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By: L. Sivert, M.A., M.D., Ph.D.
Assistant Professor, University of Chicago Pritzker School of Medicine
A condition termed pure word deafness in which patients are unable to heart attack jack 1 life 2 live discount atenolol uk understand spoken language but do not have a more general auditory agnosia or aphasia occasionally occurs arrhythmia treatment medications buy generic atenolol 50mg on line. It is caused by bilateral lesions separating the primary auditory areas from the posterior association cortex pulse pressure in shock generic 50 mg atenolol fast delivery. Patients with this condition have intact motor output and persist in uttering nonsense phrases filled with paraphasias (incorrect word or letter substitutions) that retain grammatical structure. They are not aware that people do not understand them and may become alarmed as though believing that those around them are speaking in code. A selective amusia, or the inability to recognize or appreciate pitch and melodies, may occur with right posterior temporal or inferior parietal lesions. Deficits resulting from right temporal lobe lesions are generally subtle and require specific testing for spatial orientation, fine visual discrimination, and odor discrimination. Focal seizures arising from the temporal lobe may give rise to changes in ongoing language function and to sensory, emotional, or psychic phenomena. Auditory hallucinations arising from the superior temporal gyrus range from simple sounds to complex speech, whereas visual hallucinations arising from the temporal lobe are generally complicated scenes or visual memories. The psychic and visceral experiences that occur during seizures arising from limbic structures within the temporal lobes are discussed below. It consists of the subcallosal gyrus anteriorly, includes the cingulate gyrus curving up and around the corpus callosum, and continues down the medial and inferior aspect of the temporal lobe as the parahippocampal gyrus. Some authors include the temporal poles, pyriform region of the frontal lobes, and portions of the insular cortex in the limbic lobe. As opposed to the six-layered neocortex, the cortex of the limbic lobe consists of a three-layered archeocortex (hippocampal formation and dentate gyrus), a three-layered paleocortex (parahippocampal gyrus), and a transitional juxtallocortex (cingulate gyrus). In mammals other than primates and in non-mammalian species, the limbic lobe makes up a much larger proportion of brain volume than it does in humans. Convergence of data from anatomic investigations, animal studies, and observations in humans suggests that the limbic system plays a role in mediating the experience of emotions, visceral responses, and storage of memories. The limbic system has connections to most areas of the cortex and has intimate connections with the hypothalamus, the "head ganglion" of the autonomic nervous 2038 system. In animals, electrical stimulation of the anterior cingulate cortex and the orbital-insular-temporal cortex causes changes in blood pressure, gastrointestinal motility, pupillary dilatation, salivation, bladder contraction, and respiration. In humans, seizure activity in these same areas can cause similar autonomic changes, including orgasm. Lesions of the limbic lobe usually do not induce clinically evident autonomic changes, in part because of the independence of subcortical structures such as the hypothalamus in mediating autonomic reflexes. Characteristic visceral and psychic phenomena occur with epileptic activity arising from limbic structures. Olfactory sensations, usually of an unpleasant nature, are classically associated with involvement of the uncus in the medial temporal lobe. Autonomic and gustatory sensations are seen with involvement of the opercular area within the sylvian fissure. Psychic sensations of deja vu, jamais vu, dream-like states, and depersonalization may occur along with associated impairment in consciousness. The temporal neocortex is intimately connected to the deeper limbic structures, so it is difficult to establish whether the observed seizure phenomena are due to limbic or neocortical involvement. Bilateral anterior temporal dysfunction resulting from lobectomy or other conditions (such as blunt head trauma, stroke, or herpes encephalitis) can cause a severe deficit in the ability to form new memories. Less dramatic deficits in specific items are seen with unilateral lesions, verbal memories being more impaired with left-sided lesions and non-verbal memories such as that for faces being more impaired with right anterior temporal lobe lesions. Considerable debate has arisen over the specific structures that need to be involved to produce this memory deficit. Observations suggest that the hippocampus is required to store emotionally neutral declarative memories whereas the adjacent amygdala is necessary to store emotionally laden memories. Aside from a memory deficit, bilateral lesions of the anterior temporal lobes can also induce Klu ver-Bucy syndrome. First described in monkeys, this condition consists of hypersexuality, hypermetamorphosis (excessive exploratory behavior), emotional placidity, hyperorality, and agnosia. Since then, clinical observation and countless studies have confirmed a more important role of the left hemisphere in language production and comprehension in most individuals.
Diarrhea results because of impaired absorption of water and electrolytes by the inflamed colon arrhythmia facebook buy 50 mg atenolol mastercard. Although the colonic inflammation is superficial arteria facialis cheap 100 mg atenolol amex, bacteremia occurs occasionally blood pressure chart enter numbers buy generic atenolol from india, especially in S. Susceptibility of organisms to serum complement-mediated bacteriolysis may explain the infrequency of bacteremia and disseminated infection. In this complication, fibrin thrombi are deposited in the renal glomeruli, causing cortical necrosis and fragmentation of red cells. Most patients with shigellosis begin their illness with a non-specific prodrome (see Table 342-1). The initial intestinal symptoms soon follow as cramps, loose stools, and watery diarrhea, which usually precede the onset of dysentery by 1 or more days. The dysentery consists typically of flecks and small clots of bright red blood and mucus in stools that are small in volume. Frequency of passage is often as high as 20 to 40 times a day, with excruciating rectal pain and tenesmus during defecation. The amount of blood in stools varies widely but usually is small because of the superficial colonic ulcerations. Abdominal tenderness is often most marked in the left lower quadrant over the sigmoid colon but also may be generalized. The fever is likely to abate after a few days of dysentery, making afebrile bloody diarrhea an occasional clinical presentation. After 1 to 2 weeks of untreated disease, spontaneous improvement occurs in most patients. Complications include dehydration, which can cause death, especially in children and the elderly. The leukemoid reaction and hemolytic-uremic syndrome may develop in children late in the course after antimicrobial treatment when the dysentery has started to improve. Neurologic manifestations can be striking and include delirium, seizures, and nuchal rigidity. These are non-suppurative phenomena that occur in the absence of viable Shigella organisms 1 to 3 weeks after resolution of dysentery. Shigellosis should be considered in any patient with acute onset of fever and diarrhea. Blood and pus are grossly apparent in severe bacillary dysentery; even in milder forms of the disease, microscopic examination of the stool often reveals numerous leukocytes and erythrocytes. The fecal leukocyte examination should be performed with a portion of liquid stool, preferably containing mucus. A drop of stool is placed on a microscopic slide, mixed thoroughly with two drops of methylene blue, and overlaid with a coverslip. The presence of abundant polymorphonuclear leukocytes helps distinguish shigellosis from diarrheal syndromes caused by viruses and enterotoxigenic bacteria. Amebic dysentery is excluded by the absence of trophozoites on a microscopic examination of fresh stool under a coverslip. The peripheral white cell count is of little diagnostic value, because it may range from less than 3000 to more than 30,000/mm3. Sigmoidoscopic examination reveals diffuse erythema with a mucopurulent layer and friable areas of mucosa with shallow ulcers 3 to 7 mm in diameter. A rectal swab, a swab of a colonic ulcer obtained by sigmoidoscopic examination, or a freshly passed stool specimen should be inoculated immediately on culture plates or into carrying media. Because isolation rates of shigellae from freshly passed stools of patients with shigellosis may be as low as 67%, culturing for 3 successive days is recommended. Stool cultures are generally positive within 24 hours after onset of symptoms and may remain positive for several weeks in the absence of antimicrobial therapy. Appropriate culture media include blood, desoxycholate, and Salmonella-Shigella (S-S) agars.
The afferent pathways consist of large myelinated fibers that pass to pulse pressure facts buy 50mg atenolol otc the spinal cord via the dorsal root ganglia and ascend in the ipsilateral posterior and blood pressure visual chart purchase line atenolol, to pulse pressure for athletes purchase atenolol pills in toronto a lesser extent, the posterolateral columns of the cord to reach the posterior column nuclei (gracile and cuneate nuclei) in the medulla oblongata, where they synapse with second-order neurons. The fibers from these neurons cross and then ascend in the medial lemniscus to synapse in the contralateral ventral posterolateral nucleus of the thalamus, from which third-order neurons project to the cortex. Negative symptoms are ones in which there is a loss of sensation, such as a feeling of numbness. Positive symptoms, by contrast, consist of sensory phenomena that occur without normal stimulation of receptors and include paresthesias and dysesthesias. Paresthesias may include a feeling of tingling, crawling, itching, compression, tightness, cold, or heat, and are sometimes associated with a feeling of heaviness. The term dysesthesias is used correctly to refer to abnormal sensations, often tingling, painful or uncomfortable, that occur after innocuous stimuli, while allodynia refers to the perception as painful of a stimulus that is not normally painful. Paresthesias and dysesthesias may be difficult to distinguish from pain by some patients. Hypesthesia and hypalgesia denote a loss or impairment of touch or pain sensibility, respectively, and hyperesthesia and hyperalgesia indicate a lowered threshold to tactile or painful stimuli, respectively, so that there is increased sensitivity to such stimuli. With the use of a wisp of cotton, a pin, and a tuning fork, the trunk and extremities are examined for regions of abnormal or absent sensation. Certain instruments are available for quantifying sensory function, such as the computer-assisted sensory examination, which is based on the detection of touch, pressure, vibratory, and thermal sensation thresholds. Alterations in pain and tactile sensibility can generally be detected by clinical examination. It is important to localize the distribution of any such sensory loss in order to distinguish between nerve, root, and central dysfunction. Similarly, abnormalities of proprioception can be detected by clinical examination, when patients will be unable to detect the direction in which a joint is moved. In severe cases, there may be pseudoathetoid movements of the outstretched hands, sensory ataxia, and, sometimes, postural and action tremors. Disorders of peripheral nerves commonly lead to sensory disturbances that depend upon the population of affected nerve fibers. Appreciation of movement and position are impaired, and paresthesias are 2066 common. Examination reveals that vibration, position, and movement sensations are impaired, and movement becomes clumsy and ataxic. In other neuropathies, it is the small fibers especially that are affected; spontaneous pain is common and may be burning, lancinating, or aching in quality. Pain and temperature appreciation are disproportionately affected in these neuropathies, and autonomic dysfunction may be present. Examples of small-fiber neuropathies include certain hereditary disorders, Tangier disease, and diabetes. The distribution of sensory loss should indicate the site of pathology and provide a clue to the underlying neurologic disorder. Most sensory neuropathies are characterized by a distal distribution of sensory loss, whereas sensory neuronopathies are characterized by sensory loss that may also involve the trunk and face, and which tends to be particularly severe. Sensory changes in a radiculopathy will conform to a root territory; in cauda equina syndromes, sensory deficits involve multiple roots and may lead to saddle anesthesia and loss of the normal sensation associated with the passage of urine or feces. A peripheral nerve lesion will lead to sensory loss in the distribution of a single nerve or nerve branch. Sensory loss sometimes suggests the discrete involvement of several different nerves (mononeuritis multiplex), while in other cases there is a symmetric distal sensory loss that does not conform to the territory of any individual nerves but, rather, suggests diffuse involvement of multiple nerves (polyneuropathy). Lesions of the posterolateral columns of the cord, such as occur in multiple sclerosis, vitamin B12 deficiency, and cervical spondylosis, lead often to a feeling of compression in the affected region and to a Lhermitte sign (paresthesias radiating down the back and legs on neck flexion). Examination reveals an ipsilateral impairment of vibration and joint position senses, with preservation of pain and temperature appreciation. Conversely, lesions of the anterolateral region of the cord (as by cordotomy), or central lesions interrupting fibers crossing to join the spinothalamic pathways (as in syringomyelia) lead to an impairment of pain and temperature appreciation with relative preservation of vibration and joint position sense, and of light touch. Based upon the above, certain characteristic sensory syndromes occur with cord lesions. Lateral hemisection of the cord (Brown-Se qard syndrome) leads to ipsilateral pain, hyperesthesia, and impaired vibration and joint position sense below the level of the lesion, and contralateral impairment of pain and temperature appreciation.
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