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In contrast, acute polyneuropathy that appears for the first time in mid- or late adult life is not likely to be porphyric. The neurologic manifestations are usually those of an acute polyneuropathy involving the motor nerves more severely than the sensory ones; less often both sensory and motor nerves are affected more or less equally and sometimes autonomic nerves as well. The symptoms may begin in the feet and legs and ascend, or they may begin in the hands and arms (sometimes asymmetrically) and spread in a few days to the trunk and legs. Often, the weakness predominates in the proximal muscles of the limbs and limb girdle muscles, in which case there is loss of knee jerks with preservation of reflexes at the ankles. Facial paralysis, dysphagia, and ocular palsies are features of only the most severe cases. Severe cases may progress to a fatal respiratory or cardiac paralysis in a few days, or the symptoms may advance in a saltatory fashion over several weeks, resulting in a severe sensorimotor paralysis that improves only after many months. A disturbance of cerebral function (confusion, delirium, visual field defects, and convulsions) is likely to precede the severe but not always the mild forms of polyneuropathy, or there may be none of these central features. Cerebral manifestations subside in a few days or weeks, though one of our patients was left with a lasting homonymous hemianopia. Tachycardia and hypertension are frequent in the acute phase of the disease, and fever and leukocytosis may also occur in severe cases. In general, the prognosis for ultimate recovery is excellent, though relapse of the porphyria may result in cumulative involvement of the peripheral nervous system (see discussion of relapsing polyneuropathy further on). In summary, the most characteristic features are the relapsing nature, acute onset, abdominal pain, psychotic symptoms, predominant motor neuropathy, often, an early bibrachial distribution of weakness, truncal sensory loss, and tachycardia. The pathologic findings in the peripheral nervous system vary according to the stage of the illness at which death occurs. In the first few days, the myelinated fibers may appear entirely normal, despite an almost complete paralysis. If symptoms had been present for weeks, degeneration of both axons and myelin sheaths are found in most of the peripheral nerves. The relation between the abnormality of porphyrin biosynthesis in the liver and nervous dysfunction has never been explained satisfactorily. The diagnosis is confirmed by the demonstration of large amounts of porphobilinogen and -aminolevulinic acid in the urine. The urine turns dark when standing due to the formation of porphobilin, an oxidation product of porphobilinogen. Treatment the use of intravenous glucose and intravenous hematin (4 mg/kg daily for 3 to 14 days) is recommended as the most direct and effective therapy (Windebank and Bonkovsky). Other aspects of treatment include respiratory support, use of beta-blocking agents (labetalol) if tachycardia and hypertension are severe, intravenous glucose to suppress the heme biosynthetic pathway, and pyridoxine (100 mg twice a day) on the supposition that vitamin B6 depletion has occurred.

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Natural respiration cannot be sustained; only cardiac action and blood pressure are maintained. At autopsy one finds that most if not all the gray matter of cerebral, cerebellar, and brainstem structures- and in some instances even the upper cervical spinal cord- has been severely damaged. These patients are able to walk, but their arms dangle and their hips may be weak. The interested reader may consult the appropriate chapter in the text on neurologic intensive care by Ropper and associates for further details. Myoclonus is a grave sign in most cases, but it generally recedes after several hours or a few days. Delayed Postanoxic Encephalopathy this is a relatively uncommon and unexplained phenomenon. Initial improvement, which appears to be complete, is followed after a variable period of time (1 to 4 weeks in most instances) by a relapse, characterized by apathy, confusion, irritability, and occasionally agitation or mania. Most patients survive this second episode, but some are left with serious mental and motor disturbances (Choi; Plum et al). In still other cases, there appears to be progression of the initial neurologic syndrome with additional weakness, shuffling gait, diffuse rigidity and spasticity, sphincteric incontinence, coma, and death after 1 to 2 weeks. Exceptionally, there is yet another syndrome in which an episode of hypoxia is followed by slow deterioration, which progresses for weeks to months until the patient is mute, rigid, and helpless. In such cases the basal ganglia are affected more than the cerebral cortex and white matter as in the case studied by our colleagues Dooling and Richardson. Instances have followed cardiac arrest, drowning, asphyxiation, and carbon monoxide poisoning. In exceptional cases, however, the provision of adequate fluid, vasopressor, and respiratory support allows preservation of the somatic organism in a comatose state for longer periods. Posthypoxic Neurologic Syndromes the permanent neurologic sequelae or posthypoxic syndromes observed most frequently are as follows: 1. With lesser degrees of cerebral injury, dementia with or without extrapyramidal signs 3. Extrapyramidal (parkinsonian) syndrome with cognitive impairment (discussed in relation to carbon monoxide poisoning) 4. A Korsakoff amnesic state If ischemic hypoperfusion dominates, the patient may also display the manifestations of watershed infarctions, situated between the end territories of the major cerebral vessels. Visual agnosias including Balint syndrome and cortical blindness (page 406), representing infarctions of the watershed between the middle and posterior cerebral arteries.


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All of this suggests that these special memories, or coded forms of them, through a process of relearning and habituation, come to be stored or filed in other regions of the brain; i. Not known is how a disease process, acting over a brief period of time, not only impairs all future learning but also wipes out portions of a vast reservoir of past memories that had been firmly established for many years before the onset of the illness. Also unknown are the anatomic and physiologic mech- Classification of Diseases Characterized by an Amnesic Syndrome the amnesic (Korsakoff) syndrome may be a manifestation of several neurologic disorders, identified by their mode of onset and clinical course, the associated neurologic signs, and ancillary findings (Table 21-5). Each of the amnesic states listed in Table 21-5 is considered at an appropriate point in subsequent chapters of this book. The only exception is the striking syndrome of transient global amnesia, the nature of which is not certain. It cannot be included with any assurance with the epilepsies or the cerebrovascular diseases or any other category of disease and is therefore considered here. Transient Global Amnesia this was the name applied by Fisher and Adams to a particular type of memory disorder that they observed in more than 20 middle-aged and elderly persons. The condition was characterized by an episode of amnesia and bewilderment lasting for several hours. During the attack, there was no impairment in the state of consciousness, no other sign of confusion, and no overt seizure activity; personal identification was intact, as are motor, sensory, and reflex functions. Unlike those with psychomotor epilepsy, the patient is alert, in contact with his surroundings, and capable of high-level intellectual activity and language function during the attack. As soon as the attack has ended, no abnormality of mental function is apparent except for a permanent gap in memory for the period of the attack itself and for a brief period (hours or days) preceding the attack. The condition is among the most curious in neurology but is often mistaken for a psychiatric episode. Hodges and Ward have made detailed psychologic observations in five patients during an episode. The psychologic deficit, except for its transience, was much the same as that in the permanent amnesia syndrome. Personality, cognition involving highlevel functioning, semantic language, and visuospatial discrimination were all preserved. The extent of retrograde amnesia was highly variable, but characteristically it shrank after the attack, leaving a permanent retrograde gap of about 1 h. However, some mild impairment of new learning persisted for up to a week after the acute attack. The recurrence of such attacks is not uncommon, having been noted in 66 of 277 patients who were observed for an average period of 80 months (Miller et al) and in 16 of 74 patients followed for 7 to 210 months (Hinge et al). One of our patients had more than 50 attacks, but among all the rest (more than 100 cases), 5 was the maximum. It seems children are not susceptible to the condition; however, a 13-yearold and 16-year-old with migraine were reported to have had similar attacks during participation in sports (Tosi and Righetti). No consistent antecedent events have been identified, but certain ones- such as a highly emotional experience, pain, exposure to cold water, sexual intercourse, and mild head trauma- have been reported in some cases (Haas and Ross; Fisher).

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The flow chart in Figure 37-4, which divides these disorders into dysmorphic, visceromegalic, and purely neurologic groups, is equally serviceable in the differential diagnosis of both age groups. As with the early infantile diseases, certain clusters of neurologic, skeletal, dermal, ophthalmic, and laboratory findings are highly distinctive and often permit the identification of a particular disease. Corneal clouding- several of the mucopolysaccharidoses (Hurler, Scheie, Morquio, Maroteaux-Lamy), mucolipidoses, tyrosinemia, aspartylglycosaminuria (rare) b. Optic atrophy and blindness- metachromatic leukodystrophy, neuroaxonal dystrophy. Impairment of vertical eye movements- late infantile Niemann-Pick disease, juvenile dystonic lipidosis, seablue histiocyte syndrome, Wilson disease h. Extrapyramidal signs- late-onset Niemann-Pick disease (rigidity, abnormal postures), juvenile dystonic lipidosis (dystonia, choreoathetosis), Rett, ataxia-telangiectasia (athetosis), Sanfilippo mucopolysaccharidosis, type I glutaric acidemia, Wilson disease, Segawa dopa-responsive dystonia 5. Dwarfism, spine deformities, arthropathies- Hurler, Morquio, and other mucopolysaccharidoses, Cockayne syndrome 7. Beaked thoracolumbar vertebrae- all mucopolysaccharidoses, mucolipidoses, mannosidosis, fucosidosis; aspartylglycosaminuria, multiple sulfatase deficiencies 10. Vacuolated lymphocytes- all mucopolysaccharidoses, mucolipidoses, mannosidosis, fucosidosis 13. Leigh disease may begin at the same age, with hypotonia and optic atrophy, but abnormalities of ocular movement and respiration appear early; in many cases the lactic acidosis and pyruvate decarboxylase defect will corroborate the diagnosis. Sequencing tests of the mitochondrial genome now allow definitive diagnosis in most cases, as described in a later section. Lipofuscinosis cannot always be diagnosed accurately; curvilinear bodies in nerve twigs and in the endothelial cells in skin biopsies and the recently discovered gene mutations are the most informative laboratory tests. There is a tendency for them to be less severe and less rapidly progressive, an attribute shared by many diseases with a dominant mode of inheritance. Nonetheless, there are diseases, such as Wilson disease, in which the onset of neurologic symptoms occurs after the 10th year and in rare instances after the 30th year, and the mode of inheritance is recessive in type. However, in the latter instance, the basic abnormality has existed since early childhood in the form of a ceruloplasmin deficiency with early cirrhosis and splenomegaly; only the neurologic disorder is of late onset. This brings us to another principle- that the pathogenesis of the cerebral lesion may involve a factor or factors once removed from the underlying biologic abnormality. Genetic heterogeneity poses another problem with respect to both the clinical and biochemical findings.

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Symonds elaborated this view and saw in the shearing stresses- which are maximal at the point where the cerebral hemispheres rotate on the relatively fixed brainstem. The extension of this idea, namely that diffuse axonal injury throughout the cerebral white matter is the main cause of persistent unconsciousness, has been widely adopted but- as we discuss further on- is open to dispute. Indeed, even the proponents of diffuse axonal injury as an important effect of severe brain damage have found that thalamic lesions are almost always present in cases of prolonged coma or the persistent vegetative state (Adams et al 2000). Clinical Manifestations of Concussion the immediate abolition of consciousness, suppression of reflexes (falling to the ground if standing), transient arrest of respiration, a brief period of bradycardia, and fall in blood pressure following a momentary rise at the time of impact are the characteristic clinical signs of concussive injury. Rarely, if these abnormalities are sufficiently intense, death may occur at the moment of impact, presumably from respiratory arrest. Usually the vital signs return to normal and stabilize within a few seconds while the patient remains unconscious. Brief tonic extension of the limbs, clonic convulsive movements lasting up to about 20 seconds and other peculiar movements may occur immediately after the loss of consciousness (see McCrory et al). These "concussive convulsions" are probably of little significance and have not been shown to confer an increased risk of future seizures. McCrory and colleagues noted an association between motor and convulsive movements and facial impact, and we have seen this feature twice in teenagers who collided while pursuing a ball. Then, after a variable period of time, the patient begins to stir and opens his eyes but is unseeing. Corneal, pharyngeal, and cutaneous reflexes, originally depressed, return, and the limbs are withdrawn from painful stimuli. Gradually contact is made with the environment, and the patient begins to obey simple commands and respond slowly and inadequately to simple questions. Memories are not formed during this period; the patient may even carry on a conversation which, later on, he cannot recall. Finally there is full recovery, corresponding to the time when the patient can form consecutive memories of current experiences. The time required for the patient to pass through these stages of recovery may be only a few seconds or minutes, several hours, or possibly days; but again, between these extremes there are only quantitative differences, varying with the intensity of the process. To the observer, such patients are comatose only from the moment of injury until they open their eyes and begin to speak; however, for the patient, the period of unconsciousness extends from a point before the injury occurred (retrograde amnesia) until the time when he is able to form consecutive memories- at the end of the period of anterograde amnesia. The duration of the amnesic period, particularly of anterograde amnesia, is the most reliable index of the severity of the concussive injury. If there is no disturbance or loss of consciousness, none of the lesions described below are likely to be found.

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Under pathological conditions, Th1 cells will cause diseases like Rheumatoid arthritis, Inflammatory bowel disease and other organ related autoimmune diseases such as Multiple sclerosis. It is also responsible for the general inflammatory processes we see in the tissues in general. Th2 cells are also the pathway through which allergic phenomena are mediated in pathological circumstances. In the normal organism, there is a constant oscillation between Th0, Th1 and Th2 cells and this oscillation has a chronobiology similar to most of our other regulatory systems. In factTh1/Th2 oscillation is under the control of the neuroendocrine system, and will follow its diurnal rhythm. Another mechanism which achieves this Th1/Th2 oscillation is the inhibitory effect the Th1 and Th2 secreted cytokines will have on each other. According to Heine, any substance in the dilution from 1X-14X will have the effect of generating a Th3 response, and to a lesser extent, a Th2 response. The bystander reaction this refers, as its name implies, to the induction of cells by a relative non-toxic antigen which will then have an effect on a process such as an inflammation which was started by another antigen somewhere else in the body. Figure 3: the bystander reaction Introduction 13 Antigen presentation and motif formation In order to initiate the bystander reaction we need a small dose of antigen, or a remedy containing plant extract, suis organ extract, animal venom or a nosode, each in a specific dilution. There will be a motif for each of the ingredients, thus if we give Traumeel, one for Arnica, one for Bellis perennis, etc. There will be a Th3 type cell for each of the motifs presented, thus one for Arnica, Bellis perennis and so forth. Chemotaxis and suppression the millions of cloned Th3 cells will then through chemotaxis find the inflammation caused by Th1, Th2 and Th4 lymphocytes and suppress them, thereby restoring the balance and normal oscillation between Th1/Th2 cells. Here the law of similars is at work, as each Th3 cell for Arnica or Bellis perennis for instance, will find the corresponding Th1/Th2 cell which looks similar to its motif and suppress it. Summary the immunological bystander reaction serves as a model for the working mechanism of immunomodulatory remedies which, through a non-toxic substance in a specific dilution can induce a regulatory cell, the Th3 cell. This regulatory cell, while developed at another site, and acting as an innocent bystander can bring about a balance in the immune system, by down-regulating an inflammatory process started by another noxious homotoxin remote from its own activation. The Th3 cell acts as a fulcrum on which the balance of Th1 and Th2 cells rests (Figure 4). He theorized that by giving a non-toxic substance the defense system of the body is activated through another pathway in order to bring about homeostasis. Introduction to remedies in Homotoxicology Homotoxicological medicines have been developed to serve the very specific purpose of restoring regulation in the organism.

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Treatment the slow, intermittently progressive course of cervical myelopathy with long periods of relatively unchanging symptomatology makes it difficult to evaluate therapy. Assuming that the prevailing opinion of the mechanisms of the cord and root injury is correct, the use of a soft collar to restrict anteroposterior motions of the neck seems reasonable. This form of treatment alone may be sufficient to control the discomfort in the neck and arms. Only exceptionally in our experience has arm and shoulder pain alone been sufficiently severe and persistent to require surgical decompression unless there is a laterally protruded disc or osteophytic constriction of a root foramen. Most of our patients have been dissatisfied with this passive approach and are unable to wear a collar for prolonged periods. If osteophytes have narrowed the spinal canal at several interspaces, a posterior decompressive laminectomy with severance of the dentate ligaments helps to prevent further injury. The results of such a procedure are fairly satisfactory (Epstein and Epstein); in fully two-thirds of the patients, improvement in the function of the legs occurs, and in most of the others, progression of the myelopathy is halted. The operation carries some risk; rarely, an acute quadriplegia- due presumably to manipulation of the spinal cord and damage to nutrient spinal arteries- has followed the surgical procedure. When only one or two interspaces are the site of osteophytic overgrowths, their removal by an anterior approach has given better results and carries less risk. Newer techniques have been developed in which titanium cages are used to stabilize the adjacent vertebrae thereby obviating the need for bone grafts to fuse adjacent bodies; the conventional process using bone grafts requires many weeks or longer and stabilization in a hard collar. Unfortunately, the long-term results after surgical treatment are less than ideal. Ebersold and colleagues evaluated the outcomes in 84 patients in whom the median duration of follow-up was 7 years. In the group of 33 patients who had undergone anterior decompressive procedures, 18 had improved, 9 were unchanged, and 6 had deteriorated. Of the 51 patients who underwent posterior decompression, 19 had improved, 13 were unchanged, and 19 were worse at their last follow-up examinations. These results, similar to those of most other series, indicate that the long-term outcome varies and that a significant proportion, even after adequate decompression and initial improvement, have persistent symptoms or undergo some degree of later functional deterioration. Whether the new surgical appliances previously mentioned give more satisfactory results is not known but they certainly make recovery easier and more rapid. Lumbar Stenosis this is another spondylotic abnormality, seen with particular frequency in older individuals, especially men. Usually it declares itself by numbness and weakness of the legs, sometime with poor control of sphincters. There is said to be generally little or no pain or only a spine ache that fluctuates from day to day but in our experience the majority of patients have backache and sciatica or a smiliar back or leg pain from associated osteoarthritis or discogenic disease. A notable feature is induction or aggravation of the neurologic symptoms upon standing and walking (neurologic claudication). This topic is disucssed further on page 179, which should be consulted for further discussion.

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If a woman with seizure disorder has been off epilepsy medications for a time before getting pregnant and seizes during the pregnancy, the best choice of medications is probably phenytoin. It should also be mentioned that most anticonvulsants induce the activity of hepatic enzymes, and this may result in the failure of contraceptive pills due to the accelerated metabolism of steroids. Epileptic women of childbearing age should be advised that higher doses of the estradiol component are required. Skin Eruptions from Antiepileptic Drugs As mentioned in the discussion above, these are the most common idiosyncratic reactions to the drugs used to treat epilepsy. The aromatic compounds (phenytoin, carbamazepine, phenobarbital, primidone, and lamotrigine) are the ones most often responsible. Furthermore, there is a high degree of cross-reactivity within this group, particularly between phenytoin, carbamazepine and phenobarbital, and possibly lamotrigine. The typical eruption is maculopapular, mainly on the trunk; it usually resolves within days of discontinuing the medication. More severe rashes may develop, sometimes taking the form of erythema multiforme and Stevens-Johnson syndrome, or even toxic epidermal necrolysis. A rare hypersensitivity syndrome is one of high fever, rash, lymphadenopathy, and pharyngitis. If any of these reactions require that one of the aromatic drugs be replaced, valproate, gabapentin, topiramate, or levetiracetam are reasonable substitutes, depending, of course, on the nature of the seizures. Treatment of Seizures in the Neonate Treatment of the special types of convulsions in the neonatal period and in infancy and childhood is discussed by Fenichel and by Volpe. Probably the form of epilepsy that is most difficult to treat is the childhood Lennox-Gastaut syndrome. Some of these patients have as many as 50 or more seizures per day, and every combination of anticonvulsant medications may have no effect. Valproic acid (900 to 2400 mg/day) will reduce the frequency of spells in approximately half the cases. The newer drugs- lamotrigine, topiramate, vigabatrin- are each beneficial in about 25 percent of cases. Most patients who die of epilepsy do so because of uncontrolled seizures of this type, complicated by the effects of the underlying illness or an injury sustained as a result of a seizure. Rising temperature, acidosis, hypotension, and renal failure from myoglobinuria is a sequence of life-threatening events that may be encountered in cases of status epilepticus. Prolonged convulsive status (for longer than 30 min) also carries a risk of serious neurologic sequelae ("epileptic encephalopathy"). With regard to acute medical complications, from time to time a case of neurogenic pulmonary edema is encountered during or just after the convulsions, and some patients may become extremely hypertensive, then making it difficult to distinguish the syndrome from hypertensive encephalopathy. Treatment (Table 16-9) the many regimens that have been proposed for the treatment of status attest to the fact that no one of them is altogether satisfactory and none is clearly superior (Treiman et al). A large-bore intravenous line is inserted; blood is drawn for glucose, blood urea nitrogen, electrolytes, and a metabolic and drug screen.

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There are now prospective data from three groups (see below) showing that 74 Gy is tolerable in the setting of concurrent chemotherapy. We expect that patients on the 74 Gy experimental arms will experience increased acute toxicity. Therefore, we have planned quality of life measures that will assess toxicity on all arms. The present study is based upon a combination of the data from the studies described above. The addition of biologic therapy with cetuximab to the regimen hopefully will result in even better efficacy. A subsequent report demonstrated that the difference in survival was attributed to improved intrathoracic tumor control. Criticisms of this trial include the split-course radiotherapy used in the concurrent arm and the lower doses of radiotherapy employed. Four-year survival rates were higher in the concurrent arms (12%, 17%, and 21% for sequential therapy, concurrent cisplatin/etoposide and hyperfractionated radiation, and cisplatin/vinblastine/radiation arms, respectively). Acute grade > 3 toxicities were higher for concurrent therapies and highest for the concurrent/hyperfractionation group: sequential (30%), concurrent/daily (48%), and concurrent/hyperfractionation (62%). A third trial comparing concurrent versus sequential chemoradiation reported in 2001 also explored the use of consolidation chemotherapy. However, the incidence of grade 3 esophagitis was significantly higher in the concurrent arm (28% vs. Based on these results, concurrent chemoradiation has become the standard of care since 2001. It is important to note that toxicity is significantly greater with concurrent chemotherapy. Rationale for Carboplatin and Paclitaxel the cisplatin-based regimens used in the previously cited randomized trials are less commonly employed in primary chemoradiation therapy regimens today. Treatment was generally well tolerated, although two patients died from probable radiation-induced pneumonitis. The median progression-free survival was 16 months, median survival was 26 months, and three-year survival rate was 37%. One utilizes fullstrength (systemic) chemotherapy, whereas the second approach uses lower dose chemotherapy as a radiation sensitizer. A typical regimen using the first approach would be fullstrength cisplatin/etoposide; the second common regimen is carboplatin/paclitaxel in reduced doses. Some oncologists feel that if the latter regimen is used, additional full-dose chemotherapy needs to be given. There are advocates of all these approaches, but none of them have been tested head-to-head. Local control with conventional radiotherapy is inadequate; using posttherapy bronchoscopic biopsies, Le Chevalier, et al.

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Presumably, the high-frequency electrical impulses cause a disruption of local neuronal activity that is the functional equivalent to an ablative lesion, but the effects may be more complex by way of stimulating neurotransmitter release. The observed improvement in the L-dopa-induced dyskinesias has recently led to the earlier more liberal use of subthalamic stimulators. Readjustment of the frequency of the stimulus and breakage of the wire are minor problems. Hemorrhage into the basal ganglia and local infection near the stimulator has occurred in a small number of patients so treated. The cerebral implantation of embryonic adrenal medullary tissue from 8- to 10-week-old human fetuses has provided a modest but undeniable improvement in motor function (Spencer et al, Freed et al), and some patients also appear to have benefited from the striatal implantation of human fetal and porcine nigral cells and autologous adrenal cells. The study by Freed and colleagues found a small improvement on a global scale that measures functional, psychologic, and neurologic aspects only in younger patients. These procedures are hampered by many difficulties, mainly in obtaining tissue and the failure of grafts to survive but also the problem of uncontrollable dyskinesias in some patients. Other Ancillary Treatments Finally, in the management of the patient with Parkinson disease, one must not neglect the maintenance of optimum general health and neuromuscular efficiency by a planned program of exercise, activity, and rest; expert physical therapy and exercises such as those performed in yoga may be of help in achieving these ends. Postural imbalance and falls can be greatly mitigated by the use of a cane or walking frame. A number of excellent exercise programs have been devised specifically for patients with Parkinson disease, and measures such as massage and yoga have their advocates. Our position has been that any activity that keeps the patient active and committed is of great value. Focal dystonias of the foot are partially treatable with local injections of botulinum toxin. In addition, the patient often needs a great deal of emotional support in dealing with the stress of the illness, in comprehending its nature, and in carrying on courageously in spite of it. Striatonigral Degeneration, Shy-Drager Syndrome, and Multiple System Atrophy Closely related to Parkinson disease but with a different pathologic basis is a state designated by Adams and colleagues as striatonigral degeneration. The pathologic changes were found by chance in four middle-aged patients, none with a family history of similar disease, in three of whom a parkinsonian syndrome had been described clinically. In one of the three, who had been examined carefully, the typical rigidity, stiffness, and akinesia had begun on one side of the body, then spread to the other, and progressed over a 5-year period, but with little or none of the characteristic tremor of idiopathic Parkinson disease. A flexed posture of the trunk and limbs, slowness of all movements, poor balance, mumbling speech, and a tendency to faint when standing were other elements in the clinical picture. Mental function was intact, and there were no reflex changes, no suck and grasp reflexes, and no cerebellar signs or involuntary movements. The other two patients had been seen by competent neurologists who had made a diagnosis of Parkinson disease.


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