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By: Joseph St. Geme, MD

  • Chair, Department of Pediatrics, Professor of Pediatrics and Microbiology, Perelman School of Medicine at the University of Pennsylvania
  • Physician-in-Chief, Leonard and Madlyn Abramson Endowed Chair in Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania


At its peak menstruation exercise buy 100 mg lady era amex, within minutes to pregnancy 19 weeks purchase generic lady era on line an hour breast cancer team names buy 100 mg lady era otc, the patient is forced to women's health clinic yonge street order lady era 100mg with amex lie down and to shun light and noise. Light is irritating and may be painful to the globes, or it is perceived as overly bright (dazzle), and strong odors are disagreeable. The headache lasts for hours and sometimes for a day or even longer and is always the most unpleasant feature of the illness. The temporal scalp vessels may be tender and the headache is worsened by strain or jarring of the body or rapid movement of the head. For a time, when psychosomatic medicine was much in vogue, there was insistence on a migrainous personality, characterized by tenseness, rigidity of attitudes and thinking, meticulousness, and perfectionism. Further analyses, however, have not established a particular personality type in the migraineur. Moreover, the fact that the headaches may begin in early childhood, when the personality is relatively amorphous, would argue against this idea. There is no clear relationship, despite many statements to the contrary, between migraine and neurosis. A relationship to epilepsy is also tenuous; however, the incidence of seizures is slightly higher in migrainous patients and their relatives than in the general population. There does seem to be in migraineurs an overrepresentation of motion sickness and of fainting. The headache may be exceptionally severe and abrupt in onset ("crash migraine" or "thunderclap headache"), raising the specter of subarachnoid hemorrhage. The headache may at times precede or accompany rather than follow the neurologic abnormalities of migraine with aura. Milder forms of migraine, especially if partially controlled by medication, may not force the patient to withdraw from accustomed activities. Any one of the three principal components- neurologic abnormality, headache, and nausea and vomiting- may be absent. With advancing age, there is a tendency for the headache and nausea to become less severe, finally leaving only the neurologic abnormality ("aura without migraine"), which itself recurs with decreasing frequency. Visual disturbances, by far the most common, differ in detail from patient to patient; numbness and tingling of the lips and the fingers of one hand are probably next in frequency, followed by transient aphasia or a thickness of speech and hemiparesis as mentioned earlier. Rarely, there is sudden but transient blindness or a hemianopia at the onset, accompanied by only a mild headache. Basilar Migraine A less common form of the migraine syndrome, with prominent brainstem symptoms, was described by Bickerstaff. The patients, usually young women with a family history of migraine, first develop visual phenomena like those of typical migraine except that they occupy the whole of both visual fields (temporary cortical blindness may occur). There may be associated vertigo, staggering, incoordination of the limbs, dysarthria, and tingling in both hands and feet and sometimes around both sides of the mouth. These symptoms last 10 to 30 min and are followed by headache, which is usually occipital. Some patients, at the stage when the headache is likely to begin, may faint, and others become confused or stuporous, a state that may persist for several hours or longer. The symptoms closely resemble those due to ischemia in the territory of the basilar-posterior cerebral arteries- hence the name basilar artery or vertebrobasilar migraine. Subsequent studies have indicated that basilar migraine, though more common in children and adolescents, affects men and women more or less equally over a wide age range, and that the condition is not always benign and transient (see further on, under "Complicated Migraine"). Ophthalmoplegic and Retinal Migraine the former are recurrent unilateral headaches associated with weakness of extraocular muscles. A transient third-nerve palsy with ptosis, with or without involvement of the pupil, is the usual picture; rarely, the sixth nerve is affected. The paresis often outlasts the headache by days or weeks; after many attacks, a slight mydriasis and, rarely, ophthalmoparesis may remain as permanent defects. In some cases, the retinal arterioles are attenuated and sometimes there are retinal hemorrhages; in other cases, narrowing of retinal arteries or venules has been observed during an attack, as described in the cases reported by Berger and colleagues. In still other cases, monocular blindness is associated with disc edema and peripapillary hemorrhages, and vision recovers only partially after several months (Hupp et al). Such events are referred to as retinal migraine, or, more accurately, ocular migraine, since either the retinal or the ciliary circulation may be involved. It is well to remember that in adults the syndrome of headache, unilateral ophthalmoparesis, and loss of vision may have more serious causes, including temporal (cranial) arteritis. Migraine following Head Injury A particularly troublesome migraine variant occurs in a child or adolescent who, after a trivial head injury, may lose sight, suffer severe headache, or be plunged into a state of confusion, with belligerent and irrational behavior that lasts for hours or several days before clearing. In yet another variant there is an abrupt onset of either one-sided paralysis or aphasia after virtually every minor head injury (we have seen this condition several times in college athletes) but without visual symptoms and little or no headache. Although a family history of migraine is frequent in such cases, there has been no hemiplegia in other family members. Instead of complaining of headache, the child appears limp and pale and complains of abdominal pain; vomiting is more frequent than in the adult and there may be slight fever. Also, there are the puzzling patients with bouts of fever or transient disturbances in mood (psychic equivalents) and abdominal pain (abdominal migraine), dubious entities at best. We have also seen several infants and young children who have had attacks of hemiplegia (without headache), first on one side then the other, every few weeks. Recovery was complete, and arteriography in one child, after more than 70 attacks, was normal. The only advantage of considering such attacks as migrainous is that it may protect some patients from unnecessary diagnostic procedures and surgical intervention; but, by the same token, it may delay appropriate investigation and treatment. Hemiplegic Migraine In a related disorder, known as hemiplegic migraine, an infant, child, or adult has episodes of unilateral paralysis that may long outlast the headache. Several families have been described in which this condition was inherited as an autosomal dominant trait (familial hemiplegic migraine). Linkageanalysis studies of this disorder have localized the responsible gene to chromosome 19 in one-third of families (Joutel et al); in other families, the gene has localized to chromosome 1; in yet others, no linkage has been found. The gene on chromosome 19 codes for a voltage-gated calcium channel protein, which raises the provocative possibility that other forms of migraine are also due to an ion channel disorder. Instances of hemiplegic migraine may account for some of the inexplicable strokes in young women and older adults of both sexes. The situation is, however, more complex; Ducros and colleagues have found a variety of other neurologic features in these families, including peristent cerebellar ataxia and nystagmus in 20 percent; others had attacks of coma and hemiplegia, from which they recovered. Complicating the situation is the undoubted existence of sporadic migraine with transient hemiplegia that has no familial trait. Neurologic symptoms lasting more than an hour or so should prompt investigation for alternative causes of headache, but none may be found. Some of the transient aphasic, hemianesthetic, or hemiplegic attacks of later life may be of migrainous origin ("migrainous accompaniments"); Fisher has provided support for this hypothesis. Rarely, neurologic symptoms, instead of being transitory, may leave a permanent deficit. Platelet aggregation, edema of the arterial wall, increased coagulability of the blood, and intense, prolonged spasms of vessels have all been implicated (on rather uncertain grounds) in the pathogenesis of arterial occlusion and strokes that complicate migraine (Rascol et al). At the Mayo Clinic, in a group of 4874 patients aged 50 years or younger with a diagnosis of migraine, migraine equivalent, or vascular headache, 20 patients had migraine-associated infarctions (Broderick and Swanson). There is a paucity of useful pathology by which to interpret the mechanism of migraine-associated stroke. The special problem of focal cerebral disorders associated with segmental vasospasm that follows treatment with the "triptan" group of drugs is discussed further on and a similar but spontaneous syndrome of severe headache and fluctuating focal neurologic symptoms due to vasospasm (Call-Fleming syndrome) is discussed on page 730. Other Variations In some individuals, the migraine, for unaccountable reasons, may increase in frequency for several months. As many as three or four attacks may occur each week, leaving the scalp continuously tender. An even more difficult clinical problem that arises with some regularity on our services is posed by migraine that lapses into a condition of daily or virtually severe continuous headache (status migrainosus). The pain is initially unilateral, later more generalized, more or less throbbing, and disabling; vomiting or nausea are common at the outset but generally abate. Almost without exception, there is a preceding history compatible with migraine; the absence of prior headaches should raise concern about a more serious cause. Status migrainosus has sometimes followed a head injury or a viral infection, but most cases have no explanation. Relief is sought by increasing the intake of ergot preparations or even opiate medications, often to an alarming degree, but with only temporary relief. The mechanism of migraine being obscure, one can only surmise that the basic process has been greatly intensified.

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The small muscles of the hands are also affected quickly so any simple lifesaving tasks are impossible (for example pregnancy 0 negative blood type generic lady era 100 mg with amex, using lifejacket buckles breast cancer emblem purchase lady era 100 mg on line, firing flares) women's health clinic toronto birth control generic lady era 100mg mastercard. If extremity cooling leads to women's health clinic qe gateshead purchase lady era cheap drowning and subsequent cardiac arrest the casualty will present as drowned and should be treated as submersed. Conscious level drops steadily with a fall in temperature resulting in confusion and an inability speak or give a history due to muscle spasm, and as the 431 Extremity cooling: 3-30 minutes If a casualty survives the cold shock effects, their extremities (not core) cool rapidly. At this stage if they are not wearing a lifejacket their face will enter the water and they will drown. Submersion If a casualty is not wearing a lifejacket, is a non-swimmer, or is held under the surface for a variety of reasons (for example trapped, full stomach, heavy clothes), initial breath hold will give way to swallowing, coughing then around seventy seconds of uncontrolled respiration leading to mass aspiration. Salt water will then fill the alveolar space and prevent oxygen transport, whereas fresh water will cross the lung membrane, entering the blood stream and washing out surfactant causing alveolar collapse. Either route will cause hypoxemia rapidly leading to loss of consciousness and apnea. At this point the casualty will usually be found floating face the above graph shows the realistic upper limit of survival time for people in the water wearing normal clothing, from time of entry into the water. The graph indicates the expected survival time of casualties in different water temperatures. This is used by the coast guard as an aid in determining appropriate search durations. Mike Tipton at Portsmouth University has been studying what happens if both reflexes are stimulated together causing an "autonomic conflict". What has been proven from this work is that when there is both the parasympathetic and sympathetic triggered, a significant arrhythmia is caused at the break of breath hold. Whilst this may be not too catastrophic in young fit individuals, if the casualty happened to have any cardiac predisposing factors, the arrhythmia produced could be fatal. Autonomic Conflict We have already explained that the cold shock response is driven by a huge sympathetic nervous system response triggered by large areas of bare skin in contact with cold water. Mammalian Dive Reflex the mammalian dive reflex is evoked by stimulation of the cold receptors of the face, innervated by Cranial nerves X and 434 Tipton and Shattock 2012 this evolving concept could explain the high death rates in the first three minutes of immersion, previously thought to be purely accountable to cold water shock. However, as arrhythmias are not detectable at post mortem it is hard to prove, but certainly accounts for a significant number of casualties having dry lungs and no signs of drowning. The aspiration of salt or fresh water may cause coughing, spluttering with associated wheezy or crackling noises on auscultation. They may complain of chest pain, vomiting and in serious cases have difficulty breathing with rapid shallow respirations and an associated rapid thread pulse. Pre-hospital management will need to focus on oxygenation and care of the unconscious airway. Any patient who has been at risk of aspiration must be seen in hospital by a doctor, as the latent effects of this aspiration can cause serious later complications. Water (especially salt water) irritates the lung tissue causes a localised inflammatory response, causing inflammatory damage to lung membrane leading to pulmonary oedema. Water can block the small airways due to surface tension and cause bronchospasm in others. Casualties who aspirate will develop a large ventilation-perfusion mismatch with as much as 75% of pulmonary blood reported to flow through unventilated lungs (increased shunt). This coupled with impaired gas exchange in ventilated alveoli from pulmonary oedema and inhaled fluid will result in a profound hypoxia. Much has been made of the differences between fresh and seawater in animal models but it seems to have no appreciable ef- Complications of Drowning (Previous nomenclature for this has included "secondary drowning" or "late onset near drowning". Contaminated water can cause either microbiological or chemical injury to the lung parenchyma. Serious thought should be given to any specific complications from immersion in these media. Rescue from Water Hydrostatic squeeze is the pressure the sea exerts on the casualty when they are vertical in the water. If the casualty is removed vertically from the water the rapid loss of supporting hydrostatic pressure and reintroduction of gravity creates significant effects in the body and instant cardiac arrest can occur. It is important to remove the casualty from the water horizontally to minimise the potential for collapse. Infection Prophylactic antibiotics are not recommended in all cases though in the case of contaminated water inhalation they do seem to be of some use. Clearly the possibility of an unusual organism being involved is high and early involvement of microbiologists would be advisable. Other interventions such as steroids or have not been evaluated specifically in drowning, but have roles defined in other related conditions. Therefore once released from the mud they should, ideally, be transported lying down, where practical, especially if trapped to a depth greater than the knees. Concepts based on either crush injuries or suspension trauma are not relevant to the mud environment. Concomitant injury or medical conditions Remember that drowning is usually the result of an underlying event or condition that contributes to unintentional immersion or immersion with incapacitation, such as trauma, intoxication, seizure, hypothermia, dysrhythmia, shallow-water blackout, and, for divers, a lost or improper breathing source. It is important to search for and treat any underlying triggering factors or complications. Neonates have a high body surface area to weight ratio and therefore cool quickly. At the other extreme of age, the elderly have a reduced ability to generate heat from metabolism and a higher incidence of concomitant medical and psychiatric illness. Respiratory rate falls (mainly due to decreased metabolic demand) and conscious level begins to deteriorate. The oxygen dissociation curve shifts to the left, further inhibiting oxygen release. Dry cold ears can read 2-3 degrees lower than actual body temperature, and wet cold ears can be more than 6 degrees lower. Pre-hospital Care the neuro- and cardio-protective effects of hypothermia are well demonstrated and active re-warming on scene is not advised. Before wrapping in blanket, strip some outer layers of wet clothing off of the hypothermic casualty, but again take care to avoid rough handling. Always transport head down to maximise the amount of blood in the core of the body.

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Here we mention mainly that penicillin and its derivatives such as imipenem menopause age generic lady era 100 mg amex, and to breast cancer 8mm in size order generic lady era from india a lesser degree women's health issues across the lifespan generic 100 mg lady era amex, cephalosporins are capable of causing seizures when high serum concentrations are attained menopause foods order lady era with amex. During the 1960s, more than 10,000 cases of this disease were collected in Japan by Tsubaki et al. Usually the illness began with ascending numbness and weakness of the legs, paralysis of sphincters, and autonomic disorder. The onset was acute in about two-thirds of the cases and subacute in the remainder. The occurrence of these neurologic complications was found to be related to the prolonged use of clioquinol. Two patients seen by the authors several years after onset of the disease had been left with optic atrophy and a spastic-ataxic paraparesis. Also mentioned here, because neurologists are often asked to consult on these cases, is a curious effect of the anesthetic propofol. Seizures and myoclonic-like movements have been seen in a small number of individuals, presumably as an idiosyncratic effect. Sometimes these take the form of less organized twitching, opisthotonus, or involuntary movements. While some inhaled anesthetics such as enfulrane can cause seizures in susceptible patients, propofol does not share the activating effects of the volatile anesthetics. In our own experience, the seizures have occurred in the first hour after emergence from anesthesia but as many cases are reported during induction, emergence, or after the use of the drug (see Walder). These syndromes relate to the special physiologic and anatomic features of the cord, such as its prominent function in sensorimotor conduction and relatively primitive reflex activity; its long, cylindrical shape; its small cross-sectional size; its tight envelopment by meninges; the peripheral location of myelinated fibers next to the pia; the special arrangement of its blood vessels; and its relationship to the vertebral column. Woolsey and Young estimate that there are about 30 diseases known to affect the spinal cord, of which half are seen with regularity. These processes express themselves by a number of readily recognized syndromes and, as will be evident, certain diseases preferentially evoke one syndrome and not others. The syndromic grouping of the spinal cord disorders, which is in keeping with the general plan of this book, facilitates clinical diagnosis and reduces the number of ancillary examinations needed for confirmation. In addition, an important distinction is made between lesions within the cord (intramedullary) and those that compress the cord from without (extramedullary). Most of the processes to be considered here cause one or the other of these syndromes, and each of them will be considered in the course of exposition of the major categories of spinal cord disease. The anatomic and physiologic considerations pertinent to an understanding of disorders of the cord and of the spine can be found in Chaps. Trauma to the Spine and Spinal Cord Throughout recorded medical history, advances in the understanding of spinal cord disease have coincided largely with periods of warfare. The first thoroughly documented study of the effects of sudden total cord transection was by Theodor Kocher in 1896, based on his observations of 15 patients. During World War I, Riddoch- and later Head and Riddoch- gave the classic descriptions of spinal transection in humans; Lhermitte and Guillain and Barre are credited with refining these observations. The advent of antibiotics and the ability to control skin, bladder, and pulmonary infections permitted the survival of unprecedented numbers of soldiers with spinal cord injuries and provided the opportunity for long-term observation. In special centers, such as the Long Beach, Hines, and West Roxbury Veterans Administration Hospitals in the United States and the Stoke Mandeville National Spinal Injuries Centre in England, the care and rehabilitation of the paraplegic were brought to a very high level. Studies conducted in these centers have greatly enhanced our knowledge of the functional capacity of the chronically isolated spinal cord. Kuhn, Munro, Martin and Davis, Guttmann, Pollock, and their associates, listed in the references, have made particularly important contributions to this subject. Mechanisms of Spine and Spinal Cord Injury Although trauma may involve the spinal cord alone, the vertebral column is almost invariably injured at the same time. A useful classification of spinal injuries is one that divides them into fracture-dislocations, pure fractures, and pure dislocations. Except for bullet, shrapnel, and stab wounds, a direct blow to the spine is a relatively uncommon cause of serious spinal cord injury. In civilian life, most spinal injuries are the result of force applied at a distance from the site of spinal fracture and dislocation. All three types of spinal injury previously mentioned are produced by a similar mechanism, usually a vertical compression of the spinal column to which anteroflexion is added; or, the mechanism may be one of vertical compression and retroflexion (commonly referred to as hyperextension). The most important variables in the mechanics of vertebral injury are the structure of the bones at the level of the injury and the intensity, direction, and point of impact of the force. In keeping with the mechanism of force applied at a distance, many spinal injuries are due to blows to the head. If the cranium is struck by a hard object at high velocity, a skull fracture occurs, the force of the injury being absorbed mainly by the elastic quality of the skull. Each of these categories of acute spinal cord disease is discussed in the following pages. For convenience we have included in this group radiation myelopathy, which is transverse but evolves subacutely. If the neck happens to be rigid and straight and the force is applied quickly to the head, the atlas and the odontoid process of the axis may break. If the force is applied less quickly, an element of flexion or extension is added. In the case of severe forward flexion injury, the head is bent sharply forward when the force is applied. The adjacent cervical vertebrae are forced together at the level of maximum stress. The anteroinferior edge of the upper vertebral body is driven into the one below, sometimes splitting it in two. The posterior part of the fractured body is displaced backward and compresses the cord. Concomitantly, there is tearing of the interspinous and posterior longitudinal ligaments. Vulnerability to the effects of anteroflexion (and to some extent to retroflexion injuries) is increased by the presence of cervical spondylosis or ankylosing spondylitis or by a congenital stenosis of the spinal canal. In hyperextension injuries, the mechanism is one of vertical compression with the head in an extended position. Stress is mainly on the posterior elements (the laminae and pedicles) of the midcervical vertebrae (C4 to C6), which may be fractured unilaterally or bilaterally- and on the anterior ligaments. This dual disruption in the spinal architecture allows for displacement of one vertebral body on the adjacent one. The dislocation results in the cord being caught between the laminae of the lower vertebra and the body of the one above. It should be pointed out that a hyperextension injury to the spinal cord commonly occurs without apparent damage or misalignment of the vertebrae when viewed radiologically. In these instances the spinal cord damage, which can be nonetheless profound and permanent, is caused by a sudden inward bulge of the ligamentum flavum or a transient vertebral dislocation followed by spontaneous realignment. This type of spinal cord damage, without radiologic evidence of fracture or dislocation, is particularly common in children. That rupture of the supporting ligamentous elements has nonetheless occurred can be revealed by gentle flexion and extension of the neck under radiologic observation which demonstrates slight dislocation of the vertebra (spinal instability). Another mechanism of cord and spinal root injury, involving extremes of extension and flexion of the neck, is so-called whiplash or recoil injury, most often the result of an automobile accident. When a vehicle is struck sharply from behind, the head of the occupant is flung back uncontrollably; or, if a fast-moving vehicle stops abruptly, there is sudden forward flexion of the neck, followed by retroflexion. Under these conditions the occipitonuchal and sternocleidomastoid muscles and other supporting structures of the neck and head are affected much more often than the spinal cord or roots. Nevertheless, in rare instances, quadriparesis, temporary or permanent, results from a violent whiplash injury. The exact mechanism of neural injury in these circum- stances is not clear; perhaps there is a transient posterior dislocation of a vertebral body, a momentary buckling of the ligmentum flavum, or retropulsion of the intervertebral disc into the spinal canal. The presence of a congenitally narrow cervical spinal canal or of spinal diseases such as cervical spondylosis, rheumatoid arthritis, or ankylosing spondylitis adds greatly to the hazard of damage to the cord or roots. Also, preexisting spondylotic symptoms may be aggravated and become the source of chronic pain.

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These unusual phenomena all point to women's health center hershey pa purchase lady era with visa a lesion of the upper midbrain tegmentum and are usually manifestations of vascular disease womens health dallas lady era 100mg lowest price, traumatic disease womens health kp purchase lady era uk, or tumor women's health center munster indiana generic 100mg lady era fast delivery, notably pinealoma that compresses this region. Seesaw nystagmus is a torsional-vertical oscillation in which the intorting eye moves up and the opposite (extorting) eye moves down, then both move in the reverse direction. It is occasionally observed in conjunction with chiasmatic bitemporal hemianopia due to sellar or parasellar masses. Periodic alternating nystagmus is a remarkable horizontal jerking that periodically (every 90 seconds or so) changes direction, interposed with a brief neutral period during which the eyes show no nystagmus or jerk downward. Alternating nystagmus is seen with lesions in the lower brainstem but has also been reported with Creutzfeldt-Jakob disease, hepatic encephalopathy, lesions of the cerebellar nodulus, carcinomatous meningitis, and a large number of other processes. It differs from ping-pong gaze, which is a saccadic variant with a more rapid alternating of gaze from side to side and usually the result of bilateral cerebral strokes. So-called palatal nystagmus, which is really a tremor, is due to a lesion of the central tegmental tract and may be accompanied by a convergence-retraction nystagmus that has the same beat as the palatal and pharyngeal muscles, as discussed on page 85. Other Spontaneous Ocular Movements Roving conjugate eye movements are characteristic of light coma. Slow horizontal ocular deviations that shift every few seconds from side to side ("ping-pong gaze") is a form of roving eye movement that occurs with bihemispheric infarctions or sometimes with posterior fossa lesions. Fisher has noted a similar slow, side- toside pendular oscillation of the eyes ("windshield-wiper eyes"). This phenomenon has been associated with bilateral hemispheric lesions that have presumably released a brainstem pacemaker. Ocular bobbing is a term coined by Fisher to describe a distinctive spontaneous fast downward jerk of the eyes followed by a slow upward drift to the midposition. It is observed in comatose patients in whom horizontal eye movements are absent and has been associated most often with large destructive lesions of the pons, less often of the cerebellum. The eye movements may be disconjugate in the vertical plane, especially if there is an associated third nerve palsy on one side. Other spontaneous vertical eye movements have been given a variety of confusing names: atypical bobbing, inverse bobbing, reverse bobbing, and ocular dipping. For the most part, they are observed in coma of metabolic or anoxic origin and in the context of preserved horizontal eye movements (in distinction to ocular bobbing). Ocular dipping is a term we have used to describe an arrhythmic slow conjugate downward movement followed in several seconds by a more rapid upward movement; it occurs spontaneously but may at times be elicited by moving the limbs or neck. Anoxic encephalopathy has been the most common cause, but a few cases have been attributed to drug overdose (Ropper 1981). Oculogyric crisis, formerly associated with postencephalitic parkinsonism, is now most often due to phenothiazine drugs, as discussed earlier. Opsoclonus is the term applied to rapid, conjugate oscillations of the eyes in horizontal, rotatory, and vertical directions, made worse by voluntary movement or the need to fixate the eyes. These movements are continuous and chaotic, without an intersaccadic pause (called by some by the colorful term saccadomania), and are almost unique among disorders of ocular movement in that they persist in sleep. Opsoclonus may also be observed in patients who are intoxicated with antidepressants, anticonvulsants, organophosphates, cocaine, lithium, thallium, and haloperidol; in the nonketotic hyperosmolar state; and in cerebral Whipple disease, where it is coupled with rhythmic jaw movements (oculomasticatory myorhythmia, page 603). Similar movements have been produced in monkeys by creating bilateral lesions in the pretectum. Ocular dysmetria, the analogue of limb dysmetria, consists of an overshoot of the eyes on attempted fixation followed by several cycles of oscillation of diminishing amplitude until fixation is attained. The overshoot may occur on eccentric fixation or on refixation to the primary position of gaze. It probably reflects dysfunction of the anterosuperior vermis and underlying deep cerebellar nuclei. Ocular flutter refers to occasional bursts of very rapid horizontal oscillations around the point of fixation; this abnormality is also associated with cerebellar disease. Flutter at the end of a saccade, called flutter dysmetria (fish-tail nystagmus) has the appearance of dysmetria, but careful analysis indicates that it is probably a different phenomenon. Whereas the inaccurate saccades of ataxia are separated by normal brief pause (intersaccadic interval), flutter dysmetria consists of consecutive saccades without an intersaccadic interval (Zee and Robinson). Opsoclonus, ocular dysmetria, and flutter-like oscillations may occur together, or a patient may show only one or two of these ocular tremors, either simultaneously or in sequence. One hypothesis relates opsoclonus and ocular flutter to a disorder of the saccadic "pause neurons" (see above), but their exact anatomic basis has not been elucidated. Disorders of the Eyelids and Blinking A consideration of oculomotor disorders would be incomplete without reference to the eyelids and blinking. The function of the eyelids is to protect the delicate corneal surfaces against injury and the retinae against glare; this is done by blinking and lacrimation. Eyelid movement is normally coordinated with ocular movement- the upper lids elevate when looking up and descend when looking down. Turning the eyes quickly to the side is usually attended by a single blink, which is necessarily brief so as not to interfere with vision. When the blink duration is prolonged in this context, it is indicative of an abnormally intense effort required to initiate the saccade; usually this is due to frontal lobe or basal ganglionic disease. Closure and opening of the eyelids is accomplished through the reciprocal action of the levator palpebrae and orbicularis oculi muscles. Relaxation of the levator and contraction of the orbicularis effect closure; the reverse action of these muscles effects opening of the closed eyelids. The levator is innervated by the oculomotor nerve, and the orbicularis by the facial nerve. The trigeminal nerves provide sensation to the eyelids and are also the afferent limbs of corneal and palpebral reflexes. Central mechanisms for the control of blinking, in addition to the reflexive brainstem connections between the third, fifth, and seventh nerve nuclei, include the cerebrum, basal ganglia, and hypothalamus. The eyelids are kept open by the tonic contraction of the levator muscles, which overcomes the elastic properties of the periorbital muscles. The eyelids close during sleep and certain altered states of consciousness due to relaxation of the levator muscles. Blinking occurs irregularly at a rate of 12 to 20 times a minute, the frequency varying with the state of concentration and with emotion. The natural stimuli for the blink reflex (blinking is always bilateral) are corneal contact (corneal reflex), a tap on the brow or around the eye, visual threat, an unexpected loud sound, and, as indicated above, turning of the eyes to one side. There is normally a rapid adaptation of blink to visual and auditory stimuli but not to corneal stimulation. Electromyography of the orbicularis oculi reveals two components of the blink response, an early and late one, a feature that is readily corroborated by clinical observation. The early response consists of only a slight movement of the upper lids; the immediately following response is more forceful and approximates the upper and lower lids. Whereas the early part of the blink reflex is beyond volitional control, the second part can be inhibited voluntarily. Blepharospasm, an excessive and forceful closure of the lids, which is described on page 93, is a common disorder that occurs in isolation or as part of a number of dyskinesias and druginduced movement disorders. Increased blink frequency occurs with corneal irritation, with sensitization of trigeminal nerve endings, and in oculofacial dyskinetic syndromes, such as blepharospasm. A reduced frequency of blinking (10 per minute) is characteristic of progressive supranuclear palsy and Parkinson disease. In these cases, adaptation to repeated supraorbital tapping at a rate of about 1 per second is impaired; therefore the patient continues to blink with each tap on the forehead or glabella. The failure to inhibit this response is referred to as the glabellar or Myerson sign. A lesion of the oculomotor nerve, by paralyzing the levator muscle, causes ptosis, i. The Gunn "jaw-winking" phenomenon is a synkinesis that may also occur after aberrant regeneration of the facial nerve but is otherwise a congenital and sometimes hereditary anomaly in which a ptotic eyelid retracts momentarily when the mouth is opened or the jaw is moved to one side. In other cases, inhibition of the levator muscle and ptosis occurs with opening of the mouth ("inverse Marcus Gunn phenomenon," or Marin Amat syndrome). A useful clinical rule is that a combined paralysis of the levator and orbicularis oculi muscles. This is because the third and seventh cranial nerves are rarely affected together in peripheral nerve or brainstem disease. An infrequent but overlooked cause of unilateral ptosis is a dehiscence of the tarsal muscle attachment; it can be identified by the loss of the upper lid fold just below the brow. Bilateral ptosis is a characteristic feature of certain muscular dystrophies and myasthenia gravis; congenital ptosis and progressive sagging of the upper lids in the elderly are other common forms.

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