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From time to time the authors have encountered families in which several members developed a spastic paraparesis and a gradual failure of intellectual function during the middle adult years. The patient s mental horizon narrowed gradually, and the capacity for high-level thinking diminished; in addition, the examination showed appropriately exaggerated tendon re exes, clonus, and Babinski signs. In one such family the illness had occurred in two generations; in another, three brothers in a single generation were af icted. Skre described two recessive types of hereditary spastic paraplegia in Norway, one with onset in childhood, the other in adult life. In contrast to the dominant form (see further on), the recessive types displayed evidence of more widespread involvement of the nervous system, including dementia, cerebellar ataxia, and epilepsy. Also, Cross and McKusick have observed a recessive type of paraplegia accompanied by dementia beginning in adolescence. They named it the Mast syndrome, after the af icted family. Worster-Drought and others have reported the pathologic ndings in two cases of this type. In addition to senile plaques and neuro brillary changes, there was demyelination of the subcortical white matter and corpus callosum and a patchy but gross swelling of the arterioles, which gave the staining reactions for amyloid ( Scholz s perivascular plaques ). Van Bogaert and associates published an account of similar cases that showed the characteristic pathologic features of Alzheimer disease. Adult forms of metachromatic leukodystrophy and adrenoleukodystrophy may present with a similar clinical picture (Chap. 37). Quite rare instances of the same syndrome with adult onset have turned out to be due to phenylketonuria or other aminoacidopathies (see Chap. 37). Another interesting association of familial spastic paraplegia is with progressive cerebellar ataxia. Fully one-third of the cases that we have seen with such a spastic weakness were also ataxic and would fall into the category of spinocerebellar degenerations. Yet another variant of this group of diseases has been described by Farmer and colleagues; the inheritance in their cases was autosomal dominant, and the main clinical features were deafness and dizziness, ataxia, chorea, seizures, and dementia, evolving in that order. Postmortem examinations of two patients disclosed calci cation in the globus pallidus, neuronal loss in the dentate nuclei, and destruction of myelinated bers in the centrum semiovale.
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with the primary auditory receptive areas in the temporal lobes. Complete tone deafness, which is III N. nucleus probably inherited as an autosomal dominant trait, is another central disorder. Ascending med. IV N. nucleus The two peripheral forms of deafness, conlong. fasciculus VI N. nucleus ductive and nerve deafness, must be distinguished from each other, since important remedial meaUncinate fasciculus sures are available, particularly for the former. In differentiating them, the tuning-fork tests are often of value. When a vibrating fork, preferably of 512Hz frequency, is held about 2.5 cm from the ear Fastigial (test for air conduction), sound waves can be apnucleus preciated only as they are transmitted through the middle ear; they will be reduced with disease in this location. When the vibrating fork is applied Juxtarestiform to the skull (test for bone conduction), the sound body waves are conveyed directly to the cochlea, without intervention of the sound-transmission apparatus of the middle ear, and will therefore not be reduced or lost in outer or middle ear disease. Norsup. mally air conduction is better than bone conduc- Flocculo-nodular lobe lat. tion, and the sound transmitted though the air is med. Vestibular nuclei appreciated for about twice as long as that passing inf. Vestibular nerve through the bone. These principles form the basis for several simple tests of auditory function. Med. vestibuloIn the Weber test, the vibrating fork is applied Lat. vestibulospinal spinal tract to the forehead in the midline (or to a central intract (in descending cisor). A normal person hears the bone-conducted med. long. fasciculus) sound equally in both ears. In nerve deafness, the sound is localized in the normal ear for obvious reasons; in conductive deafness, the sound is perceived as louder in the affected ear because interference from ambient sounds is muted on the affected side. In the Rinne test, the fork is applied to the mastoid process. At the moment the sound ceases, the fork is held at the auditory meatus. In middle ear deafness, the sound cannot be heard by air conduction after bone conduction has ceased Figure 15-3. A simpli ed diagram of the vestibulocerebellar and vestibulospinal pathways and (abnormal or negative Rinne test). In nerve deaf- connections between vestibular and ocular motor nuclei. The medial longitudinal fasciculi (dotness, the reverse is true (normal or positive Rinne ted vertical lines) are the main pathways for ascending vestibular impulses. (See text and also test), although both air and bone conduction may Fig. 14-1.) be quantitatively decreased. The Schwabach test Diplacusis refers to a defect in frequency discrimination that is consists of comparing the patient s bone conduction with that of manifest by a lack of clarity of spoken syllables or by the percepthe normal examiner. tion that music is out of tune and unpleasant (described by patients In general, early sensorineural deafness is characterized by a as a mushiness of sounds). partial loss of perception of high-pitched sounds and conductive Since each cochlear nucleus is connected with the cortex of deafness by a partial loss of low-pitched sounds. This can be asboth temporal lobes, hearing is unaffected by unilateral cerebral certained by the use of tuning forks of different frequencies but lesions. Deafness due to brainstem lesions is observed only rarely, most accurately by the use of an audiometer and the construction since a massive lesion is required to interrupt both the crossed and of an audiogram, which reveals the entire range of hearing at a uncrossed projections from the cochlear nuclei so massive, as a glance. The audiogram is the one essential test in the evaluation of rule, that other neurologic abnormalities make the testing of hearing hearing loss and the point of departure for subsequent diagnostic impossible. evaluation. A ticking watch or rubbing the patient s hair together The main causes of sensorineural and conductive hearing loss near the ear can be used as a surrogate test of gross hearing for the are discussed further on. bedside, but these maneuvers emit mostly high-frequency noise and will not detect low-frequency conductive loss. A cochlear type of hearing loss can be recognized by the presSpecial Audiologic Procedures ence of the symptoms of recruitment and diplacusis. Recruitment refers to a heightened perception of loudness once the threshold for A number of special tests have proved to be helpful in distinguishhearing has been exceeded; thus the common retort You don t ing cochlear from retrocochlear (nerve) lesions. Although an abhave to shout when the examiner raises his voice (see below). solute distinction cannot be made on the basis of any one test, the
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We have been talking about the normal blood pressure, which has an average or set-point level of about 120/80 mmHg. The normal BP can rise to an upper limit of about 140/90 mmHg. And it can fall down to a lower limit of about 100/60 mmHg. The distance between these upper and lower normal readings creates the normal range for blood pressure, a condition that can technically be called normotension (NOR-moh-TEN-shun). We use this term because blood pressure represents the amount of tension exerted against the blood. Figure 16.5 (A) illustrates a state of normotension: that is, a state of relative constancy or homeostasis of blood pressure within its normal range. Unfortunately, however, blood pressure doesn t always remain within its normal range. Say that a lumberjack accidentally cuts his brachial artery with a chainsaw while felling a large oak tree. The blood spurts out in hot red jets, resulting in a severe and possibly fatal hemorrhage (HEM-uh-rij) a bursting out (-orrhage) of blood (hem). When so much blood is lost, there isn t much blood left to press against the arterial wall. Thus, blood pressure steeply declines. It may even reach a state of hypotension (HIGH-pohTEN-shun). Hypotension is a condition of below normal or de cient (hypo-) blood pressure (tens). Speci cally, hypotension is a blood pressure signi cantly less than 100/60 mmHg (Figure 16.5, B). At the opposite extreme lies hypertension (HIGH-per-TEN-shun) an excessive or above normal (hyper-) blood pressure. Hypertension is a blood pressure signi cantly above the upper normal limit of approximately 140/90 mmHg (Figure 16.5, C). So what if a person has hypotension or hypertension a skeptic might inquire. With hypotension, the person may easily faint. And if the condition is severe, there may be circulatory shock or coma, due to a lack of blood pressure pushing blood up to feed the brain. In the case of hypertension, the chronically above-normal pressure may overstretch and thin out the walls of arteries, creating aneurysms (AN-yuh-riz-ums). Aneurysms are abnormally widened up arteries, which are highly susceptible to being ruptured. And when an aneurysm ruptures, there may be a large amount of internal bleeding. Persons su ering a stroke, or cerebrovascular (seh-REE-broh-VAS-kyoolar) accident, for instance, may well have experienced a ruptured aneurysm of their cerebral blood vessels covering the brain. Whatever particular body functions the oxygen-and-blood-deprived brain area carried out, are then partially or totally lost.
the initial effects. These persons, after several repetitions, recognize a high, despite the subsequent recurrence of unpleasant, or dysphoric, symptoms (nausea, vomiting, and faintness as the drug effect wanes). One of our patients described the initial effect as dying and going to heaven. The repeated self-administration of the drug is the most important factor in the genesis of addiction. Regardless of how one characterizes the state of mind that is produced by episodic injection of the drug, the individual quickly discovers the need to increase the dose in order to obtain the original effects (tolerance). Although the initial effects may not be fully recaptured, the progressively increasing dose of the drug does relieve the discomfort that arises as the effects of each injection wear off. In this way a new pharmacogenically induced need is developed, and the use of opioids becomes self-perpetuating. At the same time a marked degree of tolerance is produced, so that enormous amounts of drugs, e.g., 5000 mg of morphine daily, can eventually be administered without the development of toxic symptoms. The pharmacologic criteria of addiction, as indicated in the chapter on alcoholism, are tolerance and physical dependence. The latter refers to the symptoms and signs that become manifest when the drug is withdrawn following a period of continued use. These symptoms and signs constitute a speci c clinical state, termed the abstinence or withdrawal syndrome (see later). The mechanisms that underlie the development of tolerance and physical dependence are not fully understood. However, it is known that opioids activate an opioid antinociceptive system (enkephalins, dynorphins, endorphins), which are opioid receptors and are located at many different levels of the nervous system (these are described in Chap. 8, on pain; see also the review of Fields). The Opioid Abstinence Syndrome The intensity of the abstinence or withdrawal syndrome depends on the dose of the drug and the duration of addiction. The onset of abstinence symptoms in relation to the last exposure to the drug, however, is related to the pharmacologic half-life of the agent. With morphine, the majority of individuals receiving 240 mg daily for 30 days or more will show moderately severe abstinence symptoms following withdrawal. Mild signs of opiate abstinence can be precipitated by narcotic antagonists in persons who have taken as little as 15 mg of morphine or an equivalent dose of methadone or heroin three times daily for 3 days. The abstinence syndrome that occurs in the morphine addict may be taken as the prototype. The rst 8 to 16 h of abstinence usually pass asymptomatically. At the end of this period, yawning, rhinorrhea, sweating, piloerection, and lacrimation become manifest. Mild at rst, these symptoms increase in severity over a period of several hours and then remain constant for several days. The patient may be able to sleep during the early abstinence period but is restless, and thereafter insomnia remains a prominent feature. Dilatation of the pupils, recurring waves of goose esh, and twitchings of the muscles appear. The patient complains of aching in the back, abdomen, and legs and of hot and cold ashes ; he frequently asks for blankets. At about 36 h the restlessness becomes more severe, and nausea, vomiting, and diarrhea usually develop. Temperature, respiratory rate, and blood pressure are slightly elevated. All these symptoms reach their peak intensity 48 to 72 h after withdrawal and then gradually subside. The opioid abstinence syndrome is rarely fatal (it is life-threatening only in infants). After 7 to 10 days, the clinical signs of abstinence are no longer evident, although the patient may complain of insomnia, nervousness, weakness, and muscle aches for several more weeks, and small
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A biased coin is more predictable than a fair coin, and thus has lower entropy. As the bias becomes more pronounced, the entropy drops toward zero. We explore these notions further in Exercise 5.18 and 5.19. 145
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