromes, a careful clinical analysis is often more informative than laboratory procedures. Often, because of the cholesterol content, the tumor gives an increased signal on Tl-weighted images.
