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The cecocentral scotoma medications 6 rights cheap prochlorperazine 5mg overnight delivery, which tends to have an arcuate border symptoms of high blood pressure cheap 5mg prochlorperazine fast delivery, represents a lesion that is predominantly in the distribution of the papillomacular bundle 8h9 treatment discount prochlorperazine 5mg mastercard. However nature medicine buy genuine prochlorperazine on line, the presence of this visual field abnormality does not establish whether the primary defect is in the cells of the origin of the bundle, i. Demyelinative disease is characterized by unilateral or asymmetrical bilateral scotomas. Vascular lesions that take the form of retinal hemorrhages or infarctions of the nerve-fiber layer (cotton-wool patches) give rise to unilateral scotomas; occlusion of the central retinal artery or its branches causes infarction of the retina and, as a rule, a loss of central vision. As pointed out earlier, anterior ischemic optic neuropathy causes sudden monocular blindness or an altitudinal field defect. Since the optic nerve also contains the afferent fibers for the pupillary light reflex, extensive lesions of the nerve will cause a so-called afferent pupillary defect, which has been mentioned earlier and is considered further in Chap. With most diseases of the optic nerve, as alluded to above, the optic disc will eventually become pale (atrophic). If the atrophy is secondary to papillitis or papilledema, the disc margins are indistinct and irregular; the disc has a pallid, yellow-gray appearance, like candle tallow; the vessels are partially obscured; and the adjacent retina is altered because of the outfall of fibers. As in the case of optic neuritis, visual evoked potentials from the stimulation of one eye may be slowed even if the optic disc appears normal and there is no perimetric abnormality. Lesions of the Chiasm, Optic Tract, and Geniculocalcarine Pathway Hemianopia (hemianopsia) means blindness in half of the visual field. Bitemporal hemianopia indicates a lesion of the decussating fibers of the optic chiasm and is caused most often by the suprasellar extension of a tumor of the pituitary gland (Fig. It may also be the result of a craniopharyngioma, a saccular aneurysm of the circle of Willis, and a meningioma of the tuberculum sellae; less often, it may be due to sarcoidosis, metastatic carcinoma, ectopic pinealoma or dysgerminoma, Hand-Schuller-Christian disЁ ease, or hydrocephalus with dilation and downward herniation of the posterior part of the third ventricle (Corbett). In some instances a tumor pushing upward presses the medial parts of the optic nerves, just anterior to the chiasm, against the anterior cerebral arteries. The visual field pattern created by a lesion in the optic nerve as it joins the chiasm typically includes a scotomatous defect on the affected side coupled with a contralateral superior quadrantanopia ("junctional field defect"). Variations in the pattern of visual loss are frequent, in part accounted for by the location of the chiasm in an individual patient- a prefixed chiasm making unilateral eye findings more common. Homonymous hemianopia (a loss of vision in corresponding halves of the visual fields) signifies a lesion of the visual pathway behind the chiasm and, if complete, gives no more information than that. As a general rule, if the field defects in the two eyes are identical (congruous), the lesion is likely to be in the calcarine cortex and subcortical white matter of the occipital lobe; if they are incongruous, the visual fibers in the optic tract or in the parietal or temporal lobe are more likely to be implicated. Actually, absolute congruity of field defects is rare, even with occipital lesions. The lower fibers of the geniculocalcarine pathway (from the inferior retinas) swing in a wide arc over the temporal horn of the lateral ventricle and then proceed posteriorly to join the upper fibers of the pathway on their way to the calcarine cortex (Fig. This arc of fibers is known variously as the Flechsig, Meyer, or Archambault loop, and a lesion that interrupts these fibers will produce a superior homonymous quadrantanopia (contralateral upper temporal and ipsilateral upper nasal quadrants; Fig. This clinical effect was first described by Harvey Cushing, so that his name also has been applied to the loop of temporal visual fibers. Parietal lobe lesions are said to affect the inferior quadrants of the visual fields more than the superior ones, but this is difficult to document; with a lesion of the right parietal lobe, the patient ignores the left half of space; with a left parietal lesion, the patient is often aphasic. As to the localizing value of quadrantic defects, the report of Jacobson is of interest; he found, in reviewing the imaging studies of 41 patients with inferior quadrantanopia and 30 with superior quadrantanopia, that in 76 percent of the former and 83 percent of the latter the lesions were confined to the occipital lobe. If the entire optic tract or calcarine cortex on one side is destroyed, the homonymous hemianopia is complete. With infarction of the occipital lobe due to occlusion of the posterior cerebral artery, the macular region, represented in the most posterior part of the striate cortex, may be spared by virtue of collateral circulation from branches of the middle cerebral artery. Incomplete lesions of the optic tract and radiation usually spare central (macular) vision. We have nevertheless observed a lesion of the tip of one occipital lobe that produced central homonymous hemianopic scotomata, bisecting the maculae. Lesions of both occipital poles (as in embolization of the posterior cerebral arteries) result in bilateral central scotomas; if all the calcarine cortex or all the subcortical geniculocalcarine fibers on both sides are completely destroyed, there is cerebral or "cortical" blindness (see below and Chap. An altitudinal defect is one that is confined to the upper or lower half of the visual field but crosses the vertical meridian.
The lesion in such cases may in some patients be localized by the presence of a third nerve palsy (Weber syndrome) or other segmental abnormality on the same side as the lesion (opposite the hemiplegia) symptoms vitamin d deficiency order 5 mg prochlorperazine free shipping. With low pontine lesions treatment 2 cheap 5mg prochlorperazine fast delivery, an ipsilateral abducens or facial palsy is combined with a contralateral weakness or paralysis of the arm and leg (Millard-Gubler syndrome) treatment under eye bags order prochlorperazine 5mg otc. Lesions in the medulla affect the tongue and sometimes the pharynx and larynx on one side and the arm and leg on the other symptoms stroke 5mg prochlorperazine. These "crossed paralyses," so characteristic of brainstem lesions, are described further in Chap. Even lower in the medulla, a unilateral infarct in the pyramid causes a flaccid paralysis followed by slight spasticity of the contralateral arm and leg, with sparing of the face and tongue. Some motor function may be retained, as in the case described by Ropper and colleagues; interestingly, in this case and in others previously reported, there was considerable recovery of voluntary power even though the pyramid was almost completely destroyed. Rarely, an ipsilateral hemiplegia may be caused by a lesion in the lateral column of the cervical spinal cord. In this location, however, the pathologic process more often induces bilateral signs, with resulting quadriparesis or quadriplegia. A homolateral paralysis that spares the face, if combined with a loss of vibratory and position sense on the same side and a contralateral loss of pain and temperature, signifies disease of one side of the spinal cord (BrownSequard syndrome, as discussed in Chap. When the motor cortex and adjacent parts of the parietal lobe are damaged in infancy or childhood, normal development of the muscles as well as the skeletal system in the affected limbs is retarded. This does not happen if the paralysis occurs after puberty, by which time the greater part of skeletal growth has been attained. In hemiplegia due to spinal cord lesions, muscles at the level of the lesion may atrophy as a result of damage to anterior horn cells or ventral roots. In the causation of hemiplegia, ischemic and hemorrhagic vascular diseases of the cerebrum and brainstem exceed all others in frequency. Other important causes, less acute in onset, are, in order of frequency, brain tumor, brain abscess, demyelinative diseases, and the vascular complications of meningitis and encephalitis. Most of these diseases can be recognized by their mode of evolution and characteristic clinical and laboratory findings, which are presented in the chapters on neurologic diseases. Alternating transitory hemiparesis may be due to a special type of migraine (see discussion in Chap. From time to time, hysteria is found to be the cause of a hemiplegia, as discussed further on. Paraplegia Paralysis of both lower extremities may occur with diseases of the spinal cord, nerve roots, or, less often, the peripheral nerves. If the onset is acute, it may be difficult to distinguish spinal from neuropathic paralysis because of the element of spinal shock, which results in abolition of reflexes and flaccidity. In acute spinal cord diseases with involvement of corticospinal tracts, the paralysis or weakness affects all muscles below a given level; usually, if the white matter is extensively damaged, sensory loss below a partic- ular level is conjoined (loss of pain and temperature sense due to spinothalamic tract damage, and loss of vibratory and position sense due to posterior column involvement). Also, in bilateral disease of the spinal cord, the bladder and bowel and their sphincters are usually affected. In peripheral nerve diseases, motor loss tends to involve the distal muscles of the legs more than the proximal ones (exceptions are certain varieties of the Guillain-Barre syndrome and ґ certain types of diabetic neuropathy and porphyria); sphincteric function is usually spared or impaired only transiently. Sensory loss, if present, is also more prominent in the distal segments of the limbs, and the degree of loss is often more for one modality than another. For clinical purposes it is helpful to separate the acute paraplegias from the chronic ones and to divide the latter into two groups: those beginning in adult life and those occurring in infancy. The most common cause of acute paraplegia (or quadriplegia if the cervical cord is involved) is spinal cord trauma, usually associated with fracture-dislocation of the spine. Less common causes are hematomyelia due to a vascular malformation, an arteriovenous malformation of the cord that causes ischemia by an obscure mechanism, or infarction of the cord due to occlusion of the anterior spinal artery or, more often, to occlusion of segmental branches of the aorta (due to dissecting aneurysm or atheroma, vasculitis, and nucleus pulposus embolism). Paraplegia or quadriplegia due to postinfectious myelitis, demyelinative or necrotizing myelopathy, or epidural abscess or tumor with spinal cord compression tends to develop somewhat more slowly, over a period of hours, days, or longer. Epidural or subdural hemorrhage from bleeding diseases or warfarin therapy causes an acute or subacute paraplegia; in a few instances the bleeding has followed a lumbar puncture. Paralytic poliomyelitis and acute Guillain-Barre syndrome- the former a purely motor disorder with ґ mild meningitis (now rare), the latter predominantly motor but often with sensory disturbances- must be distinguished from the acute and subacute myelopathies and from each other. In adult life, multiple sclerosis and tumor account for most cases of subacute and chronic spinal paraplegia, but a wide variety of extrinsic and intrinsic processes may produce the same effect: protruded cervical disc and cervical spondylosis (often with a congenitally narrow canal), epidural abscess and other infections (tuberculous, fungal, and other granulomatous diseases), syphilitic meningomyelitis, motor system disease, subacute combined degeneration (vitamin B12 deficiency), syringomyelia, and degenerative disease of the lateral and posterior columns of unknown cause.
On the other hand medicine ball exercises buy generic prochlorperazine, improvement frequently occurs when the main cause is cerebral trauma symptoms checklist trusted 5 mg prochlorperazine, compression from edema treatment vaginitis purchase genuine prochlorperazine on-line, postconvulsive paralysis medicine jokes order prochlorperazine 5mg with visa, or a transient metabolic derangement such as hypoglycemia, hyponatremia, etc. Included also in this category are aphasias due to lesions that separate the more strictly receptive parts of the language mechanism itself from the purely motor ones (conduction aphasia- see below) and to lesions that isolate the perisylvian language areas, separating them from the other parts of the cerebral cortex (transcortical aphasias). The anatomic basis for most of these so-called disconnection syndromes is poorly defined. The theoretical concept, however, is an interesting one and emphasizes the importance of afferent, intercortical, and efferent connections of the language mechanisms. The weakness of the concept is that it may lead to premature acceptance of anatomic and physiologic mechanisms that are overly simplistic. The locale of the lesion that causes loss of a language function does not localize the language function itself, a warning enunciated long ago by Hughlings Jackson. Nevertheless, the language disorders described below occur with sufficient regularity and clinical uniformity to be as useful as the more classic and common types of aphasia in revealing the complexity of language functions. Conduction Aphasia As indicated earlier, Wernicke theorized that certain clinical symptoms would follow a lesion that effectively separated the auditory and motor language areas without directly damaging either of them. Since then, a number of wellstudied cases have been described that conform to his proposed model of Leitungsaphasie (conduction aphasia), which is the name he gave it. The characteristic feature is one of severely impaired repetition; the defect applies to both single words and nonwords. There is a similar fluency and paraphasia in self-initiated speech, in repeating what is heard, and in reading aloud; writing is invariably impaired. The lesion in the few autopsied cases has been located in the cortex and subcortical white matter in the upper bank of the left sylvian fissure, usually involving the supramarginal gyrus and occasionally the most posterior part of the superior temporal region. However, in most of the reported cases, including those described by the Damasios, the left auditory complex, insula, and supramarginal gyrus were also involved. In any case, the usual cause of conduction aphasia is an embolic occlusion of the ascending parietal or posterior temporal branch of the middle cerebral artery, but other forms of vascular disease, neoplasm, or trauma in this region may produce the same syndrome. The concept of conduction aphasia, as outlined above, remains a useful theoretic construct, although not all authors are in agreement as to its purity as an aphasic syndrome. A summary of the arguments against a subcortical disconnection and those favoring a cortical origin can be found in the report of the condition with focal seizures by Anderson and colleagues. Patients with pure word-deafness may declare that they cannot hear, but shouting does not help, sometimes to their surprise. Audiometric testing and auditory evoked potentials disclose no hearing defect, and nonverbal sounds, such as a doorbell, can be heard without difficulty. The patient is forced to depend heavily on visual cues and frequently uses them well enough to understand most of what is said. If able to describe the auditory experience, the patient says that words sound like a jumble of noises. Conceptually it has been thought of as an exclusive injury of the auditory processing system. In most recorded autopsy studies, the lesions have been bilateral, in the middle third of the superior temporal gyri, in a position to interrupt the connections between the primary auditory cortex in the transverse gyri of Heschl and the association areas of the superoposterior cortex of the temporal lobe. In a few cases unilateral lesions have been localized in this part of the dominant temporal lobe (see page 397). Requirements of small size and superficiality of the lesion in the cortex and subcortical white matter are best fulfilled by an embolic occlusion of a small branch of the lower division of the middle cerebral artery. Such a person can no longer name or point on command to words, although he is sometimes able to read letters or numbers. Understanding spoken language, repetition of what is heard, writing spontaneously and to dictation, and conversation are all intact. The ability to copy words is impaired but is better preserved than reading, and the patient may even be able to spell a word or to identify a word by having it spelled to him or by reading one letter at a time (letter-by-letter reading). In some cases, the patient manages to read single letters but not to join them together (asyllabia). The most striking feature of this syndrome is the retained capacity to write fluently, after which the patient cannot read what has been written (alexia without agraphia). Autopsies of such cases have usually demonstrated a lesion that destroys the left visual cortex and underlying white matter, particularly the geniculocalcarine tract, as well as the callosal connections of the right visual cortex with the intact language areas of the dominant hemisphere (page 409). In the case originally described by Dejerine (1892), the disconnection occurred in the posґ terior part (splenium) of the corpus callosum, wherein lie the connections between the visual association areas of the two hemispheres (see Fig.
Some pa- tients state that cramps are more frequent when the legs are cold and daytime activity has been excessive treatment kawasaki disease order cheap prochlorperazine line. In others medicine 54 543 generic prochlorperazine 5mg amex, the cramps are provoked by the abrupt stretching of muscles symptoms miscarriage buy discount prochlorperazine 5 mg on-line, are very painful symptoms graves disease buy prochlorperazine paypal, and tend to wax and wane before they disappear. Although of no pathologic significance, the cramps in extreme cases are so persistent and so readily provoked by innocuous movements as to be disabling. Cramps of all types need to be distinguished from sensations of cramp without muscle spasm. Contrasted to cramp is the physiologic contracture, observed in McArdle disease and carnitine palmitoyl transferase deficiency, in which increasing muscle shortening and pain gradually develop during muscular activity. Cramps are also to be distinguished from the disabling and progressive form of painful spasm of the axial and proximal muscles known as the already mentioned stiff-man syndrome; this appears to be a disease of the spinal interneurons (page 1279). Continuous spasm intensified by the action of muscles and with no demonstrable disorder at a neuromuscular level is a common manifestation of localized tetanus and also follows the bite of the black widow spider. These disorders must be differentiated from a rare but distinctive type of encephalomyelitis of unknown cause ("spinal neuronitis"), characterized by intense rigidity and myoclonic jerking of trunk and limbs and painful spasms evoked by tactile and other stimuli. The damage in this disease is thought to be mainly to spinal internuncial neurons, with disinhibition of anterior horn cells (Howell et al; see also page 1067). There may also be difficulty distinguishing cramps and spasms from the early stages of a dystonic illness and from tetanus. All the aforementioned phenomena of cramping and pathologic activity of muscle fibers are elaborated in Chap. Palpable Abnormalities of Muscle Altered structure and function of muscle are not accurately revealed by palpation. Of course, the difference between the firm, hypertrophied muscle of a well-conditioned athlete and the slack muscle of a sedentary person is as apparent to the palpating fingers as to the eye, as is also the persistent contraction in tetanus, cramp, contracture, fibrosis, and extrapyramidal rigidity. The muscles in dystrophy are said to have a "doughy" or "elastic" feel, but we find this difficult to judge. In the Pompe type of glycogen storage disease, attention may be attracted to the musculature by an unnatural firmness and increase in bulk. The swollen, edematous, weak muscles in acute rhabdomyolysis with myoglobinuria or severe polymyositis may feel taut and firm but are usually not tender. Areas of tenderness in muscles that otherwise function normally, a state called myogelosis, have been attributed to fibrositis or fibromyositis, but their nature has not been divulged by biopsy. A tumorous or granulomatous mass may develop in part of a muscle or throughout a muscle, posing a series of special clinical problems discussed on page 1282. Pain localized to a group of muscles is a feature of torticollis and other dystonias. Pain tends not to be prominent in polymyositis and dermatomyositis but there are exceptions, as commented below. Other familiar painful disorders are acute brachial neuritis (neuralgic amyotrophy), radiculitis, and Bornholm disease, or pleurodynia, but actually little is known of the cause of the pain in any of them. The same is true of the muscular discomfort that characterizes the early stages of Guillain-Barre syndrome and of paralytic ґ poliomyelitis. Intense pain is a prominent complaint in most of the muscle spasm and cramp syndromes mentioned earlier. Pain tends to be more definite in polyneuritis, poliomyelitis, and polyarteritis nodosa than it is in polymyositis, various forms of dystrophy, and other myopathies. If pain is present in polymyositis, it usually indicates coincident involvement of connective tissues and joint structures. Hypothyroidism, hypophosphatemia, and hyperparathyroidism are other sources of a myalgic myopathy. They include the "statin" lipid-lowering drugs, clofibrate, captopril, lithium, colchicine, beta-adrenergic blocking drugs, penicillamine, cimetidine, suxamethonium, and numerous others (see the table in the review by Mastaglia and Laing). Contraction under ischemic conditions- as when the circulation is occluded by a tourniquet or from atherosclerotic vascular disease- induces pain; the pain of intermittent claudication is presumably of this type and is not accompanied by cramp. It is postulated that lactic acid or some other metabolite accumulates in muscles and activates pain receptors, but this is unproven.
The most striking examples medicine quiz discount prochlorperazine 5 mg with mastercard, fortunately rare medications vertigo cheap prochlorperazine 5 mg visa, are now observed as complications of vertebral angiography medicine 968 quality prochlorperazine 5mg, resulting in high cervical infarction medications for schizophrenia buy 5mg prochlorperazine visa, similar in most ways to the aforementioned spinal infarction from extracranial dissection of the vertebral artery. The syndrome of painful segmental spasms, spinal myoclonus, and rigidity, mentioned earlier, has also been observed under these conditions. The frequency of this complication was greatly reduced by the introduction of less toxic contrast media. Treatment the approach to all forms of spinal cord infarction is largely symptomatic, with attention during the acute stage to the care of bladder, bowel, and skin; after 10 to 14 days, more active rehabilitation measures can be started. Whether the acute effects of infarction can be modified by high-dose corticosteroids, agents that increase blood flow, or anticoagulation is not known. Hemorrhage of the Spinal Cord and Spinal Canal (Hematomyelia) Hemorrhage into the spinal cord is rare compared with the frequency of cerebral hemorrhage. The apoplectic onset of symptoms that involve tracts (motor, sensory, or both) in the spinal cord, associated with blood and xanthochromia in the spinal fluid, are the identifying features of hematomyelia. Aside from trauma, hematomyelia is usually traceable to a vascular malformation or a bleeding disease and particularly to the administration of anticoagulants. Actually, most vascular malformations of the spinal cord do not cause hemorrhage, but instead produce a progressive, presumably ischemic myelopathy, as described later and mentioned in the earlier section on necrotic myelopathy. In some cases, as in those of Leech and coworkers, one cannot ascertain the source of the bleeding, even at autopsy. Epidural or subdural bleeding, like epidural abscess, represents a neurologic emergency and calls for immediate radiologic localization and, in most cases, surgical evacuation. Advances in the techniques of selective spinal angiography and microsurgery have permitted the visualization and treatment of vascular lesions that cause bleeding with a precision not imaginable a few decades ago. These angiographic procedures make it possible to distinguish among the several types of vascular malformations, arteriovenous fistulas, and vascular tumors such as hemangioblastomas and to localize them accurately to the spinal cord, epidural or subdural space, or vertebral bodies. Vascular Malformations of the Spinal Cord and Overlying Dura these are well-known lesions, occurring not infrequently and causing both ischemic and hemorrhagic lesions. The most useful categorization reflects the appearance and location of the malformation by angiography and by surgical examination. These malformations may be divided into three groups: (1) arteriovenous malformations that are strictly intramedullary or also involve the meninges and surrounding structures such as the vertebral bodies to a limited extent; (2) a variety of intradural perimedullary fistulas that lie on the subpial surface of the cord (these probably conform most closely to the lesion described by Foix and Alajouanine discussed in the earlier section on necrotic myelopathy); and (3) purely dural fistulas. There is not sufficient pathologic material to determine whether these represent distinct pathologic entities or simply differing degrees and configurations of a common developmental process. Once recognized, treatment may be an urgent matter in cases with rapid clinical deterioration and impending paralysis. Increasingly, it has been recognized that arteriovenous fistulas that lie within the dura overlying the spinal cord, are capable of causing a myelopathy, sometimes several segments distant from the vascular nidus. The majority are situated in the region of the low thoracic cord or the conus, with a limited venous draining system. Some appear to be situated in a dural root sleeve and to drain into the normal perimedullary coronal venous plexus. The presenting clinical features in our patients have included slowly progressive bilateral but asymmetric leg weakness with variable sensory loss. According to Jellema and colleagues who studied 80 patients with spinal dural fistulas, the most common initial symptoms were gait imbalance, numbness, and paresthesias. As the process progressed, the majority developed urinary problems, leg weakness, and numbness in the legs and buttocks. The myelopathy that results is subacute or saltatory in evolution, presumably from venous congestion within the cord. Characteristically, activities that increase venous pressure (Valsalva maneuver, exercise) transiently amplify the symptoms or produce irreversible, stepwise worsening. One remarkable such case involved a baritone opera singer whose legs gave way repeatedly while singing (Khurana et al). As mentioned, some cases are painless, although most of our patients have had a moderate spinal ache or sciatica. Acute cramp-like, lancinating pain, sometimes in a sciatic distribution, is often a prominent early feature.
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