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By: D. Jaroll, M.B. B.CH. B.A.O., M.B.B.Ch., Ph.D.

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He never did pain medication for dogs after surgery purchase anacin 525mg on-line, however milwaukee pain treatment services safe anacin 525mg, venture too far away from his neurologic roots pain treatment center of franklin tennessee buy anacin 525 mg with visa, as demonstrated in his work On Narcissism (1959) pain treatment satisfaction questionnaire trusted anacin 525 mg, in which he suggested that all provisional ideas on psychology will one day be explained by organic substrates. To support his beliefs, Flourens developed the ablation experiment, in which removing any part of the brain in birds led to generalized disorders of behavior. Sensory input at an elementary level is localized, but the process of perception involves the whole brain. All cerebral material is equipotential; that is, if sufficient cortical material is intact, the remaining material will take over the functions of any missing brain tissue. Flourens suggested that the brain operated in an integrated fashion, not in discrete faculties, and that mental functions depend on the brain functioning as a whole. Thus, the size of the injury, rather than its location, determines the effects of brain injury. First, he used animals with brains so small that any ablation would invade more than one functional area. Second, he observed only motor behavior-that is, behaviors such as eating or wing flapping-whereas the localizationists were mostly interested in more complex faculties such as friendship or intellect. Flourens also erroneously suggested that humans use only 10% of the brain, an idea that laypeople still commonly hold today. Despite these scientific problems, many accept Flourens as having refuted localization theory. Marie found that Leborgne had widespread damage, not a specific lesion, as Broca had suggested. In general, these researchers proposed that, although basic sensorimotor functions may be localized in the brain, higher cortical processes were too complex to confine to any one area. Two important neuropsychological findings also challenged strict localization theory. In 1881 (cited by Blakemore, 1977), Hermann Munk (1839­1912) found that experimental lesions in the association cortex of a dog produced temporary mind-blindness: the animal could see objects but failed to recognize their significance. In the experiment, Munk first had the dogs learn to associate the shape of a triangle with fear by pairing them together with an electric shock. After the dogs learned the association, Munk lesioned parts of the cortex that were not primarily involved with vision. Afterward, the dogs could see the object but could not perceive the meaning of the stimuli to which they were conditioned before the surgery. In 1914, Joseph Babinski (1857­1932), the founder of neurology, introduced the term anosognosia, which means "no knowledge of the disease," to describe an inability or refusal to recognize that one has a particular disease or disorder, thereby introducing the phenomenon of unawareness (Babinski & Joltran, 1924). Babinski observed patients who had lesions, most often in the association cortex of the right hemisphere. These patients were capable of seeing and hearing, but denied that anything was wrong with them even when they had severe neurologic damage such as hemiplegia. Karl Lashley (1890­1958), a student of the famous behaviorist John Watson, was a great exemplar of experimental neuropsychology and, according to Hebb (1983), practically its founder. He was one of the first to combine behavioral sophistication in experiments with neurologic sophistication. Although Lashley accepted the localization of basic sensory and motor skills, he supported equipotential views with experiments on rats similar to those of Flourens on birds (Lashley, 1929). Lashley found that impairment in maze running in the rat was directly related to the amount of cortex removed. From his experiments, Lashley formulated his famous principle of mass action: the extent of behavioral impairments is directly proportional to the mass of the removed tissue. Lashley also emphasized the multipotentiality of brain tissue: Each part of the brain participates in more than one function (Teuber, Battersby, & Bender, 1960). Lashley believed that his results were highly compatible with a view that brain tissue is equipotential and can be involved in tasks other than those assigned by the localizationists. Clinical observers of medical patients with very small lesions have often reported marked behavioral deficits, even though the lesion may be microscopic. Thus, equipotentiality theory fails to account for the specific deficits often seen in the absence of general impairment in intellect, abstract attitude, perception, or other global ability. The creation of one such model has been credited to the English neurologist Hughlings Jackson (1835­1911), whose primary work was written during the second half of the nineteenth century, but was not published in the United States until the 1950s.

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The moving two-point discrimination test is easy to perform rapidly with equipment available virtually everywhere: a paper clip treatment for dog gas pain buy anacin with paypal. The moving two-point discrimination test offers several advantages compared to the classic twopoint discrimination test drug treatment for shingles pain discount anacin 525mg amex. As the sensation of moving touch is recovered distally sooner than constant touch8 (see Chapter 7) pain and injury treatment center purchase anacin now, so too back pain treatment during pregnancy order anacin with mastercard, moving two-point discrimination testing will give information concerning the results of nerve repair sooner than two-point discrimination testing. In the individual patient, the ability to discriminate two-points moving from one recovers not only sooner but also to a higher degree (lower moving two-point discrimination) than does constant-touch. Expressed another way, the patient has a better functional result from his nerve repair than classic two-point discrimination testing suggests. The moving two-point discrimination test also is an accurate monitor of gains in function during sensory re-education. Another advantage of the moving two-point discrimination test is that it is a "pure" sensory test. The moving twopoint discrimination test, a test done to not by the patient, permits the tester to assess purely sensory function. Because the moving two-point discrimination test evaluates the fiber/receptor system that mediates moving touch, the moving two-point discrimination test overcomes the criticisms6-11 of classic two-point discrimination in evaluating functional sensation. But if the sensory grip in fact requires movement, such as winding a watch or buttoning a button, or if the hand function requires the fingertips to move over an object, then the moving two-point discrimination test should be more appropriate. Recently, we have demonstrated that the moving twopoint discrimination test is the only test of sensibility to correlate with the ability to recognize objects (tactile gnosis) (see Chapter 10). Less than 1% of adults with median or ulnar nerve repairs at the wrist recover to level S4. Thus, following a nerve repair, the absolute number of axons reaching the fingertip is reduced by attrition at the suture line, axonal misdirection down the wrong endoneurial sheath, ar. It is given that some minimal peripheral innervation density is critical for tactile discrimination. If only a third of fibers are slowly-adapting, and only, say, half the total number of fibers regenerate to the periphery, the critical innervation density for slow-adapters is more likely not to be met than for the quick-adapters. Furthermore, the degenerating Meissner corpuscle can be reinnervated by any one of the three to nine quickly-adapting axons that normally innervate it, while two to four degenerating Merkel cells are less likely to be reinnervated by the one slowly-adapting fiber that normally innervates them. Compounding this is the experimental observation that the Merkel cell degenerates more rapidly than Meissner corpuscle (Chapter 4). In essence, it is statistically highly more probable to reinnervate the Meissner corpuscles, the fiber/receptor system primarily tested by the moving two-point discrimination test. As the paper clip moves across the papillary ridges, it sets up not only a sequence of brief touches, but also a vibration within the area of its movement, similar to the disturbance the passenger in a car feels crossing railroad tracks. These low-frequency pertubations of the resting state in the fingertip pulp stimulate the entire Meissner afferent group of quickly-adapting fibers. Almost certainly, however, the remaining quickly-adapting fibers (the Pacinian afferents) will be stimulated as will the slowly-adapting fiber/ receptor systems. But as the paper clip moves along the fingertip due to the phenomenon of "recruitment," increasing responses will come from the quicklyadapting fiber/receptors. The slowly-adapting fiber/receptors, always in the minority, probably make only a functionally insignificant contribution to our perception of the two moving points. Therefore, I believe it is effectively correct to speak of this test as one that evaluates the innervation density of the quicklyadapting fiber/receptor system in general, and the Meissner afferents in particular. Moberg E: Future hope or thr surgical management of peripheral nerve lesions, in Michon J, Moberg E (eds): Traumatic Nerve Lesions. Amer Arbr Sci, Amer Arbor, 1977 by report to the international union, LaMotte R, Mountcastle B: Symposium on "Active Touch," Beaune, France, 1977 29. Corkin S, Milner B, Rasmussen T: Somatosensory threshold: Contrasting effects of post-central gyrus and posterior parietal lobe excision. Horch K: Guidance of regrowing sensory axons after cutaneous nerve lesions in the cat. Is there a distinct vibratory "sense" as there is a sense of smell: is the perception of a vibratory stimulus mediated by its own submodality specific neuroanatomic pathway, such as the perception of sound or light? The perception of vibration, or vibratory sense, is taught as if it were a separate sensory submodality, such as pain, temperature, and touch. The final step in this subliminal indoctrination is the constant association of this "vibratory sense" with known spinal cord anatomy; "vibratory sense" is destroyed with lesions to the posterior white columns, the fasciculus cunneatus and gracilis. Perception of a vibratory stimulus is the same as perception of successive, brief touch stimuli.

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Delayed coma after hypoxia has been reported most often after carbon monoxide or asphyxial gas poisoning pain medication for dogs surgery generic anacin 525mg online, but as shown in Patient 5­11 pain management for osteosarcoma in dogs buy anacin 525 mg with amex, cases are known in which other injuries flourtown pain evaluation treatment center cheap anacin 525mg without prescription, including hypoglycemia dna advanced pain treatment center pa anacin 525mg amex, cardiac arrest, strangulation, or a complication of surgical anesthesia, have provided the antecedent insult. Often, the neurologic changes are at first mistaken for a psychiatric disorder or even a subdural hematoma because of the lucid interval. Pathologically, the brains of patients dying of delayed postanoxic deterioration contain diffuse, severe, and bilateral leukoencephalopa- thy of the cerebral hemispheres with sparing of the immediate subcortical connecting fibers and, usually, of the brainstem. The basal ganglia are sometimes infarcted,200 but the nerve cells of the cerebral hemispheres and the brainstem remain mostly intact. This genetic defect is not known to cause cerebral disease and its relationship to the demyelination is unclear. There is no specific treatment, but bedrest for patients with acute hypoxia may prevent the complication. Another sequela of severe diffuse hypoxia is the syndrome of intention or action myoclonus. About 40% of patients who do not regain consciousness after cardiac resuscitation develop myoclonic status epilepticus. Affected patients who awaken from posthypoxic coma usually are dysarthric, and attempted voluntary movements are marked by myoclonic jerks of trunk and limb muscles. In one series of 51 patients admitted to the hospital for hypoglycemia, 41 were diabetics, 36 being treated with insulin and five with sulfonylurea drugs. In nondiabetic patients, the hypoglycemia had been induced by excessive alcohol and one patient had injected herself with insulin in a suicide attempt. In patients taking either insulin or oral hypoglycemics, the addition of fluoroquinolones, mostly gatifloxacin or ciprofloxacin, may induce severe hypoglycemia207 (gatifloxacin can also cause hyperglycemia208). The intake of alcohol and perhaps psychoactive drugs in insulin-treated diabetics with severe hypoglycemia is relatively common. In fact, alcohol alone is responsible for a significant percentage of patients with severe hypoglycemia. Fortunately, in most emergency departments a blood glucose from a fingerstick is done as a matter of course in any patient with altered mental status. Pathologically, hypoglycemia directs its main damage at the cerebral hemispheres, producing laminar or pseudolaminar necrosis in fatal cases, but largely sparing the brainstem. Clinically, the picture of acute metabolic encephalopathy caused by hypoglycemia usually presents in one of four forms: (1) as a delirium manifested primarily by mental changes with either quiet and sleepy confusion or wild mania; (2) coma accompanied by signs of multifocal brainstem dysfunction including neurogenic hyperventilation and decerebrate spasms. In this form pupillary light reactions, as well as oculocephalic and oculovestibular responses, are usually preserved to suggest that the underlying disorder is metabolic. The patients sometimes have shiver-like diffuse muscle activity and many are hypothermic (338C to 358C); (3) as a stroke-like illness characterized by focal neurologic signs with or without accompanying coma. In one series of patients requiring hospital admission, 5% suffered transient focal neurologic abnormalities. This kind of shifting deficit, as well as the fact that focal neurologic signs also occur in children in coma with severe hypoglycemia, stands against explaining the localized neurologic deficits as being caused by cerebral vascular disease; (4) as an epileptic attack with single or multiple generalized convulsions and postictal coma. The varying clinical picture of hypoglycemia often leads to mistaken clinical diagnoses, particularly when in a given patient the clinical picture varies from episode to episode, as in Patient 5­12. Patient 5­12 A 45-year-old woman was hospitalized for treatment of a large pelvic sarcoma. Her eyes were open, but she did not respond to questioning, although she moved all four extremities in response to noxious stimuli. The next day her roommate called for help when the patient did not respond to her questions. Again she was hypoglycemic, and the symptoms resolved after the infusion of glucose. Comment: the variability and neurologic findings from episode to episode make hypoglycemia a great imitator, particularly of structural disease of the nervous system, raising the question of whether prehospital blood glucose measurement should be done in all patients suspected by emergency medical services of having had a stroke. In one such series of 185 patients suspected of ``cerebral vascular accident,' five were found to be hypoglycemic and all were medication-controlled diabetics. Neither the history nor the physical examination reliably distinguishes hypoglycemia from other causes of metabolic coma, although (as is true in hepatic coma) an important clinical point is that the pupillary and vestibulo-ocular reflex pathways are almost always spared. The great danger of delayed diagnosis is that the longer hypoglycemia lasts, the more likely it is to produce irreversible neuronal loss.

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The continuity of the various cranial nerve nuclei through the different regions of the brainstem is shown diagrammatically in Figure 5-29 pain treatment for kidney infection anacin 525 mg discount. Oculomotor Trochlear Mesencephalic nucleus of trigeminal Main sensory nucleus of trigeminal Motor nucleus of trigeminal Abducent Facial Dorsal cochlear and vestibular nuclei Nucleus ambiguus Dorsal vagal nucleus Hypoglossal Nucleus of tractus solitarius Spinal nucleus of trigeminal A B Figure 5-29 Position of some of the cranial nerve nuclei in the brainstem natural treatment for post shingles pain discount 525mg anacin amex. These tracts may become involved in demyelinating diseases unifour pain treatment center hickory nc generic anacin 525mg with visa, neoplasms a better life pain treatment center flagstaff az purchase cheap anacin online, and vascular disorders. Arnold-Chiari Phenomenon the Arnold-Chiari malformation is a congenital anomaly in which there is a herniation of the tonsils of the cerebellum and the medulla oblongata through the foramen magnum into the vertebral canal (Fig. This results in the blockage of the exits in the roof of the fourth ventricle to the cerebrospinal fluid, causing internal hydrocephalus. It is commonly associated with craniovertebral anomalies or various forms of spina bifida. Signs and symptoms related to pressure on the cerebellum and medulla oblongata and involvement of the last four cranial nerves are associated with this condition. Raised Pressure in the Posterior Cranial Fossa and Its Effect on the Medulla Oblongata the medulla oblongata is situated in the posterior cranial fossa, lying beneath the tentorium cerebelli and above the foramen magnum. It is related anteriorly to the basal portion of the occipital bone and the upper part of the odontoid process of the axis and posteriorly to the cerebellum. In patients with tumors of the posterior cranial fossa, the intracranial pressure is raised, and the brain­­that is, the cerebellum and the medulla oblongata­­tends to be pushed toward the area of least resistance; there is a downward herniation of the medulla and cerebellar tonsils through the foramen magnum. This will produce the symptoms of headache, neck stiffness,and paralysis of the glossopharyngeal,vagus,accessory, and hypoglossal nerves owing to traction. In these circumstances, it is extremely dangerous to perform a lumbar Vascular Disorders of the Medulla Oblongata Lateral Medullary Syndrome of Wallenberg the lateral part of the medulla oblongata is supplied by the posterior inferior cerebellar artery, which is usually a branch of the vertebral artery. This coronal section of the skull shows the herniation of the cerebellar tonsil and the medulla oblongata through the foramen magnum into the vertebral canal. Medial Medullary Syndrome the medial part of the medulla oblongata is supplied by the vertebral artery. Tumors of the Pons Astrocytoma of the pons occurring in childhood is the most common tumor of the brainstem. The symptoms and signs are those of ipsilateral cranial nerve paralysis and contralateral hemiparesis: weakness of the facial muscles on the same side (facial nerve nucleus), weakness of the lateral rectus muscle on one or both sides (abducent nerve nucleus), nystagmus (vestibular nucleus), weakness of the jaw muscles (trigeminal nerve nucleus), impairment of hearing (cochlear nuclei), contralateral hemiparesis, quadriparesis (corticospinal fibers), anesthesia to light touch with the preservation of appreciation of pain over the skin of the face (principal sensory nucleus of trigeminal nerve involved, leaving spinal nucleus and tract of trigeminal intact), and contralateral sensory defects of the trunk and limbs (medial and spinal lemnisci). Involvement of the corticopontocerebellar tracts may cause ipsilateral cerebellar signs and symptoms. There may be impairment of conjugate deviation of the eyeballs due to involvement of the medial longitudinal fasciculus, which connects the oculomotor, trochlear, and abducent nerve nuclei. Clinical Significance of the Pons the pons, like the medulla oblongata and the cerebellum, is situated in the posterior cranial fossa lying beneath the tentorium cerebelli. It is related anteriorly to the basilar artery, the dorsum sellae of the sphenoid bone, and the basilar part of the occipital bone. In addition to forming the upper half of the floor of the fourth ventricle, it possesses several important cranial nerve nuclei (trigeminal,abducent,facial,and vestibulocochlear) and serves as a conduit for important ascending and descending tracts (corticonuclear,corticopontine,corticospinal,medial longitudinal fasciculus and medial, spinal, and lateral lemnisci). It is not surprising, therefore, that tumors, hemorrhage, or infarcts in this area of the brain produce a variety of symptoms and signs. For example, involvement of the corticopontocerebellar Pontine Hemorrhage the pons is supplied by the basilar artery and the anterior, inferior, and superior cerebellar arteries. If the hemorrhage occurs from one of those arteries and is unilateral, there will be facial paralysis on the side of the lesion (involvement of the facial nerve nucleus and, therefore, a lower motor neuron palsy) and paralysis of the limbs on the opposite side (involvement of the corticospinal fibers as they pass through the pons). There is often Clinical Notes 219 Cavity of fourth ventricle Tectospinal tract Medial lemniscus Pyramid Area supplied by vertebral artery Hypoglossal nerve Arcuate nucleus Figure 5-32 Transverse section of the medulla oblongata at the level of the inferior olivary nuclei showing the extent of the lesion producing the medial medullary syndrome. When the hemorrhage is extensive and bilateral, the pupils may be "pinpoint" (involvement of the ocular sympathetic fibers); there is commonly bilateral paralysis of the face and the limbs. The patient may become poikilothermic because severe damage to the pons has cut off the body from the heat-regulating centers in the hypothalamus. Trauma to the Midbrain Among the mechanisms of injuries to the midbrain, a sudden lateral movement of the head could result in the cerebral peduncles impinging against the sharp rigid free edge of the tentorium cerebelli. Sudden movements of the head resulting from trauma cause different regions of the brain to move at different velocities relative to one another. For example, the large anatomical unit, the forebrain, may move at a different velocity from the remainder of the brain, such as the cerebellum. Involvement of the oculomotor nucleus will produce ipsilateral paralysis of the levator palpebrae superioris; the superior, inferior, and medial rectus muscles; and the inferior oblique muscle.