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Elicitation of these reflexes in a comatose patient provides two pieces of information: (1) evidence of unimpeded function of the oculomotor nerves and of the midbrain and pontine tegmental structures that integrate ocular movements and (2) loss of the cortical inhibition that normally holds these movements in check medications in checked baggage purchase avodart pills in toronto. The presence of unimpaired reflex eye movements implies that coma is not due to compression or destruction of the upper midbrain medicine 93 948 trusted avodart 0.5mg. Instead medications zocor discount avodart, there must be widespread cerebral dysfunction medicine grapefruit interaction order avodart 0.5mg amex, such as occurs with cerebral anoxia or metabolic-toxic suppression of cortical activity. It must be conceded, however, that sedative or anticonvulsant intoxication serious enough to cause coma may obliterate the brainstem mechanisms for oculocephalic reactions and, in extreme cases, even the oculovestibular responses as noted below. Asymmetry in elicited eye movements remains a dependable sign of focal brainstem disease. In instances of coma due to a large mass in one cerebral hemisphere that secondarily compresses the upper brainstem, the oculocephalic reflexes are usually present, but the movement of the eye on the side of the mass may be impeded in adduction as a result of a third nerve paresis. Irrigation of each ear with 10 mL of cold water (or roomtemperature water if the patient is not comatose) normally causes slow conjugate deviation of the eyes toward the irrigated ear, followed in a few seconds by compensatory nystagmus (fast component away from the stimulated side). In comatose patients, the fast "corrective" phase of nystagmus is lost and the eyes are tonically deflected to the side irrigated with cold water or away from the side irrigated with warm water; this position may be held for 2 to 3 min. If only one eye abducts and the other fails to adduct, one can conclude that the medial longitudinal fasciculus has been interrupted (on the side of adductor paralysis). The opposite, abducens palsy, is indicated by an esotropic resting position and a lack of outward deviation of one eye with the reflex maneuvers. The complete absence of ocular movement in response to oculovestibular testing indicates a severe disruption of brainstem tegmental pathways in the pons or midbrain or, as mentioned, a profound overdose of sedative or anesthetic drugs. A marked asymmetry in corneal responses indicates either an acute lesion of the opposite hemisphere or, less often, an ipsilateral lesion in the brainstem. Spontaneous Limb Movements Restless movements of both arms and both legs and grasping and picking movements signify that the corticospinal tracts are more or less intact. Variable oppositional resistance to passive movement (paratonic rigidity), complex avoidance movements, and discrete protective movements have the same meaning; if these movements are bilateral, the coma is usually not profound. The occurrence of focal motor epilepsy indicates that the corresponding corticospinal pathway is intact. Often, elaborate forms of semivoluntary movement are present on the "good side" in patients with extensive disease in one hemisphere; they probably represent some type of disequilibrium or disinhibition of cortical and subcortical movement patterns. Definite choreic, athetotic, or hemiballistic movements indicate a disorder of the basal ganglionic and subthalamic structures, just as they do in the alert patient. Posturing in the Comatose Patient One of these abnormal postures is decerebrate rigidity, which in its fully developed form consists of opisthotonos, clenching of the jaws, and stiff extension of the limbs, with internal rotation of the arms and plantar flexion of the feet (see Chap. This postural pattern was first described by Sherrington, who produced it in cats and monkeys by transecting the brainstem at the intercollicular level. The decerebrate pattern was noted to be ipsilateral to a one-sided lesion, hence not due to involvement of the corticospinal tracts. Such a precise correlation is rarely possible in patients who develop stereotyped extensor posturing since it arises in a variety of settings- with midbrain compression due to a hemispheral mass; with cerebellar or other posterior fossa lesions; with certain metabolic disorders, such as anoxia and hypoglycemia; and rarely with hepatic coma and profound intoxication. Patients with an acute lesion of one cerebral hemisphere may show a similar type of extensor posturing of the contralateral and sometimes ipsilateral limbs, and this may coexist with the ability to make purposeful movements of the same limbs. Extensor postures, unilateral or bilateral, may seemingly occur spontaneously, but more often they are in response to manipulation of the limbs or a tactile or noxious stimulus. Another pattern is the extensor posturing of arm and leg on one side and flexion and abduction of the opposite arm. This reaction is analogous to the tonic reflexes described by Magnus in decerebrate animals. In some patients with the foregoing postural changes the lesions are clearly in the cerebral white matter or basal ganglia, which is difficult to reconcile with the classic physiologic explanation of decerebrate posturing; presumably there is a functional derangement of structures in the midbrain.
In advanced forms of this disorder medicine 1900s spruce cough balsam fir purchase 0.5mg avodart amex, the shriveled tongue lies inert and fasciculating on the floor of the mouth medicine that makes you throw up avodart 0.5mg mastercard, and the lips are lax and tremulous symptoms ms generic avodart 0.5 mg line. Saliva constantly collects in the mouth because of dysphagia symptoms 0f brain tumor cheap 0.5mg avodart with mastercard, and drooling is troublesome. Dysphonia- alteration of the voice to a rasping monotone due to vocal cord paralysis- is often added. As this condition evolves, speech becomes slurred and progressively less distinct. There is special difficulty in the enunciation of vibratives, such as r, and as the paralysis becomes more complete, lingual and labial consonants are finally not pronounced at all. In the past, bilateral paralysis of the palate, causing nasality of speech, often occurred with diphtheria and poliomyelitis, but now it occurs most often with progressive bulbar palsy, a form of motor neuron disease (page 940), and with certain other neuromuscular disorders, particularly myasthenia gravis. Spastic (Pseudobulbar) Dysarthria Diseases that involve the corticobulbar tracts bilaterally- usually due to vascular, demyelinative, or motor system disease (amyotrophic lateral sclerosis)- result in the syndrome of spastic bulbar (pseudobulbar) palsy. The patient may have had a clinically inevident vascular lesion at some time in the past, affecting the corticobulbar fibers on one side; however, since the bulbar muscles on each side are innervated by both motor cortices, there may be little or no impairment in speech or swallowing from a unilateral corticobulbar lesion. Should another stroke then occur, involving the other corticobulbar tract at the pontine, midbrain, or capsular level, the patient immediately becomes dysphagic, dysphonic, and anarthric or dysarthric, often with paresis of the tongue and facial muscles. These structures are innervated by the vagal, hypoglossal, facial, and phrenic nerves, the nuclei of which are controlled by both motor cortices through the corticobulbar tracts. As with all movements, those involved in speaking are subject to extrapyramidal influences from the cerebellum and basal ganglia. The act of speaking requires that air be expired in regulated bursts, and each expiration must be maintained long enough (by pressure mainly from the intercostal muscles) to permit the utterance of phrases and sentences. The current of expired air is then finely regulated by the activity of the various muscles engaged in speech. Phonation, or the production of vocal sounds, is a function of the larynx, more particularly the vocal cords. The pitch of the speaking or singing voice depends upon the length and mass of the membranous parts of the vocal cords and can be varied by changing their tension; this is accomplished by means of the intrinsic laryngeal muscles, before any audible sound emerges. The controlled intratracheal pressure forces air past the glottis and separates the margins of the cords, setting up a series of vibrations and recoils. Sounds thus formed are modulated as they pass through the nasopharynx and mouth, which act as resonators. Articulation consists of contractions of the pharynx, palate, tongue, and lips, which interrupt or alter the vocal sounds. Vowels are of laryngeal origin, as are some consonants, but the latter are formed for the most part during articulation; the consonants m, b, and p are labial, l and t are lingual, and nk and ng are guttural (throat and soft palate). Defective articulation (dysarthria) and phonation (dysphonia) are recognized at once by listening to the patient speak during ordinary conversation or read aloud from a newspaper. Amyotrophic lateral sclerosis is the main condition in which the signs of spastic and atrophic bulbar palsy are combined. When the dominant frontal operculum is damaged, speech may be dysarthric, usually without impairment in emotional control. In the beginning, with vascular lesions, the patient may be mute; but with recovery or in mild degrees of the same condition, speech is notably slow, thick, and indistinct, much like that of partial bulbar paralysis. Magnetic stimulation of the cortex in these cases reveals a delay in corticobulbar conduction. Careful testing of other language functions, especially writing, will in this instance reveal the aphasic aspect of the defect. A severe dysarthria that is difficult to classify but resembles that of cerebellar disease may occur with a left hemiplegia, usually the result of capsular or right opercular infarction. It tends to improve over several weeks but initially may be so severe as to make speech incomprehensible (Ropper). Rigid (Extrapyramidal) Dysarthria In Parkinson and other extrapyramidal diseases associated with rigidity of muscles, one observes a rather different disturbance of articulation, characterized by rapid mumbling and cluttered utterance and slurring of words and syllables with trailing off in volume at the ends of sentences. The voice is low-pitched and monotonous, lacking both inflection and volume (hypophonia). The words are spoken hastily and run together in a pattern that is almost the opposite of the slowed pattern of spastic dysarthria.
Persistent cerebral ischemia and infarction may occasionally complicate migraine in young persons medicine and science in sports and exercise avodart 0.5 mg low cost. The combination of migraine and "the Pill" is particularly hazardous medicine education buy avodart 0.5 mg visa, as detailed below symptoms dizziness nausea purchase avodart with a mastercard. Similarly symptoms 9 days past iui 0.5mg avodart amex, despite the common occurrence of mitral valve prolapse in young adults, it is probably only rarely a cause of stroke (see comments on page 710). Stroke due to either arterial or venous occlusion occurs occasionally in association with ulcerative colitis and to a lesser extent with regional enteritis. Evidence points to a hypercoagulable state during exacerbations of inflammatory bowel disease, but a precise defect in coagulation has not been identified. Meningovascular syphilis and fungal and tuberculous meningitis and other forms of chronic basal meningitis are considerations in this age group; the strokes are usually of the cavitary lacunar type, resulting from infectious-inflammatory occlusion of small basal vessels. Sickle cell anemia is a rare but important cause of stroke in children of African ancestry; acute hemiplegia is the most common manifestation, but all types of focal cerebral disorders have been observed. The pathologic findings are those of infarction, large and small; their basis is assumed to be vascular obstruction associated with the sickling process. Treatment of the cerebral circulatory disorder, based presumably on sludging of red blood cells, is with intravenous hydration and transfusion. Cerebral venous sinus thrombosis in young children and neonates represents a special problem, difficult to diagnose, and with a poor prognosis (see de Veber et al). In most of the reported fatal cases, the thrombosed artery has been free of atheroma or other disease. This has been taken to indicate that embolism is responsible for the strokes, but the source of embolism can rarely be demonstrated. Cerebral and noncerebral venous thromboses are other relatively rare complications. These observations, coupled with evidence that estrogen alters the coagulability of the blood, suggest that a state of hypercoagulability is an important factor in the genesis of contraceptive-associated infarction. The vascular lesion underlying cerebral thrombosis in women taking oral contraceptives has been studied by Irey and colleagues. It consists of nodular intimal hyperplasia of eccentric distribution with increased acid mucopolysaccharides and replication of the internal elastic lamina. Similar changes have been found in pregnancy and in humans and animals receiving exogenous steroids, including estrogens. It has also become clear that mutations of the prothrombin gene are far more frequent in patients who have cerebral venous thrombosis while on oral contraceptive pills. These genetic abnormalities are thought by Martinelli and associates to account for 35 percent of idiopathic cases of cerebral vein thrombosis; they contend that contraceptives increase the risk 20-fold. Amniotic fluid embolus may also cause stroke in this manner and should be suspected in multiparous women who have had uterine tears. In the latter, there are almost invariably signs of acute pulmonary disease from simultaneous occlusion of lung vessels. Stroke with Cardiac Surgery Incident to cardiac arrest and bypass surgery there is risk of both generalized and focal hypoxia-ischemia of the brain. Improved operative techniques have lessened the incidence of these complications, but they are still distressingly frequent. Atherosclerotic plaques may be dislodged during cross-clamping of the proximal aorta and are an important source of cerebral emboli. In the last decade the incidence of stroke related to cardiac surgery has dropped to between 2 and 3 percent in large series numbering thousands of patients (Libman et al, Algren and Aren). Advanced age, congestive heart failure, and more complex surgeries have been listed as risk factors for stroke in various reports. Mohr and coworkers examined 100 consecutive cases pre- and postoperatively and observed two types of complications- one occurring immediately after the operation and the other after an interval of days or weeks. The immediate neurologic disorder consisted of a delay in awakening from the anesthesia; subsequently there was slowness in thinking, disorientation, agitation, combativeness, visual hallucinations, and poor registration and recall of what was happening. These symptoms, in the form of a confusional state sometimes verging on delirium or acute psychosis, usually cleared within 5 to 7 days, although some patients were not entirely normal mentally some weeks later. As the confusion cleared, about half of the patients were found to have small visual field defects, dyscalculia, oculomanual ataxia, alexia, or defects of perception suggestive of lesions in the parieto-occipital regions. The immediate effects were attributed to hypotension and various types of embolism (atherosclerotic, air, silicon, fat, platelets).
Infection also reaches the ventricles treatment of lyme disease order avodart 0.5mg amex, either directly from the choroid plexuses or by reflux through the foramina of Magendie and Luschka symptoms 5 weeks into pregnancy buy avodart on line. The first reaction to bacteria or their toxins is hyperemia of the meningeal venules and capillaries and an increased permeability of these vessels symptoms for pink eye purchase discount avodart line, followed shortly by exudation of protein and the migration of neutrophils into the pia and subarachnoid space symptoms wisdom teeth buy avodart amex. The subarachnoid exudate increases rapidly, particularly over the base of the brain; it extends into the sheaths of cranial and spinal nerves and, for a very short distance, into the perivascular spaces of the cortex. During the first few days, mature and immature neutrophils, many of them containing phagocytosed bacteria, are the predominant cells. Within a few days, lymphocytes and histiocytes increase gradually in relative and absolute numbers. During this time there is exudation of fibrinogen, which is converted to fibrin after a few days. In the latter part of the second week, plasma cells appear and subsequently increase in number. At about the same time the cellular exudate becomes organized into two layers- an outer one, just beneath the arachnoid membrane, made up of neutrophils and fibrin, and an inner one, next to the pia, composed largely of lymphocytes, plasma cells, and mononuclear cells or macrophages. Although fibroblasts begin to proliferate early, they are not conspicuous until later, when they take part in the organization of the exudate, resulting in fibrosis of the arachnoid and loculation of pockets of exudate. During the process of resolution, the inflammatory cells disappear in almost the same order as they had appeared. Neutrophils begin to disintegrate by the fourth to fifth day, and soon thereafter, with treatment, no new ones appear. Lymphocytes, plasma cells, and macrophages disappear more slowly, and a few lymphocytes and mononuclear cells may remain in small numbers for several months. The completeness of resolution depends to a large extent on the stage at which the infection is arrested. From the earliest stages of meningitis, changes are also found in the small- and medium-sized subarachnoid arteries. Neutrophils and lymphocytes migrate from the adventitia to the subintimal region, often forming a conspicuous layer. In the veins, swelling of the endothelial cells and infiltration of the adventitia also occur. Subintimal layering, as occurs in arterioles, is not observed, but there may be a diffuse infiltration of the entire wall of the vessel. It is in veins so affected that focal necrosis of the vessel wall and mural thrombi are most often found. Cortical thrombophlebitis of the larger veins does not usually develop before the end of the second week of the infection. The unusual prominence of the vascular changes may be related to their anatomic peculiarities. The adventitia of the subarachnoid vessels, both of arterioles and venules, is actually formed by an investment of the arachnoid membrane, which is invariably involved by the infectious process. Thus, in a sense, the outer vessel wall is affected from the beginning by the inflammatory process- an infectious vasculitis. The much more frequent occurrence of thrombosis in veins than in arteries is probably accounted for by the thinner walls and the slower current (possibly stagnation) of blood in the former. Although the spinal and cranial nerves are surrounded by purulent exudate from the beginning of the infection, the perineurial sheaths become infiltrated by inflammatory cells only after several days. Exceptionally, in some nerves, there is infiltration of the endoneurium and degeneration of myelinated fibers, leading to the formation of fatty macrophages and proliferation of Schwann cells and fibroblasts. Occasionally cellular infiltrations may be found in the optic nerves or olfactory bulbs. The arachnoid membrane tends to serve as an effective barrier to the spread of infection into the brain substance, but some secondary reaction in the subdural space may occur nevertheless (subdural effusion). This happens far more often in infants than in adults; according to Snedeker and coworkers, approximately 40 percent of infants with meningitis who are less than 18 months of age develop subdural effusions. In an even higher percentage of cases, small amounts of fibrinous exudate are found in microscopic sections that include the spinal dura. When fibrinopurulent exudate accumulates in large quantities around the spinal cord, it blocks off the spinal subarachnoid space. An infrequent late sequela of bacterial meningitis is therefore chronic adhesive arachnoiditis or chronic meningomyelitis. In the early stages of meningitis, very little change in the substance of the brain can be detected.
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