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By: W. Gunnar, M.B.A., M.D.

Clinical Director, University of South Carolina School of Medicine

Sensitivity to light and noise attends both types medicine buddha discount 300mg lopid with mastercard, and intensification with movement of the head is common medications kidney damage buy discount lopid 300mg on line. If the pain is severe medications not to crush purchase cheapest lopid and lopid, the patient prefers to lie down in a quiet treatment locator discount lopid 300 mg on line, darkened room and tries to sleep. The hemicranial and the throbbing (pulsating) aspects of migraine are its most characteristic features in comparison to other headache types; each patient displays a proclivity for the pain to affect one side or the other of the cranium, but not exclusively. The genetic nature of classic migraine is apparent from its occurrence in several members of the family of the same and successive generations in 60 to 80 percent of cases; the familial frequency of common migraine is slightly lower. Certain rare forms of migraine, such as familial hemiplegic migraine, appear to be monogenic disorders, but the role of these genes, one of which codes for a calcium channel (see below), in classic and common migraine is speculative. Migraine, with or without aura, is a remarkably common condition; its prevalence among Caucasians is in the range of 4 to 6 percent among men and 13 to 18 percent among women (see Stewart et al). Migraine may have its onset in childhood but usually begins in adolescence; in more than 80 percent of patients, the onset is before 30 years of age, and the physician should be cautious in attributing headaches that appear for the first time after this age to migraine. In women, the headaches tend to occur during the premenstrual period; in about 15 percent of such migraineurs, the attacks are exclusively perimenstrual ("true menstrual migraine"), although estrogen and progesterone levels throughout the menstrual cycle are the same in normal and migrainous women. Menstrual migraine, discussed further on, is thought to be related to the withdrawal of estradiol rather than progesterone (based on the work of Somerville). It is now acknowledged that the influence of sex hormones on headache is more complex. The attacks cease during pregnancy in 75 to 80 percent of women, and in others they continue at a reduced frequency; less often, attacks of migraine or the associated neurologic symptoms first appear during pregnancy, usually in the first trimester. Although migraine usually diminishes in severity and frequency with age, it may actually worsen in some postmenopausal women, and estrogen therapy may either increase or, paradoxically, diminish the incidence of headaches. The use of birth control pills has been associated with an increased frequency and severity of migraine and in rare instances has resulted in a permanent neurologic deficit. Some patients link their attacks to certain dietary items- particularly chocolate, cheese, fatty foods, oranges, tomatoes, and onions- but these connections in most cases seem to us to be overrated. Some of these foods are rich in tyramine, which has been incriminated as a provocative factor in migraine. Perhaps the most common ostensible trigger is excess caffeine intake or withdrawal of caffeine. Migraine with aura frequently has its onset soon after awakening, but it may occur at any time of day. During the preceding day or so, there may have been mild changes in mood (sometimes a surge of energy or a feeling of well-being), hunger or anorexia, drowsiness, and frequent yawning. Then, abruptly, there is a disturbance of vision consisting usually of unformed flashes of white, or silver or, rarely, of multicolored lights (photopsia). This may be followed by an enlarging blind spot with a shimmering edge (scintillating scotoma), or formations of dazzling zigzag lines (arranged like the battlements of a castle, hence the term fortification spectra or teichopsia). Other patients complain instead of blurred or shimmering or cloudy vision, as though they were looking through thick or smoked glass or the wavy distortions produced by heat rising from asphalt. These luminous hallucinations move slowly across the visual field for several minutes and may leave an island of visual loss in their wake (scotomatous defects); the latter are usually bilateral and often homonymous (involving corresponding parts of the field of vision of each eye), pointing to their origin in the visual cortex. Patients almost invariably attribute these visual symptoms to one eye rather than to parts of both fields. Ophthalmologic abnormalities of retinal and optic nerve vessels have been described in some cases but are not typical (see further on). Other focal neurologic symptoms, much less common than visual ones, include numbness and tingling of the lips, face, and hand (on one or both sides); slight confusion of thinking; weakness of an arm or leg; mild aphasia or dysarthria, dizziness, and uncertainty of gait; or drowsiness. Only one or a few of these neurologic phenomena are present in any given patient, and they tend to occur in more or less the same combination in each attack. If weakness or paresthetic numbness spreads from one part of the body to another or if one neurologic symptom follows another, this occurs relatively slowly over a period of minutes (not over seconds, as in a seizure, or simultaneously in all affected parts as in a transient ischemic attack). These neurologic symptoms last for 1 to 15 min, sometimes longer; as they begin to recede, they are followed by a unilateral dull pain that progresses to a throbbing headache (usually but not always on the side of the cerebral disturbance), which slowly increases in intensity. At its peak, within minutes to an hour, the patient is forced to lie down and to shun light and noise.


  • Prolactin level (milk hormone)
  • Lung disease, such as COPD or pulmonary fibrosis
  • CO2 (carbon dioxide)
  • Growth hormone (GH) -- stimulates growth of tissues and bone
  • Includes persons with heart disease, lung disease, kidney disease, alcoholism, diabetes, cirrhosis, cochlear implants, and leaks of cerebrospinal fluid
  • MRI of the spine

This diminishes the likelihood of reaccumulation of fluid but it is not always successful symptoms zinc toxicity lopid 300 mg cheap. Other causes of operative failure are swelling of the compressed hemisphere or failure of the Cerebral Contusion Severe closed head injury is almost universally accompanied by cortical contusions and surrounding edema medicine 5277 300mg lopid amex. The mass effect of contusional swelling medicine 93 5298 order 300mg lopid, if sufficiently large medicine in french buy lopid without a prescription, is a major factor in the genesis of tissue shifts and raised intracranial pressure. In the first few hours after injury, the bleeding points in the contused area may appear small and innocuous. The main concern, however, is the tendency for a contused area to swell or to develop into a hematoma. It has been claimed, on uncertain grounds, that the swelling in the region of an acute contusion is precipitated by excessive administration of intravenous fluids (fluid management is considered further on in this chapter). Traumatic Intracerebral Hemorrhage One or several intracerebral hemorrhages may be apparent immediately after head injury, or hemorrhage may be infrequently delayed in its development by several days (Spatapoplexie). The injury is nearly always severe; blood vessels as well as cortical tissue are torn. The clinical picture of traumatic intracerebral hemorrhage is similar to that of hypertensive brain hemorrhage (deepening coma with hemiplegia, a dilating pupil, bilateral Babinski signs, stertorous and irregular respirations). It may be manifest by an abrupt rise in blood pressure and in intracranial pressure. In elderly patients, it is sometimes difficult to determine whether a fall had been the cause or the result of an intracerebral hemorrhage. Craniotomy with evacuation of the clot has given a successful result in a few cases, but the advisability of surgery is governed by several factors, including the level of consciousness, the time from the initial injury, and the associated damage (contusions, subdural and epidural bleeding) shown by imaging studies. Boto and colleagues determined that basal ganglia hemorrhages were prone to enlarge in the day or two after closed head injury and that those over 25 mL in volume were fatal in 9 of 10 cases. It should be mentioned again that subarachnoid blood of some degree is very common after serious head injury. A problem that sometimes arises in cases that display both contusions and substantial subarachnoid blood is the possibility that a ruptured aneurysm was the initial event and that a resultant fall caused the contusions. In cases where the subarachnoid blood is concentrated around one of the major vessels of the circle of Willis, an angiogram may be justified to exclude the latter possibility. This syndrome confers a high risk for slowing of development; there may be acquired microcephaly reflecting brain atrophy consequent to both contusions and infarctions. A low initial Glasgow Coma Scale score, severe retinal hemorrhages, and skull fractures are associated with poor outcomes. Old and recent fractures in other parts of the body should arouse suspicion of this syndrome. Penetrating Wounds of the Head Missiles and Fragments the descriptions in the preceding pages apply to blunt, nonpenetrating injuries of the skull and their effects on the brain. The disorders included in this section are more the concern of the neurosurgeon than the neurologist. In the past, the care of penetrating craniocerebral injuries was mainly the preoccupation of the military surgeon, but- with the increasing amount of violent crime in society- such cases have become commonplace on the emergency wards of general hospitals. In civilian life, missile injuries are essentially caused by bullets fired from rifles or handguns at high velocities. Air is compressed in front of the bullet so that it has an explosive effect on entering tissue and causes damage for a considerable distance around the missile track. Missile fragments, or shrapnel, are pieces of exploding shells, grenades, or bombs and are the usual causes of penetrating cranial injuries in wartime. The cranial wounds that result from missiles and shrapnel have been classified by Purvis as tangential, with scalp lacerations, depressed skull fractures, and meningeal and cerebral lacerations; penetrating, with in-driven metal particles, hair, skin, and bone fragments; and through-andthrough wounds. In most penetrating injuries from high-velocity missiles, the object (such as a bullet) causes a high-temperature coagulative lesion that is sterile and fortunately does not require surgery. The latter are considered to be the result of disruption of the vessel wall by the high-energy shock wave. If the brain is penetrated at the lower levels of the brainstem, death is instantaneous because of respiratory and cardiac arrest. Even through-and-through wounds at higher levels, as a result of energy dissipated in the brain tissue, may damage vital centers sufficiently to cause death immediately or within a few minutes in 80 percent of cases.

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Unlike saccades medicine etymology discount 300 mg lopid fast delivery, pursuit movements to each side are generated in the ipsilateral parieto-occipital cortex medications for depression lopid 300 mg low price, with modulation by the ipsilateral cerebellum treatment spinal stenosis purchase lopid without a prescription, especially the vestibulocerebellum (flocculus and nodulus) medicine to calm nerves buy lopid 300 mg fast delivery. Another portion of the cerebellum, the posterior vermis, modulates saccadic movements (see further on). When following a moving target, as the visual image slips off the foveas, the firing rate of the governing motor neurons increases in proportion to the speed of the target, so that eye velocity matches target velocity. If, during pursuit, the eyes fall behind the target, supplementary catch-up saccades are required for refixation. The pursuit movement is then not smooth but becomes jerky ("cogwheel" or "saccadic" pursuit). A lesion of one cerebral hemisphere may cause pursuit movements to that side to break up into saccades. Also, diseases of the basal ganglia are a common cause of a disruption of normally smooth pursuit into a ratchet-like saccadic pursuit in all directions. If a series of visual targets enters the visual field, as when one is watching trees from a moving car or the stripes on a rotating drum, repeated quick saccades refocus the eyes centrally; the resulting repeated cycles of pursuit and refixation are termed optokinetic nystagmus. The main value of this test is in revealing a lesion of the posterior parietal lobe, which causes visual pursuit to be lost in the direction of the side of the lesion; it may also be found that a frontal lobe lesion eliminates the quick nystagmoid refixation phase away from the side of the lesion, causing the eyes to continue to follow the target until it is out of view. Vestibular influences are of particular importance in stabilizing images on the retina. When objects are tracked using both eye and head movements, the vestibulo-ocular movements induced by head turning must be suppressed, otherwise the eyes would remain stabilized in space; it appears likely that the smooth pursuit signals cancel the unwanted vestibular ones (Leigh and Zee). A second, more dorsal "transthalamic" bundle is predominantly uncrossed and courses through the internal medullary lamina and paralaminar parts of the thalamus to terminate diffusely in the pretectum, superior colliculus, and periaqueductal gray matter. Also contributing to smooth pursuit movements are projections from the frontal eye fields to the ipsilateral dorsolateral pontine nuclei. The latter, in turn, project to the flocculus and dorsal vermis of the cerebellum, which provide stability for the pursuit movements. However, for the purposes of clinical work, lesions of the posterior parietal cortex are known to impair pursuit toward the damaged side, and lesions of the frontal eyefields impede pursuit to the opposite side. Brainstem (Internuclear) Pathways and Oculomotor Nuclei Ultimately, all the pathways mediating saccadic and pursuit movements in the horizontal plane as well as vestibular and optokinetic movements converge on the pontine centers for horizontal gaze. Two other ascending pathways between the pontine centers and the mesencephalic reticular for- Horizontal Gaze Saccades As already mentioned, the signals for volitional horizontal gaze saccades originate in the eye field of the opposite frontal lobe (area 8 of Brodmann, see page 387) and are modulated by the adjacent supplementary motor eye field and by the posterior visual cortical areas. The cortical-to-pontine pathways for saccadic horizontal gaze have been traced in the monkey by Leichnetz. He found that these fibers traverse the internal capsule and separate at the level of the rostral diencephalon into two bundles, the first being a primary but indirect ventral "capsular-peduncular" bundle, which descends through the most medial part of the cerebral peduncle. Yet a third class of neurons (pause cells), lying in the midline of the pons, is involved in the inhibition of unwanted saccadic discharges. Voluntary vertical movements are initiated by the simultaneous activity of both frontal cortical eye fields. Projections for upgaze cross through the commissure before descending to innervate the third nerve nucleus, while those for downgaze may travel directly to the third nerve, thus accounting for the frequency of selective upgaze palsies (see text). This phenomenon is explained by the fact that with acute, one-sided lesions of the vestibulocerebellum, the inhibitory discharges of the Purkinje cells onto the ipsilateral medial vestibular nucleus are removed and the eyes deviate away from the lesion. When gaze to the side of the lesion is attempted, the eyes drift back to the midline and can be corrected only by a saccadic jerk. The head and neck may also turn away from the lesion (the occiput toward the lesion and the face away). In addition, the vestibulo-ocular reflexes, which coordinate eye movements with head movements, are improperly adjusted (Thach and Montgomery). The interested reader will find further details concerning cerebellar influences on ocular movements in the monograph by Leigh and Zee and the review by Lewis and Zee. Testing of Conjugate Gaze It is apparent from the foregoing remarks that there is considerable clinical information to be obtained from an analysis of ocular movements. A patient with stupor and coma can be examined by passively turning the head and irrigating the external auditory canals- these being vestibular stimuli.

Recumbency for a few days thereafter permits the pressure to build up medications definitions discount lopid 300 mg amex, and there has been no recurrence in the cases that we have encountered symptoms nausea headache purchase lopid 300mg without a prescription. According to Mokri and colleagues medications elderly should not take purchase lopid online pills, biopsy of the dura and underlying meninges in these cases shows fibroblastic proliferation and neovascularity with an amorphous subdural fluid medications 2 buy lopid 300mg with visa. There may be subdural effusions and mass effect, either on the cerebral convexities, temporal lobes, optic chiasm, or cerebellar tonsils. Using ultrasound, Chen and colleagues have also described an enlarged superior ophthalmic vein and increased blood flow velocity in this vessel, both of which normalize after successful treatment. Rarely, a case of intracranial hypotension becomes chronic; the headache is then no longer responsive to recumbency. Reference has already been made to this syndrome and to the slit ventricles in children who have been treated for hydrocephalus. Usually the valve setting is too low, and readjustment to maintain a higher pressure is corrective. At least 75 percent of patients are thus relieved of the headache, according to Safa-Tisseront and colleagues; they report that after a second injection, improvement is effected in 97 percent. Many patients have transient back or radicular pain (sciatica) following the blood patch. Curiously, the headache is often relieved almost immediately even if the blood is injected at some distance from the original puncture (although the procedure is usually done at the same level as the previous spinal tap). Moreover, the volume of blood injected, usually about 20 mL, is not related to the chances of success. The mechanism of this rapid improvement may not simply be the plugging of a dural leak. A number of patients fail to benefit or have only transient effects; it is then unclear whether repeating the procedure is helpful. The administration of caffeine-ergotamine preparations or intravenous caffeine may also have a salutary though temporary effect on the headache. The addition of analgesic medication is required if the patient must get up to care for himself or to travel. In protracted cases, patience is called for, since most headaches will resolve in 2 weeks or less. As to mechanism, Panullo and colleagues have shown that there is a downward displacement of the upper brainstem and posterior fossa contents when the patient assumes the upright position; but, as pointed out in Chap. These give rise to some of the most intractable low-pressure syndromes and must be investigated by radiologic and nuclide studies in order to establish the site of leakage. Several such leaks in our experience have been intermittent, adding to the difficulty in diagnosis. The point being made here is that these structures may also be involved in a number of noninfective processes, some of obscure origin. The lower spinal roots or spinal cord alone may be implicated in "spinal arachnoiditis. This may be accompanied by a pachymeningitis, and the latter may also be restricted to the cervical dura, also discussed below. A predominant localization to these basal or cervical structures may be apparent even in cases of diffuse cerebrospinal meningeal reactions, perhaps because of an uneven concentration of the noxious agent. In other instances, the primary disease appears to have arisen in the dura, with extension only to the adjacent piaarachnoid. In yet other instances, the ependyma of the aqueduct or fourth ventricle is primarily involved. The mechanisms by which these meningeal reactions affect parenchymal structures (brain, cord, and nerve roots) are not fully understood. Progressive constriction of nerve roots and spinal cord, literally a strangulation of these structures, is another plausible mechanism, but it is difficult to separate vascular factors from mechanical ones. Since any toxic agent introduced into the subarachnoid space has free access, via VirchowRobin spaces, to the superficial parts of the brain and spinal cord, direct parenchymal injury may follow.

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