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Some individuals with moderately severe retardation are pleasant and amiable and achieve a rather satisfactory social adjustment medicine during pregnancy buy discount indinavir 400mg. At the opposite end of the behavioral scale are the syndromes of autism and that of Smith-Magenis and of DeLange symptoms 2015 flu discount indinavir 400mg with visa, in which the individual fails to 1950s medications indinavir 400 mg free shipping manifest normal interpersonal social contact medicine during the civil war 400mg indinavir amex, including communicative language. The phenylketonuric child is usually irritable, unaffectionate, and implacable, and the same is said of certain other forms of retardation, such as those with the DeLange syndrome, discussed earlier in the section on retardation with dwarfism. Regarding differences in activity levels, many retarded individuals are slow, clumsy, and relatively akinetic. Others, as many as half, display an incessant hyperactivity characterized by a restless, seemingly inquisitive searching of the environment. They may be destructive and recklessly fearless and impervious to the risk of injury. Some exhibit a peculiar anhedonia that renders them indifferent to both punishment and reward. Other aberrant types of behavior, such as violent aggressiveness and self-mutilation, are common. Rhythmic rocking, head-banging, incessant arm movements- so-called rhythmias or movement stereotypies- are observed in the majority of those who are severely and moderately severely retarded. These movements are maintained hour after hour without fatigue and may be accompanied by breathing sounds, squeals, and other exclamations. A number of them tend to be particularly common in certain forms of retardation: hand-flapping in autism, hand-wringing in Rett syndrome, and hand-waving in Down syndrome and other disorders. Self-stimulation, even hurtful- such as striking the forehead or ears or biting the fingers and forearms- seems to be compulsive or perhaps to provide some sort of satisfaction. It is not that these rhythmias are by themselves abnormal, for some of them occur for brief periods in normal babies, but that they persist. Nevertheless, many moderately retarded persons, when assigned to a simple task such as putting envelopes in a box, can continue this activity under supervision for several hours. In the least severe types of retardation, all the mental activities are intact but subnormal. The point to be made is that all aspects of intellectual life, personality, and deportment are affected in slightly but differing degrees and that these effects have a neurologic basis. There is more than a hint that in particular diseases, because of their anatomy, the cognitive experience, affective life, and behavior are affected in special ways. The group of moderately retarded, like the severely retarded, is divisible into groups with somatic systemic and neurologic abnormalities, though the proportions are not the same. There are fewer of the dysmorphic type and more of the nondysmorphic, nonneurologic group. Etiology of Severe Mental Retardation From Table 38-1 it is obvious that many diseases can blight the development and maturation of the brain, leaving it in an arrested state. Some affect all parts of the organism, giving rise to associated dermal, skeletal, and visceral abnormalities, while others affect only the nervous system in particular patterns. With respect especially to the milder degrees of mental retardation, in all populations thus far studied, as mentioned above, infants of extremely low birth weight are more likely to have disabilities, brain abnormalities, and poorer language development and scholastic achievement. Mild mental retardation also tends to correlate with lower social status, which must relate in some manner to biological factors, as pointed out in the Scottish Low-Birth-Weight Study. Viral and spirochetal infections and parturitional accidents are other common causes. The factor of malnutrition during the fetal or infantile period of life as a cause of severe mental retardation has received considerable attention because it is a worldwide problem. Animal experiments by Winick and others have demonstrated that severe undernutrition in early life leads to behavioral abnormalities and biochemical and morphologic changes in the brain, which may be permanent (see Chap. Galler studied a group of infants in Barbados who were severely malnourished during the first year of life and then given an adequate diet. These children were followed to adulthood and compared with normally nourished siblings. Galler observed no effect on physical growth, but there were persistent attention deficits in 60 percent of the undernourished group and in only 15 percent of controls.

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Periorbital and supraorbital pain medicine 7767 indinavir 400mg visa, while sometimes indicative of local disease treatment 2014 generic indinavir 400 mg overnight delivery, may reflect dissection of the cervical portion of the internal carotid artery 5 medications for hypertension generic 400 mg indinavir free shipping. Headaches localized to treatment dynamics florham park indinavir 400 mg free shipping the vertex or biparietal regions are infrequent and should raise the suspicion of sphenoid or ethmoid sinus disease or thrombosis of the superior sagittal venous sinus. The mode of onset, time-intensity curve, and duration of the headache, with respect both to a single attack and to the temporal profile of the headache over a period of years, are also useful data. At one extreme, the headache of subarachnoid hemorrhage (due to a ruptured aneurysm) occurs as an abrupt attack that attains its maximal severity in a matter of seconds or minutes; or, in the case of meningitis, it may come on more gradually, over several hours or days. Migraine of the classic type usually has its onset in the early morning hours or in the daytime, reaches its peak of severity typically over several to 30 min, and lasts, unless treated, for 4 to 24 h, occasionally for as long as 72 h. A migrainous patient having several attacks per week usually proves to have a combination of migraine and tension headaches, an analgesic "rebound headache," or, rarely, some new, unexpected intracranial lesion. By contrast, the occurrence of unbearably severe unilateral orbitotemporal pain coming on within an hour or two after falling asleep or at predictable times during the day and recurring nightly or daily for a period of several weeks to months is typical of cluster headache; usually an individual attack dissipates in 30 to 45 min. The headaches of intracranial tumor may appear at any time of the day or night; they will interrupt sleep, vary in intensity, and last a few minutes to hours; as the tumor raises intracranial pressure. With posterior fossa masses, the headache tends to be worse in the morning, on awakening. Tension headaches, described further on, may persist with varying intensity for weeks to months or even longer; when such headaches are protracted, there is usually an associated depressive illness. In general, headaches that have recurred regularly for many years prove to be vascular or tension in type. The more or less constant relationship of headache to certain biologic events and also to certain precipitating or aggravating (or relieving) factors must always be noted. Headaches that occur regularly in the premenstrual period are usually generalized and mild in degree ("premenstrual tension"), but attacks of migraine may also occur at this time. Headache from infection of the nasal sinuses may appear, with clocklike regularity, upon awakening or in midmorning; it is characteristically worsened by stooping and changes in atmospheric pressure. Eyestrain headaches, of course, follow prolonged use of the eyes, as after long-sustained periods of reading, peering into glaring headlights, or exposure to the glare of video displays. In certain individuals, alcohol, intense exercise (such as weight-lifting), stooping, straining, coughing, and sexual intercourse are known to initiate a special type of bursting headache, lasting a few seconds to minutes. If the headache is made worse by sudden movement or by coughing or straining, an intracranial source is suggested. In other patients, migraine occurs several hours or a day following a period of intense activity and stress ("weekend migraine"). Some patients have discovered that their migraine is relieved momentarily by gentle compression of the carotid or superficial temporal artery on the painful side, and others report that the carotid itself is tender during the headache. Or, pain is noticed when the scalp is stroked in fixing the hair, suggesting inflammation of the temporal arteries (temporal arteritis). Interestingly, pain is practically the only sensation produced by stimulation of these structures; the pain arises in the walls of small blood vessels containing pain fibers (the nature of vascular pain is discussed further on). Of importance also are the reference sites of pain from the aforementioned structures. Pain impulses that arise from distention of the middle meningeal artery are projected to the back of the eye and temporal area. Pain from the intracranial segment of the internal carotid artery and proximal parts of the middle and anterior cerebral arteries is felt in the eye and orbitotemporal regions. The bony skull, much of the pia-arachnoid and dura over the convexity of the brain, the parenchyma of the brain, and the ependyma and choroid plexuses lack sensitivity. The sphenopalatine branches of the facial nerve convey impulses from the naso-orbital region. The ninth and tenth cranial nerves and the first three cervical nerves transmit impulses from the inferior surface of the tentorium and all of the posterior fossa. Sympathetic fibers from the three cervical ganglia and parasympathetic fibers from the sphenopalatine ganglia are mixed with the trigeminal and other sensory fibers. The central sensory connections, which ascend through the cervical spinal cord and brainstem to the thalamus, are described in the preceding chapter. To summarize, pain from supratentorial structures is referred to the anterior two-thirds of the head, i.

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The main clinical features are a subacute and widespread sensory loss that may include the trunk and a profoundly diminished kinesthetic sense 92507 treatment code discount indinavir 400 mg online, giving rise to medications 2016 cheap indinavir 400 mg with visa sensory ataxia of the limb and of gait medicine 319 cheap indinavir 400mg mastercard. Loss of pain and temperature sensation is variable; tendon reflexes are abolished symptoms discount indinavir 400mg. In time, many of these patients develop autonomic abnormalities such as bowel atony, urinary retention, loss of sweating, and pupillary changes. Even without this confirmatory test, we have found it advisable to perform a biopsy of the lip (at the epithelial-mucosal juncture) to detect inflammatory changes in the small salivary glands. In our series of 20 cases with salivary gland biopsies that demonstrated inflammatory changes diagnostic of the syndrome, only 6 had serologic evidence of the disease and two had positive serologic tests but a negative biopsy (Gorson and Ropper). The sedimentation rate in our patients was often slightly elevated, however, only 5 of our 20 had a value greater than 40 mm/min. Mellgren and also Leger and their colleagues have stressed the point that a proportion of unexplained polyneuropathies in middle and late life are caused by Sjogren syndrome. Several other studies have corroborated this finding of inflammatory disruption of the minor salivary glands in obscure neuropathies, particularly in older women and in some men. The diagnosis in our clinics, where lip biopsies are routinely performed in patients with nondescript sensory neuropathies, has not been nearly as frequent. Nerve biopsies in some cases have revealed a necrotizing vasculitis, inflammatory cell infiltrates, and focal nerve fiber destruction. The few times a dorsal root ganglion has been examined, there were infiltrates of mononuclear cells and lymphocytes and destruction of nerve cells. Treatment Treatment of the sicca complex and the neuropathic manifestations is unfortunately largely symptomatic. Corticosteroids, cyclophosphamide, and chlorambucil have been used when the neuropathy is severe and are indicated when there is vasculitis involving renal and pulmonary structures. We have administered prednisone 60 mg daily, often in tandem with intermittent plasma exchange, with little evidence of response. Idiopathic Sensory Ganglionopathies (Chronic Ataxic Neuropathy) In addition to the subacute pansensory syndrome described above and paraneoplastic, postinfectious, or toxic processes (page 1128), there is a more chronic idiopathic variety characterized by severe global sensory loss and ataxia. We have encountered several such patients with sensory loss and pronounced ataxia resembling the cases described by Dalakas. The numbness and sensory findings progressed over months and spread to proximal parts of the arms and legs and then to the trunk. There are reports of fasciculations in a few patients (but not in the ones we have seen). Yet other instances have had all the features of a truncal-limb sensory neuropathy, with little or no ataxia and only muted reflexes; these have had a more benign course but still no cause was found (why most of our patients have been male physicians, as reported by Romero, is entirely unclear). The motor nerve conduction studies have been normal or slightly impaired, while the sensory potentials were eventually lost (but they may at first be normal). A puzzling feature in two patients has been an unexpected preservation of many sensory nerve potentials even after a year of illness. In these cases the process presumably lay in the dorsal roots rather than in the ganglia.

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In such cases symptoms graves disease 400mg indinavir overnight delivery, the blink responses are delayed ipsilaterally and contralaterally as a result of conduction block in the proximal facial nerve medications side effects order indinavir 400 mg mastercard. Direct facial nerve stimulation often fails to symptoms rectal cancer order indinavir 400 mg visa demonstrate this block because only the distal segment of the nerve is amenable to medicine used for anxiety order 400 mg indinavir study. Although this test is rarely necessary for diagnosis, most patients with hereditary neuropathy have blink response abnormalities. Large acoustic neuromas may interfere with the afferent trigeminal portion of the pathway and give rise to abnormal responses on the affected side. By applying a magnetic stimulus, which induces an electrical impulse, or by a directly delivered electrical stimulus over the lower cervical or lumbar spine, it is possible to activate the motor (anterior) roots and to measure the time required to elicit a muscle contraction (Cros and Chiappa). These root stimulation tests can be quite uncomfortable for the patient because of the contraction of muscles surrounding the stimulation site. Transcranial magnetic stimulation of the cerebral cortex permits measurement of the latency of muscle contraction after excitation of motor neurons in the cortex. Thus, the integrity of the entire corticospinal system, from the cortical motor neurons through spinal tracts, anterior horn cells, and the peripheral motor nerve can be determined. By combining this technique with the previously described root stimulation, it becomes possible to measure central and peripheral motor conduction times. These forms Special Electrodiagnostic Studies of Nerve Roots and Spinal Segments (Late Responses, Blink Responses, Segmental Evoked Responses) H Reflex Information about the conduction of impulses through the proximal segments of a nerve is provided by the study of the H reflex and the F wave. In 1918, Hoffmann, after whom the H reflex was named, showed that submaximal stimulation of mixed motor-sensory nerves, insufficient to produce a direct motor response, induces a muscle contraction (H wave) after a latency that is far longer than that of the direct motor response. This reflex is based on the activation of afferent fibers from muscle spindles (the same axons that conduct the afferent volley of the tendon reflex), and the long delay reflects the time required for the impulses to reach the spinal cord via the sensory fibers, synapse with anterior horn cells, and to be transmitted along motor fibers to the muscle (see. Thus the H reflex is therefore the electrical representation of the tendon reflex circuit and is especially useful because the impulse traverses both the posterior and anterior spinal roots. The H reflex is particularly helpful in the diagnosis of S1 radiculopathy and of other polyradiculopathies. However, it may be difficult to elicit an H reflex from nerves other than the tibial. Stimuli of increasing frequency but low intensity cause a progressive depression and finally obliteration of H waves. The latter phenomenon has been used to study spasticity, rigidity, and cerebellar ataxia, in which there are differences in the frequency-depression curves of H waves. F Wave the F response, so named because it was initially elicited in the feet, was first described by Magladery and McDougal in 1950. After a latency longer than that for the direct motor response (latencies of 28 to 32 ms in arms, 40 to 50 ms in legs), a second small muscle action potential is recorded (F wave). The F wave is the result of the impulses that travel antidromically in motor fibers to the anterior horn cells, a small number of which are activated and produce an orthodromic response that is recorded in a distal muscle. These evoked potential tests find their main use in the diagnosis of multiple sclerosis and in disorders of the sensory nerve roots as discussed in Chaps. For details of their performance and interpretation the reader is referred to specialized texts on the subject. With repeated stimuli, each response will have the same waveform and amplitude until fatigue supervenes. In certain disorders, notably myasthenia gravis, a train of 4 to 10 stimuli at rates of 2 to 5 per second (optimally 2 to 3 per second), the amplitude of the motor potentials decreases and then, after four or five further stimuli, may increase slightly. A progressive reduction in amplitude is most likely to be found in proximal muscles, but these are not easily stimulated for which reason the locations most commonly used for clinical testing are the accessory nerve in the posterior triangle of the neck (trapezius), the ulnar nerve (hypothenar muscle), the median nerve at the wrist (thenar muscle), and the facial nerve and orbicularis oculi muscle. A decrement of 10 percent or more denotes a failure of a proportion of the neuromuscular junctions that are being stimulated. The sensitivity of the procedure is improved by first exercising the tested muscle for 30 to 60 s. The induced failure of neuromuscular transmission in myasthenia is similar to the one produced by curare and other nondepolarizing neuromuscular blocking agents, and both cases can be partially corrected with anticholinesterase drugs such as neostigmine and edrophonium. The myasthenic syndrome of Lambert-Eaton, often associated with oat-cell carcinoma of the lung, is characterized by a presynaptic blockage of acetylcholine release and produces the opposite defect of neuromuscular transmission to the one recorded in myasthenia gravis. During tetanic stimulation (20- to 50-per-second repetitive stimulation of nerve), the muscle action potentials, which are small or practically absent with the first stimulus, increase in voltage with each successive response until a more nearly normal amplitude is attained (see. Exercising the muscle for 10 s before stimulation will cause a similar posttetanic facilitation (200-fold increases are not uncommon).

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