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Others treatment juvenile arthritis cheap paxil 40mg with amex, such as methyl alcohol and ethylene glycol medicine 219 purchase paxil 10mg amex, act by producing a metabolic acidosis symptoms 4 weeks pregnant 20mg paxil overnight delivery. Probably this means that each disease has a distinctive mechanism and that the locus of the metabolic effect is somewhat different from one disease to another. The sudden and excessive neuronal discharge that characterizes an epileptic seizure is a common coma-producing mechanism. Usually focal seizure activity has little effect on consciousness until it spreads from one side of the brain (and the body if there is a convulsion) to the other. Coma then ensues, presumably because the spread of the seizure discharge to deep central neuronal structures paralyzes their function. In other types of seizure, in which consciousness is interrupted from the very beginning, a diencephalic origin has been postulated (centrencephalic seizures of Penfield). In "blunt", or closed head injury, it has been shown that at the moment of the concussive injury there is an enormous increase in intracranial pressure, on the order of 200 to 700 lb/in2, lasting a few thousandths of a second. The vibration set up in the skull and transmitted to the brain was for many years thought to be the basis of the abrupt paralysis of nervous function that characterizes concussive head injury. Instead, it is more likely that the sudden swirling motion of the brain induced by the blow to the head, producing a rotation (torque) of the cerebral hemispheres around the axis of the upper brainstem, is the proximate cause of loss of consciousness. These same physical forces, when extreme, cause multiple shearing lesions or hemorrhages in the diencephalon and upper brainstem. The effects of general anesthesia had for many years been attributed to changes in the physical chemistry of neuronal membranes. More recently, it has been recognized that there are interactions with ligand-gated ion channels and alterations in neurotransmitter function that are of direct consequence in causing anesthesia-induced unconsciousness. Inhalation anesthetics are unusual among coma-producing drugs in respect to the sequence of inhibitory and excitatory effects that they produce at different concentrations. During anesthesia, sufficient inhibition of brainstem activity can be attained to eliminate the pupillary responses and the corneal reflex. Sustained clonus, exaggerated tendon reflexes, and Babinski signs are common during the process of arousal. Pre-existing focal cerebral deficits from strokes often worsen transiently with the administration of anesthetics, as is true to a lesser extent with other sedatives, metabolic encephalopathies, and hyperthermia. Recurring Stupor and Coma Aside from repeated drug overdose, recurring episodes of stupor are usually due to the decompensation of an encephalopathy from an underlying biochemical derangement, hepatic failure being the most common. A similar condition of periodic hyperammonemic coma in children and adults can come about from urea cycle enzyme defects, such as ornithine transcarbamylase deficiency. Under the title of idiopathic recurring stupor, a rare condition has been described in adult men who displayed a prolonged state of deep sleepiness lasting from hours to days intermittently over a period of many years. During the bouts, a hundredfold increase of circulating endozepine-4, a naturally occurring diazepine agonist, was found in the serum and spinal fluid. Subsequently, the authors of the original reports (Lugaresi et al) found, by the use of more advanced techniques, that intoxication with lorazepam may have accounted for at least some of the cases. Although cases such as this- in which diazepine antagonists reverse episodes of recurrent coma (Huberfeld et al)- continue to be reported, the status of this entity is ambiguous. The vigilance-producing drug, modafinil, has also been effective in one report (Scott and Ahmed). It is unclear to us whether migraine can cause a similar syndrome, as suggested in the study of familial hemiplegic migraine by Fitzsimmons and Wolfenden. Catatonic stupor and KleineLevin syndrome of periodic hypersomnolence and behavioral changes (page 344) also need to be considered. Pathologic Anatomy of Coma Coma is produced by one of two broad groups of problems: the first is clearly morphologic, consisting either of discrete lesions in the upper brainstem and lower diencephalon (which may be primary or secondary to compression) or of more widespread changes throughout the hemispheres. The second is metabolic or submicroscopic, resulting in suppression of neuronal activity. The clinical examination in coma is designed to separate these various mechanisms and to gauge the depth of brain dysfunction. The study of a large number of human cases in which coma preceded death by several days has disclosed three types of lesions, each of which ultimately deranges the function of the reticular activating system directly or indirectly. In the first type, a readily discernible mass lesion- chiefly a tumor, abscess, massive edematous infarct, or intracerebral, subarachnoid, subdural, or epidural hemorrhage- is demonstrable. Usually the lesion involves only a portion of the cortex and white matter, leaving much of the cerebrum intact, but nonetheless it distorts deeper structures. In most instances, these mass lesions in or surrounding the hemispheres cause coma by a lateral displacement of deep central structures, sometimes with herniation of the temporal lobe into the tentorial opening, resulting in compression of the midbrain and subthalamic region of the reticular activating system (see below and also Chap.
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Our success in salvaging several patients even after a period of coma- similar to symptoms upper respiratory infection buy paxil 20mg free shipping reported series by Schwab treatment xeroderma pigmentosum purchase 40 mg paxil mastercard, Carter medicine jokes generic paxil 30mg without a prescription, Delshaw, and Rengarchary and coworkers- indicates that hemicraniectomy combined with an overlying duraplasty may be undertaken if the patient is progressing from a stuporous state to coma and imaging studies show increasing mass effect. Of the 63 patients with severe brain swelling and coma in the series of Schwab et al, 46 survived and none remained severely disabled. The value of surgical decompression has not been limited to patients with right-hemispheric strokes; those with initially limited degrees of aphasia may also be appropriate candidates, but the family must understand the risks involved and the likelihood that the stroke deficits will persist. After a protracted period of coma with bilaterally enlarged pupils or with evidence that the midbrain has been irrevocably damaged, the procedure is probably futile but there have been exceptions. Many in the field remain skeptical of these aggressive approaches, and a randomized trial is under way to settle the issue. In the special case of large cerebellar infarctions, usually from occlusion of a vertebral artery, swelling may compress the lower brainstem. Hydrocephalus usually develops as a prelude to this event and is manifest as drowsiness and stupor, increased tone in the legs, and Babinski signs; other sentinel signs are gaze paresis, sixth nerve palsy, or hemiparesis ipsilateral to the ataxia (Kanis and Ropper). At times it may be difficult to differentiate the effects of increasing hydrocephalus from those of a thrombus propagation in the basilar artery (Lehrich et al). Cerebellar swelling may occur with or without an associated lateral medullary stroke. The situation is comparable to medullary compression caused by cerebellar hemorrhage (page 715). Surgical decompression of the infarcted and swollen tissue should be undertaken almost as soon as cerebellar edema becomes clinically apparent by the emergence of hydrocephalus or brainstem signs, since further swelling can be anticipated. This complication can usually be anticipated in the first 3 or 4 days after a large cerebellar stroke. A brief period of observation before committing to surgery is not unreasonable if the fourth ventricle and peribrainstem cisterns are patent and the patient is awake. Mannitol may be used to prepare the patient for surgery or if a period of observation is anticipated. As in the case of cerebellar hemorrhage, ventricular drainage alone is usually inadequate and, in any case, is unnecessary if the pressure is relieved by craniectomy and resection of infarcted tissue. Anticoagulant Drugs Several considerations weigh in any discussion of the use of anticoagulant treatment of stroke. As discussed further on, several studies point conclusively to a role for anticoagulation in certain cardioembolic cases, while the indications in atherothrombotic disease are less certain. These anticoagulants may halt the advance of a progressive thrombotic stroke, but they are clearly not effective in all cases and numerous recent studies and position papers have questioned their value altogether (see for example, the Report of the Joint Stroke Guideline Development Committee authored by Coull et al). In deciding whether to use anticoagulants, one faces the question of where in the course of the stroke the patient stands when first examined. One fact seems definite- that the administration of anticoagulants is not of great value once the stroke is fully developed, whether in a patient with a lacunar infarct or one with a massive infarction and hemiplegia. It is as yet uncertain whether the long-term use of anticoagulants prevents the recurrence of a thrombotic stroke; in these cases, the incidence of complicating hemorrhage probably outweighs the value of anticoagulants (atrial fibrillation is an exception- see further on). The two situations in which the immediate administration of heparin has drawn the most support from our own clinical practice are in fluctuating basilar artery thrombosis and in impending carotid artery occlusion from thrombosis or dissection (see further on). In these situations, the administration of heparin may be initiated while the nature of the illness is being clarified; the drug is then discontinued if contraindicated by new findings. It must be acknowledged that satisfactory clinical studies in support of this approach of acute anticoagulation have not been carried out. The issue of heparinization in cases of recent cardioembolic cerebral infarction is addressed further on in this chapter, under "Embolic Infarction. In a limited randomized trial, there was no increase in the frequency of hemorrhagic transformation of the ischemic region when compared to placebo treatment (Kay et al). Because the outcome measures in this study were coarse (death or dependence 6 months after stroke), further investigations of this approach need to be carried out. We can only infer that the use of low-molecular-weight heparin (approximately 4000 U subcutaneously, twice daily) appears to be safe and is possibly beneficial. However, there was in these series a low incidence, estimated as 2 percent, of recurrent stroke in the first weeks after a cerebral infarction in the untreated groups. An early recurrent stroke rate this low almost precludes demonstrating a benefit from the use of heparin or heparinoid drugs.
Since that time medicine werx discount paxil 20 mg without prescription, highly sophisticated biochemical techniques have greatly expanded the study of fatty acid metabolism and the identification of many of the primary defects treatment zamrud buy discount paxil 20mg on-line. Biochemistry of Fatty Acid Metabolism Carnitine ( -hydroxygamma-N-trimethylamino-butyrate) symptoms gout buy paxil 20mg mastercard, derived from lysine and methionine, plays a central role in the metabolism of fatty acids. About 75 percent of carnitine comes from dietary sources (red meat and dairy products); the remainder is synthesized in the liver and kidneys. Practically all of the body carnitine is stored in muscle, where it has two main functions: (1) transporting long-chain fatty acylCoAs from the cytosol compartment of the muscle fiber into the mitochondria, where they undergo -oxidation, and (2) preventing the intramitochondrial accumulation of acyl-CoAs, thus protecting the muscle cell from the membrane-destabilizing effects of these substances. In order to be oxidized, the long-chain fatty acids undergo a series of biochemical transformations. First they are activated to corresponding acyl-CoA esters by acyl-CoA synthetase, which is located on the outer mitochondrial membrane. Since the inner mitochondrial membrane is impermeable to acyl-CoA esters, they are transferred into the mitochondria as acylcarnitine esters. The steps in the transport of long-chain fatty acids into the mitochondrial matrix (the carnitine cycle) are described in detail in the reviews of DiMauro et al, DiDonato, and Roe and Coates. Isoforms of carnitine palmityltransferase are critically involved in this process at the inner and outer membranes of the mitochondria. Clinical Features of Disordered Fatty Acid Metabolism Despite the many biochemical abnormalities that have been identified in the fatty acid metabolic pathways, there are essentially three clinical patterns by which these defects are expressed: One constellation of symptoms referred to as the encephalopathic syndrome has its onset in infancy or early childhood. A second (myopathic) syndrome appears in late infancy, childhood, or adult life and takes the form of a progressive myopathy, with or without cardiomyopathy. The myopathy may follow episodes of hypoketotic hypoglycemia or may develop de novo. It is induced by a sustained period of physical activity or fasting and is characterized by repeated episodes of rhabdomyolysis with or without myoglobinuria. Summarized below are the main disorders of fatty acid metabolism that affect skeletal muscle; these are all rare but interesting disorders: Primary Systemic Carnitine Deficiency To date, this is the only form of carnitine deficiency that can be considered primary. Its main clinical features are progressive lipid storage myopathy and cardiomyopathy, sometimes associated with the signs of hypoketotic hypoglycemia. There is no dicarboxylic aciduria, in distinction to the secondary -oxidation defects, in all of which dicarboxylic aciduria is present. The cardiomyopathy, which is fatal if untreated, responds dramatically to oral administration of L-carnitine, 2 to 6 g/day. In these families there is frequently a history of sudden unexplained death in siblings, so that early identification of affected children is essential. Attacks of myalgia, cramps, and muscle weakness, "tightness," and stiffness are precipitated by sustained (though not necessarily intense) exercise and less often by a prolonged period of fasting. Fever, anesthesia, drugs, emotional stress, and cold are rare precipitating events. They are usually accompanied by myoglobinuria, and renal failure occurs in about one fourth of cases (DiMauro et al). The attacks are not aborted by rest and, once initiated, there is no second-wind phenomenon. In type I deficiency, necrosis of muscle fibers, particularly type I fibers, occurs during attacks, followed by regeneration. Treatment There is no specific therapy except that directed at the myoglobinuria and its renal complications. However, a high-carbohydrate, low-fat diet, ingestion of frequent meals, and additional carbohydrate before and during exercise appear to reduce the number of attacks. Patients need to be instructed about the risks of prolonged exercise and skipped meals. Secondary Systemic Carnitine Deficiency this is occasionally the result of severe dietary deprivation or impaired hepatic and renal function. Such instances have been observed in patients with alcoholic-nutritional diseases and kwashiorkor, in premature infants receiving parenteral nutrition, in patients with chronic renal failure undergoing dialysis, and rarely as a complication of valproate therapy. However, most cases of systemic carnitine deficiency are due to defects of -oxidation, described below. The abnormal organic acids in each case are determined by analysis of blood and urine; identification of the specific enzyme deficiency requires tissue analysis (liver and muscle homogenates, cultured fibroblasts). At the time of this writing, no less than eight specific defects of -oxidation affecting muscle have been described; they are tabulated below.
The neurologic symptoms and signs vary slightly with the precise site and size of the extravasation abro oil treatment buy paxil 40 mg, but hemiplegia from interruption of the capsule is a consistent feature of medium-sized and large clots hair treatment cheap paxil 30 mg. With large hemorrhages medications vascular dementia paxil 30 mg sale, patients lapse almost immediately into a stupor with hemiplegia, and their condition visibly deteriorates as the hours pass. More often, however, the patient complains of headache or of some other abnormal cephalic sensation. Within a few minutes the face sags on one side, speech becomes slurred or aphasic, the arm and leg gradually weaken, and the eyes tend to deviate away from the side of the paretic limbs. These events, occurring gradually over a period of a few minutes to a half hour, are strongly suggestive of intracerebral bleeding. The paralysis may worsen; a Babinski sign appears, at first unilaterally and then bilaterally; the affected limbs become flaccid; painful stimuli are not appreciated; speaking becomes impossible; and confusion gives way to stupor. The most advanced stages are characterized by signs of upper brainstem compression (coma); bilateral Babinski signs; deep, ir- regular, or intermittent respiration; dilated, fixed pupils, first on the side of the clot; and occasionally by decerebrate rigidity. With hemorrhages confined to the anterior segment of the putamen, the hemiplegia and hyperreflexia tend to be less severe and to clear more rapidly (Caplan). There is also prominent abulia, motor impersistence, temporary unilateral neglect, and- with left-sided lesions- nonfluent aphasia and dysgraphia. With posterior lesions, weakness is also less and is attended by sensory loss, hemianopia, impaired visual pursuit to the opposite side, Wernicke-type aphasia (leftsided lesions), and anosognosia (right-sided). Those extending laterally and posteriorly into the internal capsule behave much like large putaminal hemorrhages. Those extending medially into the lateral ventricle give rise to drowsiness, stupor, and either confusion and underactivity or restlessness and agitation. Thalamic Hemorrhage the central feature here is severe sensory loss on the entire contralateral body. If large or moderate in size, thalamic hemorrhage also produces a hemiplegia or hemiparesis by compression or destruction of the adjacent internal capsule. The sensory deficit is usually severe and involves all of the opposite side, including the trunk, and may exceed the motor weakness. A fluent aphasia may be present with lesions of the dominant side, and amorphosynthesis and contralateral neglect with lesions of the nondominant side. Compression of the adjacent third ventricle leads to enlargement of the lateral ventricles, and this requires temporary drainage of the ventricles in a small proportion of patients. Small and moderate-sized hemorrhages that rupture into the third ventricle are seemingly associated with fewer neurologic deficits and better outcomes, but early hydrocephalus is almost invariable. Pontine Hemorrhage Here deep coma usually ensues in a few minutes, and the clinical picture is dominated by total paralysis, decerebrate rigidity, and small (1-mm) pupils that react to light. Lateral eye movements, evoked by head turning or caloric testing, are impaired or absent. Death usually occurs within a few hours, but there are rare exceptions in which consciousness is retained and the clinical manifestations indicate a smaller lesion in the tegmentum of the pons (disturbances of lateral ocular movements, crossed sensory or motor disturbances, small pupils, and cranial nerve palsies) in addition to signs of bilateral corticospinal tract involvement. In a series of 60 patients with pontine hemorrhage reviewed by Nakajima, 19 survived (8 of these had remained alert). Louis reported that 21 percent made a good recovery- mostly those who were alert on admission. Cerebellar Hemorrhage this usually develops over a period of one to several hours, and loss of consciousness at the onset is unusual. Repeated vomiting is a prominent feature, along with occipital headache, vertigo, and inability to sit, stand, or walk. Often these are the only abnormalities, making it imperative to have the patient attempt to stand and walk; otherwise the examination may be falsely normal. In the early phase of the illness, other clinical signs of cerebellar disease may be minimal or lacking; only a minority of cases show nystagmus or cerebellar ataxia of the limbs, although these signs must always be sought. Contralateral hemiplegia and ipsilateral facial weakness do not occur unless there is displacement and compression of the medulla against the clivus. There is often paresis of conjugate lateral gaze to the side of the hemorrhage, forced deviation of the eyes to the opposite side, or an ipsilateral sixth nerve weakness. Other ocular signs include blepharospasm, involuntary closure of one eye, skew deviation, "ocular bobbing," and small, often unequal pupils that continue to react until very late in the illness. Occasionally, at the onset, there is a spastic paraparesis or a quadriparesis with preservation of consciousness. Louis et al, those with vermian clots and hydrocephalus were at the highest risk for deterioration.
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