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These terms refer to a distinctive cerebral disease in which a rapidly progressive and profound dementia is associated with diffuse myoclonic jerks, and a variety of other neurologic abnormalities, mainly visual or cerebellar. The major neuropathologic changes are in the cerebral and cerebellar cortices; the outstanding features are widespread neuronal loss and gliosis accompanied by a striking vacuolation or spongy state of the affected regions hence the designation subacute spongiform encephalopathy (SSE). Less severe changes in a patchy distribution are found in cases with a briefer clinical course. These changes, both clinical and pathologic, occur with such uniformity from case to case that they doubtless form a nosologic entity. It is generally referred to as Creutzfeldt-Jakob disease, an inappropriate eponym, since it is most unlikely that the patient described by Creutzfeldt and at least 3 of the 5 patients described by Jakob had the same disease that we now recognize as subacute
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cerebrum. (The term operculum refers to the cortex that borders the sylvian ssure and covers or forms a lid over the insula, or island of Reil.) In other words, the lesion in the usual form of Broca s aphasia extends well beyond the so-called Broca s area (Brodmann s areas 44 and 45). Furthermore, persistence of Broca s aphasia is associated with the larger type of lesion, illustrated in Fig. 23-2. It is noteworthy that in one of Broca s original patients, whose expressive language had been limited to a few verbal stereotypes for 10 years before his death, inspection of the surface of the brain (the brain was never cut, although CT scans have since been made) disclosed an extensive lesion encompassing the left insula; the frontal, central, and parietal operculum; and even part of the inferior parietal lobe posterior to the sylvian ssure. The Wernicke s area was spared, refuting the prediction at the time of Marie. Inexplicably, Broca attributed the aphasic disorder to the lesion of the frontal operculum alone. Broca ignored the rest of the lesion, which he considered to be a later spreading effect of the stroke. Perhaps he was in uenced by the prevailing opinion of the time (1861) that articulation was a function of the inferior parts of the frontal lobes. The fact that Broca s name later became attached to a discrete part of the inferior frontal cortex helped to entrench the idea that Broca s aphasia equated with a lesion in the Broca s area. However, as pointed out above, a lesion con ned only to this area gives rise to a relatively modest and transient motor speech disorder (Mohr et al) or to no disorder of speech at all (Goldstein). Motor speech disorders, both severe Broca s aphasia and the more restricted and transient types, are most often due to a vascular lesion. Embolic infarction in the territory of the upper (rolandic, superior) division of the middle cerebral artery is the most frequent type of stroke and results in the most abrupt onset and sometimes the most rapid regression of aphasia (hours or days), depending on whether the ischemia proceeds to tissue necrosis. Even with the latter, however, ischemia around the zone of infarction causes a more extensive syndrome than one might expect from the infarct itself, i.e., the physiologic impairment initially exceeds the pathologic. Because of the distribution of the superior branch of the middle cerebral artery, there are a frequently associated right-sided faciobrachial paresis and a left-sided manual-brachial apraxia (socalled sympathetic apraxia), due probably to interruption of the bers that connect the left and right motor cortices. Atherosclerotic thrombosis, primary or metastatic tumor, subcortical hypertensive, traumatic or anticoagulant-induced hemorrhage, and seizure, should they involve the appropriate parts of the motor cortex, may also declare themselves by a Broca s aphasia. A closely related syndrome, pure word mutism (aphemia), causes the patient to be wordless (mute) but leaves inner speech intact and writing undisturbed. Anatomically, this is believed to be in the nature of a disconnection of the motor cortex for speech from lower centers and is described with the dissociative speech syndromes discussed further on in this chapter. Wernicke s Aphasia This syndrome comprises two main elements: (1) an impairment in the comprehension of speech, basically an inability to differentiate word elements or phonemes, both spoken and written, and (2) a relatively uent but paraphasic speech (further de ned below). The location of the lesion in cases of Wernicke s aphasia is the left superior lateral temporal lobe near the primary auditory cortex reveals the major role of the auditory region in the regulation of language. The defect in language is manifest further by a varying inability to repeat spoken and written
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CHAPTER 5 Exponents and Roots
4.7. DISCRETE-TIME EQUIVALENT MODELS Example 4.20 Assume that for a system of interest, 0 F12 0 F = 0 0 F23 0 0 F33
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menu.add(0, INSERT_ID, R.string.menu_insert).setShortcut('3', 'a'); Intent intent = new Intent(null, getIntent().getData()); intent.addCategory(Intent.ALTERNATIVE_CATEGORY); menu.addIntentOptions( Menu.ALTERNATIVE, 0, new ComponentName(this, FindAFriend.class), null, intent, 0, null); return true; } @Override public boolean onPrepareOptionsMenu(Menu menu) { super.onPrepareOptionsMenu(menu); final boolean haveItems = mCursor.count() > 0; if (haveItems) { Uri uri = ContentUris.withAppendedId(getIntent().getData(), getSelectedItemId()); Intent[] specifics = new Intent[1]; specifics[0] = new Intent(Intent.EDIT_ACTION, uri); Menu.Item[] items = new Menu.Item[1]; Intent intent = new Intent(null, uri); intent.addCategory(Intent.SELECTED_ALTERNATIVE_CATEGORY); menu.addIntentOptions(Menu.SELECTED_ALTERNATIVE, 0, null, specifics, intent, 0, items); menu.add(Menu.SELECTED_ALTERNATIVE, DELETE_ID, R.string.menu_delete) .setShortcut('2', 'd'); menu.add(Menu.SELECTED_ALTERNATIVE, FIND_FRIENDS, R.string.find_friends).setShortcut('4', 'f'); if (items[0] != null) { items[0].setShortcut('1', 'e'); } } else { menu.removeGroup(Menu.SELECTED_ALTERNATIVE); } menu.setItemShown(DELETE_ID, haveItems); return true; } @Override public boolean onOptionsItemSelected(Menu.Item item) { switch (item.getId()) { case DELETE_ID: deleteItem();
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roidism, accounting for the complaint of uncomfortable tightness of proximal limb muscles. A curious rippling phenomenon in muscles called myokymia, inherited as an autosomal dominant trait, has been observed in several families (Chap. 55). After a period of relaxation, a stiffening and rippling occurs in the contracting or stretched muscles. The stiffness is reduced by dantrolene but not by tocainamide. Acquired forms of myokymia are due to diverse processes, in particular nerve injury and regeneration (especially in the face, as noted in Chap. 47), hypothyroidism, and obscure causes such as thymoma. A prolonged failure of relaxation following contraction of a muscle is characteristic of the myotonic phenomenon, which typi es certain diseases congenital myotonia (of Thomsen), myotonic dystrophy, and the paramyotonia of Eulenberg (Chap. 54). True myotonia, with its prolonged discharge of membrane action potentials, requires strong contraction to elicit, is more evident after a period of relaxation, and tends to disappear with repeated contractions (pages 1265 and 1363). Paradoxical myotonia refers to an increase in the degree of myotonia during a series of contractions (the reverse of what happens in the usual type of myotonia). It also occurs in some cases of Eulenberg paramyotonia. This persistence of contraction is demonstrable also by tapping a muscle (percussion myotonia), a phenomenon easily distinguished from the electrically silent local bulge (myoedema) induced by tapping the muscle of a myxedematous or cachetic patient and from the brief fascicular contraction that is induced by tapping a normal or partially denervated muscle; the latter is referred to as idiomuscular contraction. It should be noted that in patients with hyperactive tendon re exes, striking the muscle rather than its tendon can elicit a stretch re ex. An increment in power with a series of several voluntary contractions in the absence of myotonia is a feature of the inverse myasthenic (Lambert-Eaton) syndrome, which is associated in about 50 percent of cases with small-cell carcinoma of the lung. The same increment occurs in botulism. In both instances there is an electromyographic (EMG) equivalent a rapid increase in the voltage of a series of action potentials upon appropriate stimulation (pages 1101 and 1259). The effect of cold on muscle contraction may also prove informative; either paresis or myotonia, lasting for a few minutes, may be evoked or enhanced by cold. This is most prominent in the paramyotonia of Eulenberg, but it may occur to some degree in all the other myotonic disorders. Myotonia and myoedema must also be distinguished from the recruitment and spread of involuntary spasm induced by strong and repeated contractions of limb muscles in patients with mild or localized tetanus, with the stiff-man syndrome (Chap. 55), and with dystonias of various types. These are not primary muscle phenomena but are neural in origin, due to an abolition of inhibitory mechanisms. The repeated contraction of forearm or leg muscles after the application of a tourniquet (exceeding arterial pressure) to the proximal part of a limb will often elicit latent tetany (carpopedal spasms). Its special mode of development in conditions that decrease the concentration of ionized calcium as well as its duration, its enhancement by hyperventilation, and the association of tingling, prickling paresthesias separate tetany from ordinary cramp and also from true physiologic contracture. In practice, the term contracture is applied (somewhat indiscriminately, as discussed below) to all states of xed muscle shortening. Several distinct types can be recognized. In true physiologic contracture a group of muscles, after a series of strong contractions,
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