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The following statements concern the autonomic nervous system: (a) An Argyll Robertson pupil indicates that the accommodation reflex for near vision is normal but that the light reflex is lost symptoms 97 jeep 40 oxygen sensor failure discount dilantin 100mg online. The following general statements concern the autonomic nervous system: (a) the hypothalamus has little control over the autonomic nervous system medications canada generic 100mg dilantin fast delivery. View Answer Directions: Each of the numbered items or incomplete statements in this section is followed by answers or completions of the statement treatment 1 degree av block dilantin 100 mg. The sympathetic outflow: (a) arises from nerve cells that are situated in the posterior gray column (horn) of the spinal cord (b) has preganglionic nerve fibers that leave the spinal cord in the posterior roots of the spinal nerves (c) is restricted to medications emt can administer 100mg dilantin overnight delivery the T1-L2 segments of the spinal cord (d) receives descending fibers from supraspinal levels that pass down the spinal cord in the posterior white column (e) has many preganglionic nerve fibers that synapse in the posterior root ganglia of the spinal nerves View Answer 6. Norepinephrine is secreted at the endings of the: (a) preganglionic sympathetic fibers (b) preganglionic parasympathetic fibers (c) postganglionic parasympathetic fibers (d) postganglionic sympathetic fibers (e) preganglionic fibers to the suprarenal medulla View Answer 7. The parasympathetic innervation controlling the parotid salivary gland arises from the: (a) facial nerve. Which of the following statements best describes the parasympathetic part of the autonomic nervous system? Anticholinesterase drugs act at synapses by: (a) mimicking the action of acetylcholine at its receptor sites (b) preventing the release of acetylcholine (c) increasing the secretion of acetylcholine (d) blocking the breakdown of acetylcholine (e) preventing the uptake of acetylcholine by the nerve ending View Answer 10. Atropine has the following effect on the autonomic nervous system: (a) It is an anticholinesterase drug. The following statements concern autonomic innervation of the urinary bladder: (a) the parasympathetic part brings about relaxation of the bladder wall muscle and contraction of the sphincter vesicae. The following statements concern the autonomic innervation of the heart: (a) the parasympathetic part causes dilation of the coronary arteries. Directions: Match the numbered glands with the most appropriate lettered autonomic ganglion listed below. Submandibular gland (a) Otic ganglion (b) Submandibular ganglion (c) Pterygopalatine ganglion (d) Ciliary ganglion (e) None of the above View Answer 15. Lacrimal gland (a) Otic ganglion (b) Submandibular ganglion (c) Pterygopalatine ganglion (d) Ciliary ganglion (e) None of the above View Answer 16. Nasal glands (a) Otic ganglion (b) Submandibular ganglion (c) Pterygopalatine ganglion (d) Ciliary ganglion (e) None of the above View Answer 17. Parotid gland (a) Otic ganglion (b) Submandibular ganglion (c) Pterygopalatine ganglion (d) Ciliary ganglion (e) None of the above View Answer 18. Sublingual gland (a) Otic ganglion (b) Submandibular ganglion (c) Pterygopalatine ganglion (d) Ciliary ganglion (e) None of the above View Answer Match the numbered autonomic ganglia with the most appropriate lettered viscus or muscle listed below. Superior cervical ganglion (a) Levator palpebrae superioris (smooth muscle only) (b) Vermiform appendix (c) Constrictor pupillae (d) Descending colon (e) None of the above View Answer 20. Ciliary ganglion (a) Levator palpebrae superioris (smooth muscle only) (b) Vermiform appendix (c) Constrictor pupillae (d) Descending colon (e) None of the above View Answer 21. Celiac ganglion (a) Levator palpebrae superioris (smooth muscle only) (b) Vermiform appendix (c) Constrictor pupillae (d) Descending colon (e) None of the above View Answer 22. Inferior mesenteric ganglion (a) Levator palpebrae superioris (smooth muscle only) (b) Vermiform appendix (c) Constrictor pupillae (d) Descending colon (e) None of the above View Answer 23. Superior mesenteric ganglion (a) Levator palpebrae superioris (smooth muscle only) (b) Vermiform appendix (c) Constrictor pupillae (d) Descending colon (e) None of the above View Answer Match the numbered cranial nerves with the appropriate lettered nuclei listed below. Facial nerve (a) Inferior salivatory nucleus (b) Edinger-Westphal nucleus (c) Lacrimatory nucleus (d) None of the above View Answer 25. Oculomotor nerve (a) Inferior salivatory nucleus (b) Edinger-Westphal nucleus (c) Lacrimatory nucleus (d) None of the above View Answer 26. Glossopharyngeal nerve (a) Inferior salivatory nucleus (b) Edinger-Westphal nucleus (c) Lacrimatory nucleus (d) None of the above View Answer 27. Hypoglossal nerve (a) Inferior salivatory nucleus (b) Edinger-Westphal nucleus (c) Lacrimatory nucleus (d) None of the above View Answer the following questions apply to Figure 14-19. Match the numbered areas of referred pain with the appropriate lettered viscus originating the pain listed below. Number 1 (a) Heart (b) Appendix (c) Gallbladder (d) Stomach (e) None of the above View Answer 29.

Syndromes

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Not surprisingly treatment syphilis discount dilantin 100 mg otc, in view of the above symptoms xanax is prescribed for buy 100mg dilantin, differing opinions have been held about the causation of dystonia from time to medications qid effective dilantin 100 mg time medications during breastfeeding buy 100 mg dilantin mastercard. Many examples, and particularly the focal forms, were long considered to be psychogenic in origin, for example torticollis and blepharospasm. However, evidence now increasingly favours the view that both focal and generalised dystonias form part of a spectrum, founded in some subtle disturbance of brain biochemistry and physiology. One model focuses on the role of the basal ganglia in regulating motor activity, suggesting that there is functional impairment in output from the globus pallidus interna and the substantia nigra pars reticulata. This reduced activity leads to disinhibition of the thalamus and the motor cortex, producing abnormal movements (Berardelli et al. Vitek (2002) further suggests that dystonias arise from alterations in the rate, pattern, somatosensory responsiveness and synchronisation of neural activity in the pallidothalamo-cortical circuits. The resurgence of such a view has depended on a number of factors: the demonstration of relationships between the different forms, observation of transitions from one form to another, the similarities in clinical picture between symptomatic and idiopathic cases, and not least the provocation of classic examples by a range of pharmacological agents. Moreover, careful control comparisons have increasingly failed to confirm an excess of personality In a small proportion of cases it is nonetheless still accepted, even by experienced observers, that the dystonia is primarily psychogenic in origin. And of course in many patients there will be a strong interaction between organic predisposition and the modulating influence of emotional and environmental factors. Dystonia musculorum deformans (generalised torsion dystonia) Generalised torsion dystonia leads to severe and progressive crippling. Within families who inherit the major disease other members may show formes frustes of the disorder: abnormalities of gait, abnormal arm postures, minor speech defects, or static postural abnormalities such as pes equinovarus or kyphoscoliosis. The gene produces a mutant form of the protein torsin A, whose precise role awaits clarification. Pathological studies have occasionally reported abnormal findings in the basal ganglia, substantia nigra and elsewhere, but these are regarded as non-specific or even artefactual. However, the evidence points to involvement of the basal ganglia, both by analogy with examples that are symptomatic of known brain lesions and the response that may be observed to stereotactic surgery. Clinical features the symptoms usually commence in childhood or early adolescence. The first symptom is commonly a disturbance of gait, with plantar flexion, inversion and adduction of the foot when walking. At first the picture is sometimes bizarre with respect to the precise functions affected, as already mentioned. More rarely the initial disturbance may appear in the upper limbs with abnormal postures or actions. A characteristic dystonic posture consists of extension and hyperpronation of the arms, with flexion of the wrist and extension of the fingers. In the early stages the motor abnormalities may become apparent only when activity is attempted and nothing unusual can be found on examination at rest. Remissions lasting for several months at a time may occur, all adding to the erroneous impression that the disorder is psychogenic in origin. Indeed, a hysterical disturbance is not infrequently diagnosed initially, particularly when there are coexistent emotional problems or adverse environmental factors. The mistake is easily made in view of the rarity of the disorder and the bizarre nature of the symptoms. Other objective signs of a cerebral lesion are absent, with normal tendon reflexes and unimpaired intelligence. Moreover, the dystonic postures that can occur in conversion hysteria are sometimes indistinguishable from the transient early disturbances of dystonia musculorum deformans. Later, the muscle spasms occur even when the body is relaxed, producing irregular spontaneous movements or fixed dystonic postures. Other parts of the body come to be affected, usually with symmetrical involvement of all four limbs, the trunk and the neck. The proximal muscles tend to be affected more than the distal, and a rotatory element in the axial musculature is typical. The trunk is forced into marked lordosis or scoliosis, and fixed contractures of the limbs lead eventually to severe crippling and permanent deformity. Tendon reflexes become difficult to obtain or may be exaggerated, but the plantar responses remain down-going. Rapid progress and widespread involvement is usual when the onset is in childhood or adolescence.

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For example medicine nobel prize 2015 buy 100mg dilantin otc, in a randomised study of patients and their families a few weeks after stroke xanthine medications order dilantin 100mg with mastercard, one-third of caregivers were visited at home to medicine questions dilantin 100 mg otc be taught problem-solving skills using a systematic four-step approach (Grant et al symptoms breast cancer proven 100 mg dilantin. Telephone contact, initially weekly, was then used to consolidate the intervention. After 3 months the intervention group, compared with a sham intervention and a control treatment-as-usual group, showed better problemsolving and were less depressed. The study did not attempt to examine any impact the intervention might have had on the patients themselves. In a study of 240 stroke patients randomised to receive visits from a specialist outreach nurse to provide information, advice and support over the first 12 months compared with treatment as usual, there was no reduction in stress in carers (Forster & Young 1996). Therefore it is not yet possible to give firm advice as to what technique to use to reduce carer stress, and whether in fact it will make much difference anyway. Depression and other mood disorders It is scarcely surprising that depressive reactions should be common in survivors of strokes. Ullman (1962) vividly describes the subjective impact which the experience may have. The patient finds himself abruptly in the grip of something novel, frightening and ill understood. Even slight interference in free communication with those around will greatly intensify feelings of isolation, threat or loss. When the acute stage is over there is a variety of factors around which depression may come to be organised: the frustrations of physical handicaps, uncertainty about the prospects of their resolution, the enforced dependency and imposition of the invalid role. In the longer term the patient may face loss of job and status, financial insecurity, a sense of uselessness or the prospect of permanent loss of independence. At what stage should such depressive reactions be regarded as a case of depression? It could be argued that there is a danger of overestimating depression after stroke if physical symptoms of stroke are interpreted as evidence of depression (Box 8. Patients diagnosed with depression after stroke, compared with primary depression (depression that is not secondary to brain disease or other factors), have more physical symptoms and less evidence of melancholia (Beblo & Driessen 2002). Depressed stroke patients are much more likely to endorse symptoms like fatigue and sleep disturbance than stroke patients who are not depressed (Williams et al. Most studies find that survivors of stroke, when compared with age-matched controls, are more depressed. Indeed stroke patients have been found to show a higher incidence of depression than orthopaedic controls or patients suffering from traumatic brain injuries, despite equivalent levels of disability in terms of activities of daily living or cognitive dysfunction (Folstein et al. However, one study comparing survivors of stroke with Cerebrovascular Disorders 485 Box 8. A systematic review of studies of depression after stroke found that the estimates of the prevalence of depression vary according to which rating scales have been used (Hackett & Anderson 2005), but that even using clinical assessments. Nevertheless, when the findings across studies were collated the pooled estimates were fairly consistent, indicating that about one-third of patients had significant depressive symptoms, regardless of whether the cases were ascertained from the community, from hospital or from rehabilitation settings. The pooled estimates of the time course of depression were largely based on different cross-sectional studies, each study assessing depression at a different time after stroke; only a small minority of studies had longitudinally assessed depression. Whether the study was early, in the first few weeks and months after stroke, or late, on average the rate of depression did not change. However, even though the rate of depression at each time point remains fairly constant, depression early after stroke has a good chance of remitting over the course of the first year; this is counterbalanced by the finding that other patients become depressed for the first time many months after stroke. Based on the same systematic review of papers, Hackett and Anderson (2005) found that the best predictor of depression was stroke severity, including the extent of physical disability and cognitive impairment. One matter of interest is whether the laterality of the stroke is related to depression. Early studies suggested that left hemisphere infarcts, particularly if located anteriorally, were more likely to produce depression (Robinson & Price 1982; Robinson et al.

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The neural crest cells will form the first afferent sensory neurons in the posterior root ganglia of the spinal nerves and the sensory ganglia of the cranial nerves medicine woman dr quinn order dilantin 100 mg visa. Level of Decussation of Pyramids A transverse section through the inferior half of the medulla oblongata treatment x time interaction generic dilantin 100mg with visa. In the superior part of the medulla symptoms 7 dilantin 100 mg free shipping, the corticospinal fibers occupy and form the pyramid medications 5 rs order 100mg dilantin with mastercard, but inferiorly, about three-fourths of the fibers cross the median plane and continue down the spinal cord in the lateral white column as the lateral corticospinal tract. As these fibers cross the midline, they sever the continuity between the anterior column of the gray matter of the spinal cord and the gray matter that surrounds the central canal. The fasciculus gracilis and the fasciculus cuneatus continue to ascend superiorly posterior to the central gray matter. The nucleus gracilis and the nucleus cuneatus appear as posterior extensions of the central gray matter. The substantia gelatinosa in the posterior gray column of the spinal cord becomes continuous with the inferior end of the nucleus of the spinal tract of the trigeminal nerve. The fibers of the tract of the nucleus are situated between the nucleus and the surface of the medulla oblongata. The lateral and anterior white columns of the spinal cord are easily identified in these sections, and their fiber arrangement is unchanged. Level of Decussation of Lemnisci A transverse section through the inferior half of the medulla oblongata, a short distance above the level of the decussation of the pyramids, passes through the decussation of lemnisci, the great sensory decussation. The decussation of the lemnisci takes place anterior to the central gray matter and posterior to the pyramids. It should be understood that the lemnisci have been formed from the internal arcuate fibers, which have emerged from the anterior aspects of the nucleus gracilis and nucleus cuneatus. The internal arcuate fibers first travel anteriorly and laterally around the central gray matter. They then curve medially toward the midline, where they decussate with the corresponding fibers of the opposite side. The nucleus of the spinal tract of the trigeminal nerve lies lateral to the internal arcuate fibers. The lateral and anterior spinothalamic tracts and the spinotectal tracts occupy an area lateral to the decussation of the lemnisci. They are very close to one another and collectively are known as the spinal lemniscus. The spinocerebellar, vestibulospinal, and the rubrospinal tracts are situated in the anterolateral region of the medulla oblongata. Level of the Olives A transverse section through the olives passes across the inferior part of the fourth ventricle. Figure 5-12 Transverse section of the medulla oblongata at the level of decussation of the pyramids. Figure 5-15 Transverse section of the medulla oblongata at the level of the middle of the olivary nuclei. The gray matter is shaped like a crumpled bag with its mouth directed medially; it is responsible for the elevation on the surface of the medulla called the olive. The cells of the inferior olivary nucleus send fibers medially across the midline to enter the cerebellum through the inferior cerebellar peduncle. Afferent fibers reach the inferior olivary nuclei from the spinal cord (the spino-olivary tracts) and from the cerebellum and cerebral cortex. Vestibulocochlear Nuclei the vestibular nuclear complex is made up of the following nuclei: (1) medial vestibular nucleus, (2) inferior vestibular nucleus, (3) lateral vestibular nucleus, and (4) superior vestibular nucleus. The medial and inferior vestibular nuclei can be seen on section at this level. The anterior cochlear nucleus is situated on the anterolateral aspect of the inferior cerebellar peduncle, and the posterior cochlear nucleus is situated on the posterior aspect of the peduncle lateral to the floor of the fourth ventricle. The Nucleus Ambiguus the nucleus ambiguus consists of large motor neurons and is situated deep within the reticular formation.

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