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Among the autosomal dominant cerebellar ataxias of later onset virus with diarrhea order 400 mg norfloxacin with visa, molecular and gene studies have identified mutant genes at 14 chromosomal loci infection 5 weeks after c-section trusted 400 mg norfloxacin, including three associated with episodic ataxia infection movie purchase 400mg norfloxacin mastercard. However virus 360 cheap norfloxacin 400mg with mastercard, as has been affirmed antibiotics questions pharmacology norfloxacin 400 mg online, the precise mechanisms by which the expanded polyglutamine molecule leads to neuronal cell death remain uncertain antibiotics for uti not sulfa cheap norfloxacin 400 mg amex. Some cases of ataxia are alcoholic-nutritional in origin, and a few are related to abuse of drugs, especially anticonvulsants, which may in a few cases cause a slowly progressive and permanent ataxia; rarely, organic mercury induces subacute cerebellar degeneration, and adulterated heroin causes a more abrupt and severe ataxic syndrome. The paraneoplastic variety of cerebellar degeneration often enters into the differential diagnosis; as a rule it occurs mostly in women with breast or ovarian cancers and evolves much more rapidly than any of the heredodegenerative forms. The more rapid onset of ataxia and the presence of anti-Purkinje cell antibodies (anti-Yo; page 583) are central to identifying the nature of this disease. From time to time one observes a similar idiopathic variety of subacute cerebellar degeneration, particularly in women who have no neoplasm and lack the specific antibodies of the paraneoplastic disease (Ropper). Rare cases of ataxia have been associated with celiac disease and Whipple disease, as noted in Chap. Ataxia may also be an early and prominent manifestation of Creuutzfeldt-Jakob disease caused by a transmissible prion (see Chap. Rare cases of aminoacidopathy manifesting for the first time in adult life have also provoked a cerebellar syndrome. Treatment this has been unsatisfactory and is limited largely to supportive measures such as the prevention of falling. Amantadine 200 mg daily for several months has shown limited benefit in some studies (Boetz et al). Whether thalamic electrical stimulators, or the type used for the treatment of Parkinson disease, have a role in suppressing the cerebellar tremor is not known. Hereditary Polymyoclonus the syndrome of quick, arrhythmic, involuntary single or repetitive twitches of a muscle or group of muscles was described in Chap. Familial forms are known, one of which, associated with cerebellar ataxia, was discussed earlier (dyssynergia cerebellaris myoclonica of Ramsay Hunt). But there is another disease, known as hereditary essential benign myoclonus, that occurs in relatively pure form unaccompanied by ataxia (page 87). In the latter condition, it may at times be difficult to evaluate coordination because willed movement is interrupted by the myoclonus and may be mistaken for intention tremor. Only by slowing the voluntary movement can the myoclonus be reduced or eliminated. It becomes manifest early in life; once established, it persists with little or no change in severity throughout life, often with rather little disability. It can, by its natural course, be differentiated from some of the hereditary metabolic diseases such as the Unverricht and Lafora types of myoclonic epilepsy, the lipidoses, tuberous sclerosis, and myoclonic disorders that follow certain viral infections and anoxic encephalopathy. Of interest is the response of this form of movement disorder, as in the case of acquired postanoxic myoclonus (page 89), to certain pharmacologic agents, notably clonazepam, valproic acid, and 5-hydroxytryptophan, the amino acid precursor of serotonin, particularly when these agents are used in combination. The main clinical distinctions to be made are from Creutzfeldt-Jakob subacute spongiform encephalopathy; drug-induced myoclonus, particularly lithium; renal failure and other acquired metabolic disorders; asterixis; and from the startle responses (page 90). Myoclonus as one component of a more complex movement disorder in corticobasal-ganglionic degeneration has already been mentioned. It is a disease of middle life, for the most part, and progresses to death in a matter of 2 to 5 years or longer in exceptional cases. Customarily, motor system disease is subdivided into several subtypes on the basis of the particular grouping of symptoms and signs. Less frequent are cases in which weakness and atrophy occur alone, without evidence of corticospinal tract dysfunction; for these the term progressive spinal muscular atrophy is used. When the weakness and wasting predominate in muscles innervated by the motor nuclei of the lower brainstem (i. This is designated as primary lateral sclerosis, a rare form of motor system disease in which the degenerative process remains confined to the corticospinal pathways (Pringle et al). The present authors believe that the pure spastic paraplegias without amyotrophy represent a special class of disease, hence they are described separately. There is also a relatively common familial form of spastic paraplegia in which the disease process is confined to the corticospinal tracts or, in some cases, combined with posterior column or other neurologic signs. In addition, a special type of spinal muscular atrophy disease occurs in infancy and childhood. Indeed, this condition is the leading cause of heritable infant mortality and, after cystic fibrosis, the most frequent form of serious autosomal recessive disease (Pearn). History Credit for the original delineation of amyotrophic lateral sclerosis is appropriately given to Charcot. With Joffroy in 1869 and Gombault in 1871, he studied the pathologic aspects of the disease. In a series of lectures given from 1872 to 1874, he provided a lucid account of the clinical and pathologic findings. Although called Charcot disease in France, amyotrophic lateral sclerosis (the term recommended by Charcot) has been preferred in the Englishspeaking world. Duchenne had earlier (1858) described labioglossolaryngeal paralysis, a term that Wachsmuth in 1864 changed to progressive bulbar palsy. Most authors credit Aran and Duchenne with the earliest descriptions of progressive spinal muscular atrophy, which they believed to be of myogenic origin. Amyotrophic Lateral Sclerosis this is a common disease, with an annual incidence rate of 0. Most patients are more than 45 years old at the onset of symptoms, and the incidence increases with each decade of life (Mulder). In about 10 percent of cases, the disease is familial, being inherited as an autosomal dominant trait with agedependent penetrance. The familial cases do not differ much in their symptoms and clinical course from nonfamilial ones, although as a group the former have a somewhat earlier age of onset, an equal distribution in men and women, and a slightly shorter survival. In the most typical forms of disease, the onset is perceived by the patient as weakness in a distal part of one limb. Or there may be awkwardness in tasks requiring fine finger movements (in handling buttons and automobile ignition keys), stiffness of the fingers, and slight weakness or wasting of the hand muscles. In other words, features related to upper and to lower motor neuron degeneration (or both) may appear insidiously in one limb. Cramping beyond what seems natural and fasciculations of the muscles of the forearm, upper arm, and shoulder girdle also appear. The earliest manifestation of the lower motor neuron component of this disease is often volitional cramping- for example, leg cramps as the patient turns in bed during the early morning hours. Before long, the triad of atrophic weakness of the hands and forearms, slight spasticity of the arms and legs, and generalized hyperreflexia- all in the absence of sensory change- leaves little doubt as to the diagnosis. Muscle strength and bulk diminish in parallel or there is a relative preservation of power early in the illness. Abductors, adductors, and extensors of fingers and thumb tend to become weak before the long flexors, on which the handgrip depends, and the dorsal interosseous spaces become hollowed, giving rise to the "cadaveric" or "skeletal" hand. When an arm is the first limb affected, all this occurs while the thigh and leg muscles seem relatively normal, and there may come a time in some cases when the patient walks about with useless, dangling arms. Later the atrophic weakness spreads to the neck, tongue, pharyngeal, and laryngeal muscles, and eventually those in the trunk and lower extremities yield to the onslaught of the disease. The affected parts may ache and feel cold, but true paresthesias, except from poor positioning and pressure on nerves, do not occur or are minor. Sphincteric control is well maintained even after both legs have become weak and spastic, but many patients acquire urinary and sometimes fecal urgency in the advanced stages of the disease. The abdominal reflexes may be elicitable even when the plantar reflexes are extensor. Coarse fasciculations are usually evident in the weakened muscles but may not be noticed by the patient until the physician calls attention to them. The course of this illness, irrespective of its particular mode of onset and pattern of evolution, is progressive. There may be periods lasting weeks or months during which the patient observes no advance in symptoms but clinical changes can nonetheless be detected. Half the patients succumb within 3 years of onset and 90 percent within 6 years (Mulder et al). The clinical variants of motor neuron disease that occur with regularity and have distinguishing clinical features are described below. Other Patterns of Evolution In addition to the special configurations discussed further on, there are many patterns of neuromuscular involvement other than the one just described. In our experience this crural amyotrophy is somewhat less frequent than the brachial-manual type. Another variant is the early involvement of thoracic, abdominal, or posterior neck muscles, the last being one of the causes of head lolling in older individuals. Yet another pattern is of early diaphragmatic weakness; such cases come to attention because of respiratory failure. The pattern of more symmetrical proximal limb or shoulder-girdle amyotrophy with onset at an early age is also well known and simulates muscular dystrophy (Wohlfart-Kugelberg-Welander disease- page 946). On several occasions we have observed a pattern involving the arm and leg on the same side, first with spasticity and then with some degree of amyotrophy; this is sometimes called the hemiplegic or Mills variant. However, this condition more frequently turns out to be due to multiple sclerosis. The first manifestations may be a spastic weakness of the legs, in which case a diagnosis of primary lateral sclerosis may be made (discussed further on); only after a year or two do the hand and arm muscles weaken, waste, and fasciculate. Early on, a spastic bulbar palsy with dysarthria and dysphagia, hyperactive jaw jerk and facial reflexes, but without muscle atrophy, may be the initial phase of disease. From time to time, as the disease advances, very mild distal sensory loss is observed in the feet without explanation, but always, if the sensory loss is a definite and early feature, the diagnosis must remain in doubt. In about half the patients, the illness takes the form of a symmetrical (sometimes asymmetrical) wasting of intrinsic hand muscles, slowly advancing to the more proximal parts of the arms; less often, the legs and thighs are the sites of the initial atrophic weakness; less often still, the proximal parts of the limbs are affected before the distal parts. Progressive Bulbar Palsy Here reference is made to a condition in which the first and dominant symptoms relate to weakness and laxity of muscles innervated by the motor nuclei of the lower brainstem, i. This weakness gives rise to an early defect in articulation, in which there is difficulty in the pronunciation of lingual (r, n, l), labial (b, m, p, f ), dental (d, t), and palatal (k, g) consonants. In other patients, slurring is due to spasticity of the tongue, pharyngeal, and laryngeal muscles; the speech sounds as if the patient were eating food that is too hot. Usually the voice is modified by a combination of atrophic and spastic weakness, as indicated below. Defective modulation of the voice with variable degrees of rasping and nasality is another characteristic. The pharyngeal reflex is lost, and the palate and vocal cords move imperfectly or not at all during attempted phonation. Mastication and deglutition also become impaired; the bolus of food cannot be manipulated and may lodge between the cheek and teeth; and the pharyngeal muscles do not force it properly into the esophagus. Fasciculations and focal loss of tissue of the tongue are usually early manifestations; eventually the tongue becomes shriveled and lies useless on the floor of the mouth. The chin may also quiver from fascicular twitchings, but diagnosis of the disease should not be made on the basis of fasciculations alone, i. The jaw jerk may be present or exaggerated at a time when the muscles of mastication are markedly weak. In fact, spasticity of the jaw muscles may be so pronounced that the slightest tap on the chin will evoke clonus and blinking; rarely, attempts to open the mouth elicit a "bulldog" reflex (jaws snap shut involuntarily). Commonly, when a jaw jerk is present, a positive snout reflex can also be detected, both of these reflect degeneration of the posterior frontal lobe. Spastic weakness of the oropharyngeal muscles may be the initial manifestation of bulbar palsy and may at times surpass signs of atrophic weakness; pseudobulbar signs (pathologic laughter and crying) may reach extreme degrees. This is the only common clinical situation in which spastic and atrophic bulbar palsy coexist. As with other forms of motor system disease, the course of bulbar palsy is inexorably progressive. Eventually the weakness spreads to the respiratory muscles and deglutition fails entirely; the patient dies of inanition and aspiration pneumonia, usually within 2 to 3 years of onset. About 25 percent of cases of motor system disease begin with bulbar symptoms, but rarely if ever does the sporadic form of progressive bulbar palsy run its course as an independent syndrome (pure heredofamilial forms of progressive bulbar palsy in the adult are known but rare). In general, the earlier the onset of the bulbar involvement, the shorter the course of the disease. These cases have distinctive neuropathologic features and are designated as primary lateral sclerosis, a term originally suggested by Erb in 1875. A historical review of the subject appears in the article by Pringle and colleagues. The typical case begins insidiously in the fifth or sixth decade with a stiffness in one leg, then the other; there is a slowing of gait, with spasticity predominating over weakness as the years go on. Walking is still possible with the help of a cane for many years after the onset, but eventually this condition acquires the characteristic features of a severe spastic paraparesis. Over the years, finger movements become slower, the arms become spastic, and, if the illness persists for decades, speech takes on a pseudobulbar tone. The legs are often found to be surprisingly strong, the difficulty in locomotion being attributable mainly to rigid spasticity. Pringle and associates suggest that an important diagnostic criterion of the disease is progression for 3 years without evidence of lower motor neuron dysfunction. A rare type begins in the oropharyngeal muscles, as mentioned above, but almost always, atrophy and fasciculations in this same region are evident within months. Pathologic studies in a limited number of cases have disclosed a relatively stereotyped pattern of reduced numbers of Betz cells in the frontal and prefrontal motor cortex, degeneration of the corticospinal tracts, and preservation of motor neurons in the spinal cord and brainstem (Beal and Richardson, Fisher, Pringle et al). Whether some of these cases are examples of late-onset familial spastic paraplegia (see further on) has not been explored with molecular techniques. Almost unique among cases of this type have been a few linked to an adult onset of phenylketonuria or other aminoacidopathies, or to vitamin B12 deficiency.
Usually antibiotics for uti cipro generic norfloxacin 400mg without prescription, by the fourth week antibiotics for urinary tract infection not working discount 400mg norfloxacin with amex, sometimes later antibiotic before root canal norfloxacin 400 mg for sale, the hematoma becomes hypodense infection 1 month after surgery effective norfloxacin 400 mg, typical of a chronic subdural hygroma antibiotic resistance related to natural selection cheap norfloxacin 400mg without prescription. Other formerly used investigative measures are seldom necessary but are mentioned here for completeness and in the event that the diagnosis is made in the course of evaluating some other neurologic problem virus 90 mortality rate norfloxacin 400 mg low price. Skull films are helpful when there is calcification surrounding a chronic hematoma, a calcified pineal that is Figure 35-10. The lesion is isodense to the adjacent brain tissue, but its margin can be appreciated with contrast enhancement. In an arteriogram, the cortical branches of the middle cerebral artery are separated from the inner surface of the skull, and the anterior cerebral artery may be displaced contralaterally. A xanthochromic fluid with relatively low protein content should always raise the suspicion of chronic subdural hematoma. The chronic subdural hematoma becomes gradually encysted by fibrous membranes (pseudomembranes) that grow from the dura. Some hematomas- probably those in which the initial bleeding was slight (see below)- resorb spontaneously. This hypothesis, which came to be widely accepted, is not supported by the available data. According to the latter authors, the most important factor in the accumulation of subdural fluid is a pathologic permeability of the developing capillaries in the outer pseudomembrane of the hematoma. In any event, as the hematoma enlarges, the compressive effects increase gradually. The difficulty of managing these patients surgically should not be underestimated. Elderly patients may be slow to recover after removal of the chronic hematoma or may have a prolonged period of confusion. Although no longer a common practice, the administration of corticosteroids is an alternative to surgical removal of subacute and chronic subdural hematomas in patients with minor symptoms or with some contraindication to surgery. Headache and other symptoms, such as gait difficulty or limb clumsiness, may resolve satisfactorily after several weeks of medication and may remain abated when the steroids are slowly reduced. Subdural Hygroma this encapsulated collection of clear or xanthochromic fluid in the subdural space may form after an injury as well as after meningitis (in an infant or young child). More often subdural hygromas appear without infection, presumably due to a ball-valve effect of an arachnoidal tear that allows cerebrospinal fluid to collect in the space between the arachnoid and the dura; brain atrophy is conducive to this process. It may be difficult to differentiate a long-standing subdural hematoma from hygroma, and some chronic subdural hematomas are probably the result of repeated small hemorrhages that arise from the membranes of hygromas. Shrinkage of the hydrocephalic brain after ventriculoperitoneal shunting is also conducive to the formation of a subdural hematoma or hygroma, in which case drowsiness, confusion, irritability, and low-grade fever are relieved when the subdural fluid is aspirated or drained. Chronic subdural hematomas over both cerebral hemispheres, without shift of the ventricular system. The bilaterally balanced masses result in an absence of horizontal displacement, but they may compress the upper brainstem. Why somewhat less than one-half of all subdural hematomas remain solid and nonenlarging and the remainder liquefy and then enlarge is not known. The experimental observations of Labadie and Glover suggest that the volume of the original clot is a critical factor: the larger its initial size, the more likely it will be to enlarge. An inflammatory reaction, triggered by the breakdown products of blood elements in the clot, appears to be an additional stimulus for growth as well as for neomembrane formation and its vascularization. Treatment of Subdural Hematoma In most cases of acute hematoma, it is sufficient to place burr holes and evacuate the clot before deep coma has developed. Treatment of larger hematomas, particularly after several hours have passed and the blood has clotted, consists of wide craniotomy to permit control of the bleeding and removal of the clot. As one would expect, the interval between loss of consciousness and the surgical drainage of the clot is perhaps the most important determinant of outcome in serious cases. Thin, crescentic clots can be observed and followed over several weeks and surgery undertaken only if focal signs or indications of increasing intracranial pressure arise (headache, vomiting, and bradycardia). If the acute clot is too small to explain the coma or other symptoms, there is probably extensive contusion and laceration of the cerebrum. To remove the more chronic hematomas, a craniotomy must be performed and an attempt made to strip the membranes that surround the clot. This diminishes the likelihood of reaccumulation of fluid but it is not always successful. 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. The mass effect of contusional swelling, if sufficiently large, 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. If vital centers are untouched, the immediate problem is intracranial bleeding and rising intracranial pressure from swelling of the traumatized brain tissue. Once the initial complications are dealt with, the surgical problems, as outlined by Meirowsky, are reduced to three: prevention of infection by rapid and radical (definitive) debridement, accompanied by the administration of broad-spectrum antibiotics; control of increased intracranial pressure and shift of midline structures by removal of clots of blood and the vigorous administration of mannitol or other dehydrating agents as well as dexamethasone; and the prevention of life-threatening systemic complications. When first seen, the majority of patients with penetrating cerebral lesions are comatose. A small metal fragment may have penetrated the skull without causing concussion, but this is not true of high-velocity missiles. In a series of 132 patients of the latter type analyzed by Frazier and Ingham, consciousness was lost in 120. The depth and duration of coma seemed to depend on the degree of cerebral necrosis, edema, and hemorrhage. In the series of the Acute Brain Swelling in Children this condition is seen in the first hours after injury and may prove rapidly fatal. There is usually no papilledema in the early stages, during which the child hyperventilates, vomits, and shows extensor posturing. The assumption has been that this represents a loss of regulation of cerebral blood flow and a massive increase in the blood volume of the brain. The administration of excessive water in intravenous fluids may contribute to the problem and should be avoided. As the name implies, the inciting trauma is typically violent shaking of the body or head of an infant, resulting in rapid acceleration and deceleration of the cranium combined with cervical whiplash. The presence of this type of injury must often be inferred from the combination of lesions on imaging studies or autopsy examination, but precision in examination is paramount because of its forensic and legal implications. The diagnosis is suspected from the combination of subdural hematomas and retinal hemorrhages, as summarized by Bonnier and colleagues. Sometimes there are occult skull fractures, but more often, there is little or no direct cranial trauma. On emerging from coma, the patient passes through states of stupor, confusion, and amnesia, not unlike those following severe closed head injuries. Headache, vomiting, vertigo, pallor, sweating, slowness of pulse, and elevation of blood pressure are other common findings. Focal or focal and generalized seizures occur in the early phase of the injury in some 15 to 20 percent of cases. Frazier and Ingham comment on the "loss of memory, slow cerebration, indifference, mild depression, inability to concentrate, sense of fatigue, irritability, vasomotor and cardiac instability, frequent seizures, headaches and giddiness, all reminiscent of the residual symptoms from severe closed head injury with contusions. The classic articles by Feiring and Davidoff and also by Russell and by Teuber, listed at the end of this chapter, are still very useful references on this subject. Crushing Injuries of the Skull Aside from the absence of concussion, these relatively rare cerebral lesions present no special clinical features or neurologic problems not already discussed. Birth Injuries these involve a unique combination of physical forces and circulatory-oxygenation factors and are discussed separately in Chap. As one might expect, the risk of developing posttraumatic epilepsy is also related to the overall severity of the closed head injury. In a civilian cohort of 2747 head-injured patients described by Annegers and colleagues, the risk of seizures after severe head injury (loss of consciousness or amnesia for more than 24 h, including subdural hematoma and brain contusion) was 7 percent within 1 year and 11. If the injury was only moderate (unconsciousness or amnesia for 30 min to 24 h or caus- ing only a skull fracture), the risk fell to 0. After mild injury (loss of consciousness or amnesia of less than 30 min), the incidence of seizures was not significantly greater than in the general population. In a subsequent study (1998), Annegers et al expanded the original cohort to include 4541 children and adults with cerebral trauma. The results were much the same as those of the first study except that in patients with mild closed head injuries, there was only a slight excess risk of developing seizures- a risk that remained elevated only until the fifth year after injury. The likelihood of epilepsy is said to be greater in parietal and posterior frontal lesions, but it may arise from lesions in any area of the cerebral cortex. Also, the frequency of seizures is considerably higher after penetrating cranial injury, as cited above. A small number of patients have a generalized seizure within moments of the injury (immediate epilepsy). Usually this amounts to a brief tonic extension of the limbs, with slight shaking movements immediately after concussion, followed by awakening in a mild confusional state. Whether this represents a true epileptic phenomenon or, as appears more likely, is the result of arrest of cerebral blood flow or a transient brainstem dysfunction is unclear. Some 4 to 5 percent of hospitalized head-injured individuals are said to have one or more seizures within the first week of their injury (early epilepsy). The immediate seizures have a good prognosis and we tend not to treat them as if they represented epilepsy; on the other hand, late seizures are significantly more frequent in patients who had experienced epilepsy in the first week after injury (not including the convulsions of the immediate injury) (Jennett). In medical writings, the term posttraumatic epilepsy usually refers to late epilepsy, i. Approximately 6 months after injury, half the patients who will develop epilepsy have had their first episode; by the end of 2 years, the figure rises to 80 percent (Walker). The interval between head injury and development of seizures is said to be longer in children. The longer the interval, the less certain one is of its relation to the traumatic incident.
A fuller review of this subject can be found in the text the Child with Delayed Speech antibiotic 875 discount 400mg norfloxacin free shipping, edited by Rutter and Martin antibiotic japanese buy 400mg norfloxacin overnight delivery. Stuttering and Stammering these difficulties occur in an estimated 1 to 2 percent of the school population antimicrobial properties of garlic order norfloxacin 400 mg with amex. Often the conditions disappear in late childhood and adolescence; by adulthood infection 3 weeks after tonsillectomy order norfloxacin 400 mg free shipping, only about 1 in every 300 individuals suffers from a persistent stammer or stutter antimicrobial list cheap norfloxacin 400 mg overnight delivery. In some respects they belong to and are customarily included in the developmental language disorders antibiotic guidelines 2014 norfloxacin 400mg with amex, but they differ in being largely centered in articulation. Essentially they represent a disorder of rhythm- an involuntary, repetitive prolongation of speech- due to an insuppressible spasm of the articulatory muscles. The spasm may be tonic and result in a complete blocking of speech (at one time referred to specifically as stammering) or clonic speech, i. There is no valid reason to distinguish between these two forms of the disorder, since they are intermingled, and the terms stammer and stutter are now used synonymously. Certain sounds, particularly p and b, offer greater difficulty than others; paperboy comes out p-p-paper b-bboy. The problem is usually not apparent when single words are being spoken and dysfluency tends to be worse at the beginning of a sentence or an idea. The severity of the stutter is increased by excitement and stress, as when speaking before others, and is reduced when the stutterer is relaxed and alone or when singing in a chorus. When severe, the spasms may overflow into other groups of muscles, mainly of the face and neck and even of the arms. The muscles involved in stuttering show no fault in actions other than speaking, and all gnostic and semantic aspects of receptive language are intact. The time of onset of stuttering is mainly at two periods in life- between 2 and 4 years of age, when speech and language are evolving, and between 6 and 8 years, when these functions extend to reciting and reading aloud in the classroom. If stuttering is mild, it tends to develop or to be present only during periods of emotional stress, and in four out of five children it disappears entirely or almost so during adolescence or the early adult years (Andrews and Harris). If severe, it persists throughout life regardless of treatment but tends to improve as the patient grows older. Slowness in developing hand and eye preference, ambidexterity, or an enforced change from leftto right-hand use have been popular explanations of which Orton and Travis were leading advocates. According to their theory, stuttering results from a lack of the necessary degree of unilateral control in the synchronization of bilaterally innervated speech mechanisms. However, these explanations probably apply to only a minority of stutterers (Hecaen and de Ajuriaguerra). Recently, several groups have reported subtle structural anomalies in the gray matter of the perisylvian region, but no common theme has emerged, and others are skeptical of these findings (see editorial by Packman and Onslow). It has been commented in the literature on this subject that speech production is a highly distributed system and that compensatory mechanisms used by stutterers may confound interpretation of functional imaging studies. The disappearance of mild stuttering with maturation has been attributed incorrectly to all manner of treatment (hypnosis, progressive relaxation, speaking in rhythms, etc. Since stuttering may reappear at times of emotional strain, a psychogenesis has been proposed, but- as pointed out by Orton and by Baker and colleagues- if there are any psychologic abnormalities in the stutterer, they are secondary rather than primary. We have observed that many stutterers, probably as a result of this impediment to free social interaction, do become increasingly fearful of talking and develop feelings of inferiority. By the time adolescence and adulthood are reached, emotional factors are so prominent that many physicians have mistaken stuttering for neurosis. Usually there is little or no evidence of any personality deviation before the onset of stuttering, and psychotherapy has not in our experience had a significant effect on the underlying defect. A strong family history in many cases and male dominance point to a genetic origin, but the inheritance does not follow a readily discernible pattern. Stuttering is not associated with any detectable weakness or ataxia of the speech musculature. The muscles of speech go into spasm only when called upon to perform the specific act of speaking. The spasms are not invoked by other actions (which may not be as complex or voluntary as speaking), differing in this way from an apraxia and the intention spasm of athetosis. Also, palilalia is a different condition in which a word or phrase, usually the last one in a sentence, is repeated many times with decreasing volume. Rarely, in adults as well as in children, stuttering may be acquired as a result of a lesion in the motor speech areas. The latter is said to interfere with the enunciation of any syllable of a word (not just the first), to favor involvement of grammatical and substantive words, and to be unaccompanied by anxiety and facial grimacing. The reported lesion sites in acquired stuttering are so variable (right frontal, corpus striatum, left temporal, left parietal) as to be difficult to reconcile with proposed theories of developmental stuttering (Fleet and Heilman). Another form of acquired stuttering is manifestly an expression of an extrapyramidal disorder. Here there occurs a prolonged repetition of syllables (vowel and consonant), which the patient cannot easily interrupt. The abnormality involves throat-clearing and other vocalizations, similar to what is seen in tic disorders. Treatment the therapy of stuttering is difficult to evaluate and, on the whole, the therapy of speech-fluency disorders has been a frustrating effort. As remarked above, all speech-fluency distur- bances are modifiable by environmental circumstances. Thus a certain proportion of stutterers will become more fluent under certain conditions, such as reading aloud; others will stutter more severely at this time. Again, a majority of stutterers will be adversely affected by talking on the telephone; a minority are helped by this device. Schemes such as the encouragement of associated muscular movements ("penciling," etc. Common to all such efforts has been the difficulty of achieving carryover into the natural speaking environment. Progressive relaxation, hypnosis, delayed auditory feedback, loud noise that masks speech sounds, and many other ancillary measures may help, but only temporarily. Canevini and colleagues have made the interesting observation that stuttering improved in an epileptic treated with levetiracetam, and Rosenberger has commented on other drug therapies. It is characterized by uncontrollable speed of speech, which results in truncated, dysrhythmic, and often incoherent utterances. Omissions of consonants, elisions, improper phrasing, and inadequate intonation occur. It is as though the child were too hurried to take the trouble to pronounce each word carefully and to compose sentences. Speech therapy (elocutionary) and maturation may be attended by a restoration of more normal rhythms. Other Articulatory Defects these are most common in preschool children, having an incidence of up to 15 percent. Another common condition, lallation, or dyslalia, is characterized by multiple substitutions or omissions of consonants. For example, the letter r may be incorrectly pronounced, so that it sounds like w or y; running a race becomes wunning a wace or yunning a yace. The child seems to be unaware that his or her speech differs from that of others and is distressed at not being understood. These and similar abnormalities of speech are often present in otherwise normal children and are referred to as "infantilisms. More important is the fact that in more than 90 percent of cases, these articulatory abnormalities disappear by the age of 8 years, either spontaneously or in response to speech therapy. Presumably the natural cycle of motor speech acquisition has only been delayed, not arrested. Such abnormalities, however, are more frequent among the mentally retarded than in normal children; with mental defect, many consonants are persistently mispronounced. Another type is a congenital form of spastic bulbar speech described by Worster-Drought in which words are spoken slowly, with stiff labial and lingual movements, hyperactive jaw and facial reflexes, and sometimes mild dysphagia and dysphonia. The limbs may be unaffected, in contrast to those of most children with cerebral palsy. Many of these patients also have a harelip; the two abnormalities together interfere with sucking and later in life with the enunciation of labial and guttural consonants. The aforementioned developmental abnormalities of speech are sometimes associated with disturbances of higher-order language processing. In one, which they call the "semantic pragmatic syndrome," a failure to comprehend complex phrases and sentences is combined with fluent speech and well-formed sentences that are, however, lacking in content. In another, "semantic retrieval-organization syndrome," a severe anomia blocks word finding in spontaneous speech. Developmental Dyslexia (Congenital Word Blindness) this condition, first described by Hinshelwood in 1896, becomes manifest in an older child who lacks the aptitude for one or more of the specific skills necessary to derive meaning from the printed word. Also defined as a significant discrepancy between "measured intelligence" and "reading achievement" (Hynd et al), it has been found in 3 to 6 percent of all schoolchildren. There are several excellent writings on the subject, to which the interested reader is referred for a detailed account (Orton; Critchley and Critchley; Rutter and Martin; Kinsbourne; Shaywitz; Rosenberger). The main problem is an inability to read words and also to spell and to write them, despite the ability to see and recognize letters. There is no loss of the ability to recognize the meaning of objects, pictures, and diagrams. According to Shaywitz, these children lack an awareness that words can be broken down into individual units of sound and that each segment of sound is represented by a letter or letters. This has been summarized as a problem in "phonologic processing," referring to the smallest unit of spoken language, the phoneme, and the inability of dyslexic individuals to appreciate a correspondence between phonemes and their written representation (graphemes). In addition to the essential visuoperceptual defect, some individuals also manifest a failure of sequencing ability, lack of phonemic segmentation, and altered cognitive processing of langauge. Much of what has been learned about dyslexia applies to native speakers of English more so than to those who speak Romance languages. English is more complex phonologically than most other languages- for example, using 1120 graphemes to represent 40 phonemes, in contrast to Italian, which uses 33 graphemes to represent 22 phonemes (see Paulesu). Children with native orthographic languages, such as Chinese and Japanese, apparently have a far lower incidence of dyslexia. Often, before the child enters school, reading failure can be anticipated by a delay in attending to spoken words, difficulty with rhyming games, and speech characterized by frequent mispronunciations, hesitations, and dysfluency; or there may be a delay in learning to speak or in attaining clear articulation. In the early school years there are difficulties in copying, color naming, and formation of number concepts as well as the persistent reversal of letters. Writing appears to be defective because of faulty perception of form and a kind of constructional and directional apraxia. Not infrequently, there is an associated vagueness about the serial order of letters in the alphabet and months in the year, as well as difficulty with numbers (acalculia) and an inability to spell and to read music. The complex of symptoms of dyslexia, dyscalculia, finger agnosia, and right-left confusion, found in a few of these children, is interpreted as a developmental form of the Gerstmann syndrome (page 402). Lesser degrees of dyslexia are more common than the severe ones and are found in a large segment of the school population. Some 10 percent of schoolchildren have some degree of this disability, but the problem is complex because the condition is unquestionably influenced by the way reading is taught. This disorder is stable and persistent; however, as a result of effective methods of training, only a few children are unable to read at all after many years in school. This form of language disorder, unattended by other neurologic signs, is strongly familial, being almost in conformity with an autosomal dominant or sex-linked recessive pattern. There is also a statistically higher incidence of left-handedness among these persons and members of their families. Shaywitz et al have suggested that the reported predominance of reading disabilities in boys (male-to-female ratios of 2:1 to 5:1) represents a bias in subject selection- many more boys than girls being identified because of associated hyperactivity and other behavioral problems; but this does not seem the entire explanation to us. Our casual clinical experience suggests that there is a genuine male preponderance. An estimated 12 to 24 percent of dyslexic children will also have an attention-deficit disorder (see further on). In the study of dyslexic and dysgraphic children, a number of other apparently congenital developmental abnormalities have been documented, such as inadequate perception of space and form (poor performance on form boards and in tasks requiring construction); inadequate perception of size, distance, and temporal sequences and rhythms; and inability to imitate sequences of movements gracefully, as well as degrees of clumsiness and reduced proficiency in all motor tasks and games (the clumsy-child syndrome as described by Gubbay et al and mentioned earlier in the chapter under "Delays in Motor Development"). These disorders may also occur in brain-injured children; hence there may be considerable difficulty in separating simple delay or arrest in development from a pathologic process in the brain. However, in the majority of dyslexic children these additional features are absent or so subtle as to require special testing for their detection. A few careful morphometric studies provide insight into the basis of this disorder. Galaburda and associates have studied the brains of four males (ages 14 to 32 years) with developmental dyslexia. In each case there were developmental anomalies of the cerebral cortex, consisting of neuronal ectopias and architectonic dysplasias, located mainly in the perisylvian regions of the left hemisphere. Also, all of the brains were characterized by relative symmetry of the planum temporale, in distinction to the usual pattern of cerebral asymmetry, favoring the planum temporale of the left side. Similar changes have been described in three women with developmental dyslexia (Humphreys et al). It is important to note, however, that not all patients with developmental dyslexia (or autism) show this anomalous anatomic asymmetry (Rumsey et al). They found, in the planum temporale and neighboring parietal operculum of both hemispheres, that some gyri were missing and others were duplicated. Also, in some dyslexic individuals, the visual evoked responses to rapid low-contrast stimuli are diminished. The latter abnormality may be related to a deficit of large neurons in the lateral geniculate bodies (see Livingstone et al). Stein et al has found that 20 percent of dyslexic children have unstable ocular fixation and that monocular occlusion improves both binocular control and reading.
Syndromes
In a series of 12 such patients described by Michel and colleagues virus on iphone proven norfloxacin 400 mg, burning or constrictive pain infection vs disease cheap norfloxacin 400 mg with mastercard, identical to the thalamic pain syndrome (page 141) antibiotic beads for osteomyelitis cheap 400 mg norfloxacin mastercard, resulted from vascular lesions restricted to the cortex antibiotic resistance genes generic norfloxacin 400 mg without a prescription. The discomfort involved the entire half of the body or matched the region of cortical hypesthesia; in a few cases the symptoms were paroxysmal virus encrypted my files purchase norfloxacin 400 mg mastercard. Head and Holmes drew attention to a number of interesting points about patients with parietal sensory defects- the easy fatigability of their sensory perceptions; the inconsistency of responses to painful and tactile stimuli; the difficulty in distinguishing more Clinical Effects of Parietal Lobe Lesions Within the brain antibiotic resistance map norfloxacin 400 mg fast delivery, no other territory surpasses the parietal lobes in the rich variety of clinical phenomena exposed under conditions of disease. Our current understanding of the effects of parietal lobe disease contrasts sharply with that of the late nineteenth century, when these lobes, in the classic textbooks of Oppenheim and Gowers, were considered to be "silent areas. Close to the core of the complex behavioral features that arise from lesions of the parietal lobes is the problem of agnosia. Allusion has already been made to agnosia in the discussion of lesions of the temporal lobes that affect language, and similar findings occur with lesions of the occipital lobe as discussed further on. In those contexts, the term refers to a loss of recognition of an entity that cannot be attributed to a defect in the primary sensory modality. As a result of the extension of the term agnosia to a loss of more complex integrated functions as described below, a number of intriguing deficits arise. These syndromes expose properties of the parietal lobe that have implications regarding a map of the body schema and of external topographic space, of the ability to calculate, to differentiate left from right, to write words, and other problems discussed below. Of these, the testing of sensory extinction by the presentation of two tactile stimuli simultaneously on both sides of the body has become a component of the routine neurologic examination for parietal lesions. With anterior parietal lobe lesions there is often an associated mild hemiparesis, since this portion of the parietal lobe contributes a considerable number of fibers to the corticospinal tract. Or, more often, there is only a poverty of movement or a weak effort of the opposite side in the absence of somatic neglect. The affected limbs, if involved with this apparent weakness, tend to remain hypotonic and the musculature may undergo atrophy of a degree not explained by inactivity alone. In some cases, as noted below, there is clumsiness in reaching for and grasping an object under visual guidance (optic ataxia), and exceptionally, at some phase in recovery from the hemisensory deficit, there is incoordination of movement and intention tremor of the contralateral arm and leg, simulating a cerebellar deficit (pseudocerebellar syndrome). With parietal lesions, the arm and hand may sometimes be held in a fixed dystonic posture. Long before their time, however, it was suggested that such information was the basis of our emerging awareness of ourselves as persons, and philosophers had assumed that this comes about by the constant interplay between percepts of ourselves and of the surrounding world. The formation of the body schema is thought to be based on the constant influx and storage of sensations from our bodies as we move about; hence, motor activity is important in its development. Always, however, a sense of extrapersonal space is central to this activity, and this depends upon visual and labyrinthine stimulation. The mechanisms upon which these perceptions depend are best appreciated by studying their derangements in the course of neurologic disease of the parietal lobes. Anosognosia (Unilateral Asomatognosia; Anton-Babinski Syndrome) and Hemispatial Neglect the observation that a patient with a dense hemiplegia, usually of the left side, may be indifferent to the paralysis or unaware of it was first made by Anton; later, Babinski named this disorder anosognosia. It may express itself in several ways: the patient may act as if nothing were the matter. If asked to raise the paralyzed arm, he may raise the intact one or do nothing at all. If told it is paralyzed, the patient may deny that this is so or offer an excuse: "My shoulder hurts. This mental derangement, which Hughlings Jackson referred to as "a kind of imbecility," obviously includes a somatosensory defect that encompasses loss of the stored body schema as well as a conceptual negation of paralysis and a disturbed visual perception and neglect of half of the body. It should be pointed out that the allied symptoms of loss of body scheme and the lack of appreciation of a left hemiplegia are seperable, some patients displaying only one feature. The term anosognosia for hemiplegia has been used to describe the latter phenomenon. The lesion responsible for the various forms of one-sided asomatognosia lies in the cortex and white matter of the superior parietal lobule but may extend variably into the postcentral gyrus, frontal motor areas, and temporal and occipital lobes, accounting for some of the associated abnormalities described below. Rarely, a deep lesion of the ventrolateral thalamus and the juxtaposed white matter of the parietal lobe will produce a similar contralateral neglect. The patient looks dull, is inattentive and apathetic, and shows varying degrees of general confusion. There may be an indifference to performance failure, a feeling that something is missing, visual and tactile illusions when sensing the paralyzed part, hallucinations of movement, and allocheiria (one-sided stimuli are felt on the other side). Another common group of parietal symptoms consists of neglect of one side of the body in dressing and grooming, recognition only on the intact side of bilaterally and simultaneously presented stimuli (sensory extinction) as mentioned above, deviation of head and eyes to the side of the lesion, and torsion of the body in the same direction (failure of directed attention to the body and to extrapersonal space on the side opposite the lesion). The patient may fail to shave one side of the face, apply lipstick or comb the hair only on one side, or find it impossible to put on eyeglasses, insert dentures, or put on a shirt or gown when one sleeve has been turned inside out (the problem dressing, when it is apparent on both sides of the body, is more of a dressing apraxia). Unilateral spatial neglect is brought out by having the patient bisect a line, draw a daisy or a clock, or name all the objects in the room. Homonymous hemianopia and varying degrees of hemiparesis may or may not be present and interfere with the interpretation of the lack of application on the left side of the drawing. A number of tests have been designed to elicit these disturbances, such as indicating the time by placement of the hands on a clock, drawing a map, copying a complex figure, reproducing stick-pattern constructions and block designs, making three-dimensional constructions, and reconstructing puzzles. According to Denny-Brown and Banker, the basic disturbance in such cases is an inability to summate a series of "spatial impressions"- tactile, kinesthetic, visual, or auditory- a defect they referred to as amorphosynthesis. In their view, imperception or neglect of one side of the body and of extrapersonal space is the essential feature and represents the full extent of the disturbance, which in lesser degree consists only of tactile and visual extinction. More recent observations indicate that patients with right parietal lesions show variable but lesser elements of ipsilateral neglect in addition to the striking degree of contralateral neglect, suggesting that, in respect to spatial attention, the right parietal lobe is truly dominant (Weintraub and Mesulam). A clever observation of Bisiach and Luzzatti has suggested that the loss of attention to one side of the environment extends to the mental representation of space. Their patient with a right parietal lesion was asked to describe from memory the buildings lining the Piazza del Duomo, first as if seen from one corner of the piazza and then from the opposite corner. Perhaps another aspect of parietal lobe physiology, revealed by human disease, is the loss of exploratory and orienting behavior with the contralateral arm and even a tendency to avoid tactile stimuli. DennyBrown and Chambers attribute the released grasping and exploring that follow frontal lobe lesions to a disinhibition of inherent parietal lobe automatisms, but we have no way of confirming this. It is of interest that demented patients with prominent grasp reflexes tend not to grasp parts of their own bodies unless there has been a parietal lesion, in which case there may be "self-grasping" of the forearm opposite the lesion (Ropper). Conventional treatments for hemispatial neglect use prismatic glasses and training in visual exploration of the left side. Of some interest has been an approach that demonstrates improvement by the application of vibratory stimulation to the right side of the neck as reported by Karnath and colleagues or of the ipsilateral labyrinth by caloric or electrical means (a similar treatment has been successful in some cases of dystonic torticollis, see Chap. Gerstmann Syndrome this syndrome provides the most striking example of what might be viewed as a bilateral asomatognosia and is due to a left or dominant parietal lesion. The characteristic features are inability to designate or name the different fingers of the two hands (finger agnosia), confusion of the right and left sides of the body, and inability to calculate (dyscalculia) and to write (dysgraphia). One or more of these manifestations may be associated with word-blindness (alexia) and homonymous hemianopia or a lower quadrantanopia, of which the patient is usually unaware. The lesion is in the inferior parietal lobule (below the interparietal sulcus), particularly the angular gyrus or subjacent white matter of the left hemisphere. There has been a dispute as to whether the four main elements of the Gerstmann syndrome have a common basis or only an association. Benton states that they occur together in a parietal lesion no more often than do constructional apraxia, alexia, and loss of visual memory and that every combination of these symptoms and those of the Gerstmann syndrome occurs with equal frequency in parietal lobe disease. Others, including the authors, tend to disagree and believe that right-left confusion, digital agnosia, agraphia, and acalculia have special significance, possibly being linked through a unitary defect in spatial orientation of fingers, body sides, and numbers. The relationship between the fingers and the ability to enumerate is especially intriguing and relates to other arithmetic difficulties, discussed below. Dyscalculia has attracted little critical attention, perhaps because it occurs most often as a by-product of aphasia and an inability of the patient to appreciate numerical language. Primary dyscalculia is usually associated with the other elements of the Gerstmann syndrome. Computational difficulty may also be part of the more complex visuospatial abnormality of the nondominant parietal lobe; there is then difficulty in the placing of numbers in specific spatial relationships while calculating. In such cases, there is no difficulty in reading or writing the numbers or in describing the rules governing the calculation, but the computation cannot be accomplished correctly with pencil and paper. An analysis of how computation goes awry in each individual case is therefore required. Lesions of the superior parietal lobule may interfere with voluntary movement of the opposite limbs, particularly the arm, as pointed out by Holmes. In reaching for a visually presented target in the contralateral visual field and to a lesser extent in the ipsilateral field, the movement is misdirected and dysmetric (the distance to the target is misjudged). This disorder of movement, mentioned above in the general discussion of parietal signs and sometimes referred to as optic ataxia, resembles cerebellar ataxia and may be explained by the fact that cortical areas 7 and 5 receive visual projections from the parastriate areas and proprioceptive ones from the cerebellum, both of which are integrated in the multimodal parietal cortex. Areas 5 and 7, in turn, project to frontal areas 6, 8, and 9, where ocular scanning and reaching are coordinated. They can no longer use common implements and tools, either in relation to their bodies. It is of interest that, in both agraphia and acalculia, the motor defect is intertwined with some of these agnosic defects; hence the term apractognosia seems appropriate for the combined problem. From the above descriptions, it is evident that the left and right parietal lobes function differently. The most obvious difference, of course, is that language and arithmetical functions are centered in the left hemisphere. It is hardly surprising, therefore, that verbally mediated or verbally associated spatial and praxic functions are more affected with left-sided than with right-sided lesions. It must also be realized that language function involves cross-modal connections and is central to all cognitive functions. Hence cross-modal matching tasks (auditory-visual, visual-auditory, visual-tactile, tactile-visual, auditory-tactile, etc. Such patients can read and understand spoken words but cannot grasp the meaning of a sentence if it contains elements of relationship. The recognition and naming of parts of the body and the distinction of right from left and up from down are learned, verbally mediated spatial concepts that are disturbed by lesions in the dominant parietal lobe. If the lesion is small and predominantly cortical, optokinetic nystagmus is usually retained; with deep lesions, it is abolished, with the target moving ipsilaterally (see Chap. From time to time, severe left-sided visual neglect results from a lesion in the right angular gyrus (see Mort and colleagues). With posterior parietal lesions, as noted by Holmes and Horrax, there are deficits in localization of visual stimuli, inability to compare the sizes of objects, failure to avoid objects when walking, inability to count objects, disturbances in smooth-pursuit eye movements, and loss of stereoscopic vision. Cogan observed that the eyes may deviate away from the lesion on forced lid closure, a "spasticity of conjugate gaze"; we have been able to elicit this sign only rarely. Visual Disorientation and Disorders of Spatial (Topographic) Localization Spatial orientation depends on the integration of visual, tactile, and kinesthetic perceptions, but there are instances in which the defect in visual perception predominates. Patients with this disorder are unable to orient themselves in an abstract spatial setting (topographagnosia). Such patients cannot draw the floor plan of their house or a map of their town- or of the United States- and cannot describe a familiar route, as from home to work, for example, or find their way in familiar surroundings. This disorder is almost invariably caused by lesions in the dorsal convexity of the right parietal lobe, and it is separable from the anosognosia discussed earlier. A common and striking disorder of motor behavior of the eyelids is seen in many patients with large acute lesions of the right parietal lobe. This gives the erroneous impression that the patient is drowsy or stuporous, but it will be found that a quick reply is given to whispered questions. In more severe cases, the lids are held shut and opening is strongly resisted, to the point of making an examination of the pupils and fundi impossible. Auditory Neglect this defect in appreciation of the left side of the environment is less apparent than is visual neglect, but it is no less striking when it occurs. Many patients with acute right parietal lesions are initially unresponsive to voices or noises on the left side, but the syndrome is rarely persistent. Special tests, however, demonstrate, in many of these patients, a displacement of the direction of the perceived origin of sounds toward the left. This defect is separable from visual agnosia (see De Renzi et al); curiously, it may be worsened by the introduction of visual cues. Subtle differences between the allocation of spatial attention to sound (auditory neglect) and a distortion in its localization may be found in different cases, but the main lesion usually lies in the right superior lobule, and the same bias for left hemispheric lesions applies as for visual inattention. Corticosensory syndrome and sensory extinction (or total hemianesthesia with large acute lesions of white matter) B. Mild hemiparesis (variable), unilateral muscular atrophy in children, hypotonia, poverty of movement, hemiataxia (all seen only occasionally) C. Homonymous hemianopia or inferior quadrantanopia (incongruent or congruent) or visual inattention D. Abolition of optokinetic nystagmus with target moving toward side of the lesion E. Effects of unilateral disease of the dominant (left) parietal lobe (in right-handed and most left-handed patients)- additional phenomena include A. Gerstmann syndrome (dysgraphia, dyscalculia, finger agnosia, right-left confusion) C. Anosognosia, dressing and constructional apraxias (these disorders may occur with lesions of either hemisphere but one observed more frequently and are of greater severity with lesions of the nondominant one) D. Visual spatial imperception, spatial disorientation, and complete or partial Balint syndrome (optic apraxia, described below) With all these parietal syndromes, if the disease is sufficiently extensive, there may be a reduction in the capacity to think clearly as well as inattentiveness and slightly impaired memory. It is still not possible to present an all-embracing formula of parietal lobe function. In this way, parietal lesions cause disorders of specific types of self-consciousness or self-awareness that are tied to sensory modalities, but they do not do so in the fundamental way that results from lesions of the temporal lobe. And, as Hubel and Wiesel have shown, the response patterns of neurons in both occipital lobes to edges and moving visual stimuli, to onand-off effects of light, and to colors are much different from what was originally supposed. Hence, form, location, color, and movement each have separate localizable mechanisms. The monographs of Polyak and of Miller contain detailed information about the anatomy and physiology of this part of the brain.
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