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By: Abul K. Abbas, MBBS

  • Distinguished Professor and Chair, Department of Pathology, University of California San Francisco, San Francisco, California

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Although more pronounced during moments of stuttering treatment breast cancer buy pepcid with american express, reversals were also expressed during perceptually fluent speech 4 medications safe pepcid 40 mg. First medicine grace potter cheap 20mg pepcid fast delivery, the timing disruptions are seen to treatment ingrown toenail order pepcid line take the form of a faulty programming of the procedural aspects of motor sequencing (the reversals), and delays in attempting to correct for the mistimed motor programming resulting in a delay in sound production. This account of mistiming in some ways provides a very similar picture of stuttering to that proposed by Harrington (1988), and described in the previous chapter; the important difference being that Harrington believed these timing misperceptions are related to the perception of the rhythmic structure of speech, whereas Guitar et al. Second, stuttering ­ and specifically secondary stuttering ­ is seen to arise as a result of anticipatory hypertension. In this theory sequencing reversals represent an active programming decision taken, with the anticipatory contraction occurring as a consequence of attempts to reduce the effects of lip perturbation from the anticipated stutter. They argue that "the persistence of inappropriate efferent activity could produce a vicious cycle effect (positive feedback) leading to progressively increasing levels of cocontraction" (p. At a physiological level this explanation is also consistent with the findings of Freeman and Ushijima (1978). The client is taught techniques to gradually reduce tension, and therefore to change the pitch of the auditory signal. Although there are some limited data that this approach can be successful in reducing tension in stuttered speech, it is now nearly 25 years since Van Riper (1982, p. Using cinefluorographic evidence, Zimmerman (1980a, 1980b, 1984) argued that the lower articulatory velocities and smaller articulatory displacements seen in the speech of adults who stutter were associated with processes that ensured brainstem pathway activation was kept below a certain threshold, and that once this threshold was exceeded, stuttering would result. Further, he found that the interarticulator positionings seen in both perceptually fluent and stuttered utterances were dissimilar to those found in the fluent speech of nonstuttering speakers. The effects of anxiety, for example, can be seen in this neuromotor model as being associated with increased activation of brainstem pathways resulting in activity exceeding the "normal" threshold. In turn, this results in aberrant tuning or triggering inputs for the motorneuron pools implicated in the gestural task required, thus altering the relationships of the appropriate muscle groups and leading to stuttered speech. First, speech breakdowns may be either due to "more variable motorics" resulting from an unstable motor system, or second, that the motor systems of those who stutter are essentially the same as normal speakers but 70 Stuttering and cluttering may show less tolerance to variability, which in normal speakers would have no significant effect on either subcortical activition and gestural-motor behaviour. Articulator sequencing and single data-point studies One way of evaluating the effectiveness of coordinative articulatory systems is by examining the temporal order of movement onsets and peak velocities for combined articulator movements. One of the major findings of the mid1980s was that nonstuttering speakers produced a highly consistent sequence pattern of upper lip, lower lip, jaw, when these three articulators began to move from a vowel towards a bilabial closure target (/p/) (Gracco, 1986; Gracco & Abbs, 1986). Caruso, Abbs, and Gracco (1988) replicated this result with a group of control subjects, but noticed a remarkable difference in performance from a group of adults who stuttered, whose responses showed many reversals and deviations to this pattern during fluent episodes. Unfortunately, a number of subsequent studies failed to replicate this difference, noting that nonstuttering subjects also lack consistency in sequencing patterns (Alfonso, 1991; Max, Gracco, & Caruso, 2004; Ward, 1997a, 1997b). Despite these findings, it does not necessarily follow that adults who stutter do not experience problems with articulatory control, even during fluent episodes, and significant differences between the two groups have been observed. Ward (1997a) found that his group of adults who stuttered reached their articulatory targets with less precision than those of the control speakers, and that this imprecision became more pronounced as greater demands were placed on the speech motor system; for example, when an increased rate of speech or a change in stress pattern was required. One interpretation of this finding is that it might reflect an impairment in intergestural motor timing, albeit one that cannot be characterized in terms of a sequencing deficit. But at what level within the motor output processes is this increased variability occurring? Peters, Hulstijn, and Van Lieshout (2000) argue that the various data point not to an underlying deficit in ability to construct the necessary motor speech plans, but rather to a difference in the parameter settings which are undertaken to adjust the motor programs to the specific demands of each speech situation. That is, although speech movement is controlled in a different way, it may not reflect an impairment with motor speech control so much as either unskilled or perhaps compensatory articulatory strategies. However, one recent study (McClean, Tasko, & Runyan, 2004) analyzed lip, tongue and jaw movement relationships from a group of 37 adults who stuttered and 43 who did not. Results indicated that subgroups of those with more severe 4 Motor speech control and stuttering 71 stuttering displayed more elevated lip­jaw, and tongue­jaw speed ratios. They suggest that kinematic variables could act as predictors for certain stuttering subgroups. For the most part, disturbances to motor speech activity have been ascribed to hemispheric anomalies (in the form of functional and structural asymmetries; see chapter 2) but the cerebellum has also been implicated in the (mis)timing of rhythmic speech and nonspeech tasks in those who stutter (Boutsen, Brutten, & Watts, 2000; Howell, AuYeung, & Rustin, 1997). Max and Yudman (2003) on the other hand failed to find either speech or nonspeech differences in those who stuttered, thus concluding that the cerebellum was not concerned with the mediation of rhythmic timing in speech. A speech motor control model of stuttering has not met with universal acclaim (Conture, 2001; Ingham, 1998). Ingham (1998) has forcefully questioned both the motives and the procedures used in motor speech control studies and articulatory dynamics. Citing a study by McClean, Kroll, and Loftus (1990) which failed to find differences between a group of stutterers and nonstutterers across measures of movement amplitude, duration and velocity, Ingham also notes that one study found that the most severe stuttering was associated with the least articulatory variability (McClean, Levandowski, & Cord, 1994). The authors suggest that increased variability might be a sign of a more stable motor system, rather than a less stable one. Furthermore there is now some suggestion that reduced rather than increased variability characterizes a dysfunctional speech motor system. As Van Lieshout, Hulstijn, and Peters (2004) point out, speech motor control has already been shown to differ considerably depending on both task level complexity and environmental factors amongst those suffering from a number of disorders implicating motor speech control, including Parkinsonism. It would therefore be expected that a disorder such as stuttering, whose essence is likely to be multicausal (Smith & Kelly, 1997; Starkweather & Gottwald, 1990), would be similarly influenced. There needs to be sufficient variability to perform a complex task, but too much variability will result in a failure of that task. Thus the acceptability of variability may depend on the nature of the linguistic data being collected; more automatic speech results from single point data analyses, whilst more complex data arises from connected speech samples and phrase length data (see section below). It may then be that different levels of variability are needed for different tasks depending on the loading of a range of factors such as different levels of complexity both motorically and linguistically (Grosjean, Van Galen, de Jong, Van Lieshout, & Hulstijn, 1997; Kleinow & Smith, 2000; Van Lieshout, Rutjens, & Spauwen, 2002). An overly stable (= rigid) movement pattern would rather impede than facilitate speech motor control under such conditions. On the other hand, in performing highly automatic simple movement patterns, for example repeating the word "apa" repeatedly at the same rate, would not require much movement flexibility, and might actually benefit from a [sic] absolute stable pattern. For example, Ward (1997a) found no difference between adults who stuttered and those who did not when analyzing lip and jaw sequencing patterns, but when the same movement traces were analyzed as phase plane trajectories (Kelso & Tuller, 1987) significant differences between the two groups were uncovered when increased linguistic and motoric demands were introduced. Despite some protestations, research into stuttering and motor variability still continues apace (see section below). Even if the speech of those who stutter is found to be consistently associated with increased variability, and that this variability in turn is shown to correlate with a more stable motor speech system, we would still need to know why such differences exist between those who stutter and those who do not. The analysis of phrase length data One limitation of all these studies lies in the fact that the research focus is on very short periods of time. Articulatory movement from vowel to bilabial closure at normal speech rate takes around 200 ms (0. But speech is a dynamic process, with coarticulation effects extending across a number of phonemes, and some have argued that if we are to fully understand the motor speech control strategies that underlie fluent speech, and any deviance which characterizes stuttered speech, then we need to look at bigger time frames and longer speech sequences. There are now a number of methods that allow the analysis of articulatory patterns across phrase length data (Lucero, Munhall, Gracco, & Ramsey, 1997; Smith, Goffman, Zelaznik, Ying, & McGillem, 1995; Ward & Arnfield, 2001). All work by having subjects repeat a phrase a number of times, whilst the movement of the lower lip is recorded. The variability in the lower lip movement over the phrase is then compared over the repeated trials, resulting in an index of movement variability. In all methods, greater variability in spatio-temporal movement is considered to reflect reduced ability to control motor-speech programming, but different methods of modelling the variability of the movement traces will result in different indices of articulator stability (see Ward & Arnfield, 2001). Surprisingly, they also observed that a slow speech rate did not improve stability, as predicted, and as was the case with the control speakers. In addition, they suggest that the very act of changing timing relations (from the unstable habitual speech rate mode to a new slow mode) changes the operating parameters and may help to establish new sets of timing relationships. There may be some limited clinical evidence for the latter in a report by Onslow, Costa, Andrews, Harrison, and Packman (1996) who found that high levels of fluency were maintained following a period of prolonged speech therapy with faster speech rates than those usually targeted by prolonged speech programs. However, there is rather little data to corroborate this finding and as we will see, particularly in part 2, the issue of maintaining high levels of fluency remains a significant problem with all therapies. However, in a further study, Kleinow and Smith (2000) observed that motor control amongst those who stutter showed greater variability with increased syntactic complexity. This does seem consistent with those therapeutic approaches which constrain length of utterance (see chapters 10, 11, 12). A problem in almost all of the research on speech kinematics and stuttering is that we only have detailed information from the adult population. Because of this, we can only speculate as to the control mechanisms in place at the onset of stuttering. Equally, we cannot be sure that where group differences have been found between adults who stutter and adults who do not, that these may reflect the use of varied control strategies on behalf of the speakers, rather than the direct effects of the stuttering, itself.

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The thalamic reticular nucleus also receives an excitatory collateral projection from the thalamocortical neuron (not shown) and sends an inhibitory -aminobutyric acid­ergic projection to symptoms when quitting smoking buy generic pepcid 40mg online the thalamic relay neuron symptoms norovirus buy pepcid without prescription. The reciprocal thalamocorticothalamic interactions gate the relay of information at the level of the thalamus and control thalamocortical synchronization medications a to z purchase pepcid once a day. These functions change during the sleep-wake cycle under the modulatory influence of cholinergic and monoaminergic neurons of the brainstem treatment interventions proven 40 mg pepcid, which project to the thalamic relay and reticular nuclei as well as to the cerebral cortex. Excessive synchronized inhibitory input from the reticular nucleus elicits rhythmic postsynaptic inhibitory potential on thalamocortical neurons, deactivating T-type calcium channels and leading to a rebound burst of action potentials in thalamocortical cells. Deep Brain Stimulation the thalamic nuclei are a common target for deep brain stimulation for various conditions (Table 14. The hypothala mus maintains homeostasis by integrating cortical, lim bic, and spinal inputs and by affecting hormone release, temperature regulation, intake of food and water, sexual behavior and reproduction, emotional responses, and diurnal rhythms. As the link from the nervous system to the endocrine system, the hypothalamus synthesizes and secretes neurohormones that stimulate or inhibit the secretion of pituitary hormones. Clinical disorders related to endocrine dysfunction are discussed in Volume 2, Chapter 79, "Endocrine Disease. The hypothalamus is bordered laterally by the optic tracts and posteriorly by the mammillary bodies (Figure 15. Functionally, the hypothalamus and the adjacent pre optic area form a unit that is subdivided into 3 distinct longitudinal zones: the periventricular, medial, and lat eral zones (Figure 15. The hypothalamic nuclei situated in these zones are often difficult to differentiate because they do not have sharply delineated borders and may extend into different zones. The periventricular zone of the hypothalamus includes the suprachiasmatic nucleus, which is involved in circadian rhythms, and the magnocellular and parvocellular nuclei, which control endocrine function (see below). The medial zone contains several nuclei that are involved in maintaining homeostasis and controlling reproduction. The medial preoptic nucleus contains ther mosensitive neurons involved in thermoregulation. The medial preoptic area also contains osmosensitive neu rons that receive inputs from circumventricular organs of the anterior wall of the third ventricle, such as the subfornical organ and the vascular organ of the lamina terminalis, which lack a bloodbrain barrier. The medial hypothalamus also contains the paraventricular nucleus, which is involved not only in endocrine function but also in autonomic control and is critical in stress responses. The arcuate (infundibular), ventromedial, and dorsomedial nuclei participate in the regulation of food intake, metabolism, and reproductive function. A, Midline section shows the different regions of the hypothalamus, the pituitary gland (hypophysis) in the sella turcica, and the mammillary bodies. B, View of the base of the brain shows the optic chiasm, the pituitary, and the mammillary bodies. Posterolateral hypo thalamic neurons secrete orexin, which regulates the switch between wakefulness and sleep. This leads to reciprocal inhibitory interactions between the sleeppromoting neurons of the ventrolateral preoptic nucleus and the excitatory projections to the arousalpromoting monoaminergic and cholinergic nuclei. Orexin neurons also stimulate food intake and are part of the reward circuit involved in drug addiction via their pro jections to dopaminergic neurons of the ventral tegmental nucleus. Principles of Neuroendocrinology and Hypothalamic Function 131 A Third ventricle Fornix Optic tract Table 15. The cells of the magnocellular system of the hypothalamus project to the posterior pituitary; together they constitute the neurohypophysis (Figure 15. Magnocellular neurosecretory cells are largediameter hypothalamic neurons located in the paraventricular nucleus and the supraoptic nucleus. These neurosecretory cells produce vasopressin and oxytocin, which are trans ported via axons through the stalk of the pituitary to the posterior lobe of the pituitary where these peptides are stored. Vasopressin and oxytocin can also be released from dendrites into the hypophyseal portal circulation. The medial zone contains several nuclei (medial preoptic, paraventricular, arcuate, ventromedial, and dorsomedial) that are involved in maintaining homeostasis and controlling reproduction. The medial hypothalamus contains the paraventricular nucleus, which is involved not only in endocrine function but also in autonomic control and is critical in stress responses. Neuroscience and Neuroanatomy hypotensive state even in the presence of low serum osmo lality. The magnocellular system also includes oxytocin, which initiates uterine contraction and ejection of milk in lactation. Oxytocin release is stimulated by distention of the cervix, labor, breastfeeding, and estrogen. Vasopressin (also called antidiuretic hormone) maintains the osmolality of the blood. Parvocellular System Neurovascular Transmission the parvocellular system regulates pituitary hormone release by neurovascular transmission. The parvocellular system comprises smalldiameter neurons in several hypo thalamic nuclei in the periventricular zone. Parvocellular neurosecretory cells project to the median eminence, where their nerve terminals release peptides into the hypothalamohypophysial portal system (Figure 15. These blood vessels carry peptides to the anterior lobe of the pituitary gland, where they influence the secretion of hormones into the systemic circulation. Systemic hor mones then exert negative feedback to control the secretion of the releasing hormones. Neurons in the paraventricular nucleus and the supraoptic nucleus produce vasopressin and oxytocin. Corticotropin stimulates the adrenal cortex to synthesize and release the glucocorticoid hor mone cortisol. Prolonged administration of exogenous glucocorticoids (eg, prednisone) is the overall most common cause of Cushing syndrome. The most common cause of Cushing dis ease is pituitary adenoma leading to excess corticotropin Vasopressin (also called antidiuretic hormone) main tains the osmolality of the blood. Vasopressin is secreted in response to an increase in plasma osmolality that is sensed directly at the supraoptic and paraventricular neu rons on separate hypothalamic osmoreceptors. Vasopressin acts on vasopressin V2 receptors in the renal tubules, increasing the reabsorption of water and the concentration of the urine. Alterations in blood pressure and volume also affect vasopressin release through baroreceptors and mechanoreceptors conveyed via the vagus and glossopha ryngeal nerves. The blood pressure stimulus predominates over osmolarity: Vasopressin release continues in a Chapter 15. Typical clinical features include truncal obe sity with abdominal striae, thinning of the skin with easy bruising and dryness, hirsutism, osteoporosis, proximal muscle weakness, osteoporosis, and insulin resistance. Prolactin stimulates lactation; the hypothalamicpituitary axis is responsible for milk pro duction that responds to sensory stimuli from the nipples. Dopamine exerts an inhibitory effect on prolactin; clinically, this may account for galactorrhea and reproductive disorders if dopamine transport from the hypothalamus is disrupted. Prolactinsecreting tumors (eg, prolactinomas) may clinically manifest as anovulatory infertility, amenorrhea, unexpected lactation, and sexual dysfunction in women. Thyrotropin increases the synthesis of thyroid hormone and stimulates the release of thyroxine and triiodothyronine. Neuroscience and Neuroanatomy stalk (or both) may result in antidiuretic hormone defi ciency. This deficiency may be due to trauma, surgery, pituitary apoplexy, or infiltration of the pituitary gland (through an infectious, inflammatory, or neoplastic proc ess). Patients often present with polyuria, nocturia, and elevated levels of serum sodium. Hyperprolactinemia Prolactin levels may be elevated in pituitary microadenomas and macroadenomas; however, several other conditions may result in elevated prolactin. These include pregnancy, primary hypothyroidism, postictal states, stress, and kid ney or liver disease. Dopamine inhibits prolactin; thus, another cause of hyperprolactinemia is the use of dopa mine receptor antagonists (eg, metoclopramide, antipsy chotics, and certain antidepressants). The medial zone of the hypothala mus is important in regulating motivated behavior (eg, defensive behavior). Clinical Correlations Diabetes Insipidus Diabetes insipidus can be central or nephrogenic. The term limbic system is also a misnomer because the "system" involves several cortical and subcortical structures.

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The Schwann cells of a myelinated axon are spaced a small distance from one another; the intervals between them are called nodes of Ranvier symptoms diverticulitis pepcid 40mg fast delivery. The specialized contact zone between a motor nerve fiber and the muscle it supplies is called the neuromuscular junction or motor end plate symptoms 4-5 weeks pregnant buy pepcid 20 mg overnight delivery. Impulses arising in the sensory receptors of the skin symptoms 6dp5dt purchase genuine pepcid line, fascia symptoms 6 days post embryo transfer discount pepcid online visa, muscles, joints, internal organs, and other parts of the body travel centrally through the sensory (afferent) nerve fibers. These fibers have their cell bodies in the dorsal root ganglia (pseudounipolar cells) and reach the spinal cord by way of the dorsal roots. The hindbrain or rhombencephalon (infratentorial portion of the brain) comprises the pons, the medulla oblongata (almost always called "medulla" for short), and the cerebellum. Its upper end is continuous with the medulla; the transition is defined to occur just above the level of exit of the first pair of cervical nerves. Its tapering lower end, the conus medullaris, terminates at the level of the L3 vertebra in neonates, and at the level of the L1­2 intervertebral disk in adults. The cervical, thoracic, lumbar, and sacral portions of the spinal cord are defined according to the segmental division of the vertebral column and spinal nerves. Argo light Argo Overview Diencephalon Cerebrum (telencephalon) Midbrain (mesencephalon) Pons and cerebellum Medulla oblongata Prosencephalon, brain stem Central nervous system Conus medullaris Filum terminale Dorsal root Spinal ganglion Ventral root Spinal nerve Mixed peripheral nerve Epineurium Spinal cord Ramus communicans Sympathetic trunk Node of Ranvier Schwann cell nucleus Perineurium of a nerve fascicle Myelinated nerve Fibrocyte Endoneurium Capillary Unmyelinated nerve Muscle fibers Capillary Motor end plate Cutaneous receptors Peripheral nervous system Rohkamm, Color Atlas of Neurology © 2004 Thieme All rights reserved. Overview 3 Telencephalon midline structures Argo light Argo Skull the skull (cranium) determines the shape of the head; it is easily palpated through the thin layers of muscle and connective tissue that cover it. It is of variable thickness, being thicker and sturdier in areas of greater mechanical stress. The thinner bone in temporal and orbital portions of the cranium provides the so-called bone windows through which the basal cerebral arteries can be examined by ultrasound. The only joints in the skull are those between the auditory ossicles and the temporomandibular joints linking the skull to the jaw. Scalp the layers of the scalp are the skin (including epidermis, dermis, and hair), the subcuticular connective tissue, the fascial galea aponeurotica, subaponeurotic loose connective tissue, and the cranial periosteum (pericranium). The connection between the galea and the pericranium is mobile except at the upper rim of the orbits, the zygomatic arches, and the external occipital protuberance. Scalp injuries superficial to the galea do not cause large hematomas, and the skin edges usually remain approximated. Wounds involving the galea may gape; scalping injuries are those in which the galea is torn away from the periosteum. The outer and inner tables of the skull are connected by cancellous bone and marrow spaces (diploл). The bones of the roof of the cranium (calvaria) of adolescents and adults are rigidly connected by sutures and cartilage (synchondroses). The sagittal suture lies in the midline, extending backward from the coronal suture and bifurcating over the occiput to form the lambdoid suture. The area of junction of the frontal, parietal, temporal, and sphenoid bones is called the pterion; below the pterion lies the bifurcation of the middle meningeal artery. The inner skull base forms the floor of the cranial cavity, which is divided into anterior, middle, and posterior cranial fossae. The anterior fossa lodges the olfactory tracts and the basal surface of the frontal lobes; the middle fossa, the basal surface of the temporal lobes, hypothalamus, and pituitary gland; the posterior fossa, the cerebellum, pons, and medulla. The anterior and middle fossae are demarcated from each other laterally by the posterior edge of the (lesser) wing of the sphenoid bone, and medially by the jugum sphenoidale. The middle and posterior fossae are demarcated from each other laterally by the upper rim of the petrous pyramid, and medially by the dorsum sellae. Skull Viscerocranium the viscerocranium comprises the bones of the orbit, nose, and paranasal sinuses. The superior margin of the orbit is formed by the frontal bone, its inferior margin by the maxilla and zygomatic bone. The frontal sinus lies superior to the roof of the orbit, the maxillary sinus inferior to its floor. The nasal cavity extends from the anterior openings of the nose (nostrils) to its posterior openings (choanae) and communicates with the paranasal sinuses-maxillary, frontal, sphenoid, and ethmoid. The infraorbital canal, which transmits the infraorbital vessels and nerve, is located in the superior (orbital) wall of the maxillary sinus. The portion of the sphenoid bone covering the sphenoid sinus forms, on its outer surface, the bony margins of the optic canals, prechiasmatic sulci, and pituitary fossa. Argo light Argo Skull Scalp Galea aponeurotica Diploл Coronal suture Pterion Squamous suture Parietomastoid suture Lambdoid suture Occipitomastoid suture Skull Mastoid process Coronal suture Outer and inner table Skull (cross section) Glabella Supraorbital foramen Orbit Infraorbital foramen Zygomatic bone Mental foramen Frontal sinus Supraorbital margin Nasal bone Infraorbital margin Perpendicular lamina (ethmoid bone, nasal septum) Vomer Viscerocranium Foramen magnum Dorsum sellae Anterior clinoid process Crista galli Cribriform plate Prechiasmatic sulcus Jugum sphenoidale Lesser wing of sphenoid bone Inner skull base (yellow = anterior fossa, green = middle fossa, blue = posterior fossa) Sphenoid sinus Maxillary sinus Upper jaw (maxilla) Lower jaw (mandible) Superior margin of petrous bone Pituitary fossa (sella turcica) Rohkamm, Color Atlas of Neurology © 2004 Thieme All rights reserved. Skull 5 Temporomandibular joint Argo light Argo Meninges the meninges lie immediately deep to the inner surface of the skull and constitute the membranous covering of the brain. The pericranium of the inner surface of the skull and the dura mater are collectively termed the pachymeninges, while the pia mater and arachnoid membrane are the leptomeninges. Pain can thus be felt in response to noxious stimulation of the dura mater, while the cerebral parenchyma is insensitive. Some of the cranial nerves, and some of the blood vessels that supply the brain, traverse the dura at a distance from their entry into the skull, and thereby possess an intracranial extradural segment, of a characteristic length for each structure. Thus the rootlets of the trigeminal nerve, for instance, can be approached surgically without incising the dura mater. Pachymeninges the pericranium contains the meningeal arteries, which supply both the dura mater and the bone marrow of the cranial vault. The pericranium is fused to the dura mater, except where they separate to form the dural venous sinuses. The virtual space between the pericranium and the dura mater-the epidural space-may be forced apart by a pathological process, such as an epidural hematoma. Immediately beneath the dura mater, but not fused to it, is the arachnoid membrane; the intervening virtual space-the subdural space-contains capillaries and transmits bridging veins, which, if injured, can give rise to a subdural hematoma. The falx cerebri separates the two cerebral hemispheres and is bordered above and below by the superior and inferior sagittal sinuses. It attaches anteriorly to the crista galli, and bifurcates posteriorly to form the tentorium cerebelli, with the straight sinus occupying the space between the falx and the two halves of the tentorium. The much smaller falx cerebelli separates the two cerebellar hemispheres; it encloses the occipital sinus and is attached posteriorly to the occipital bone. The tentorium cerebelli separates the superior aspect of the cerebellum from the inferior aspect of the occipital lobe. The opening between the two halves of the tentorium, known as the tentorial notch or incisura, is traversed by the midbrain; the medial edge of the tentorium is adjacent to the midbrain on either side. The tentorium attaches posteriorly to the sulcus of the transverse sinus, laterally to the superior rim of the pyramid of the temporal bone, and anteriorly to the anterior and posterior clinoid processes. The tentorium divides the cranial cavity into the supratentorial and infratentorial spaces. The pituitary stalk, or infundibulum, accompanied by its enveloping arachnoid membrane, Meninges Pia Mater the cranial pia mater is closely apposed to the brain surface and follows all of its gyri and sulci. The cerebral blood vessels enter the brain from its surface by perforating the pia mater. Except for the capillaries, all such vessels are accompanied for a short distance by a pial sheath, and thereafter by a glial membrane that separates them from the neuropil. The perivascular space enclosed by this membrane (Virchow­Robin space) contains cerebrospinal fluid. The choroid plexus of the cerebral ventricles, which secretes the cerebrospinal fluid, is formed by an infolding of pial blood vessels (tela choroidea) covered by a layer of ventricular epithelium (ependyma). Arachnoid Membrane the dura mater is closely apposed to the arachnoid membrane; the virtual space between them (subdural space) contains capillaries and bridging veins. Between the arachnoid membrane and the pia mater lies the subarachnoid space, which is filled with cerebrospinal fluid and is spanned by a network of delicate trabecular fibers. Argo light Argo Meninges Pacchionian corpuscles Galea aponeurotica Diploл Cerebral arteries Pericranium and dura mater Epidural space Subdural space Superior sagittal sinus Subarachnoid space Arachnoid membrane Pia mater Virchow-Robin space Superior sagittal sinus Scalp, skull, meninges Falx cerebri Supratentorial compartment Straight sinus Falx cerebelli Tentorium Infratentorial compartment Sigmoid sinus Superior sagittal sinus Falx cerebri Cranial cavity (dorsal view) Inferior sagittal sinus Straight sinus Tentorial edge Tentorium of cerebellum Infratentorial compartment Diaphragma sellae Pituitary stalk (infundibulum) Internal acoustic meatus Cranial cavity (lateral view) Rohkamm, Color Atlas of Neurology © 2004 Thieme All rights reserved. Each of the two lateral ventricles communicates with the third ventricle through the interventricular foramen of Monro (one on each side). The cerebellomedullary cistern (cisterna magna) lies between the posterior surface of the medulla and the undersurface of the cerebellum. The ambient cistern lies lateral to the cerebral peduncle and contains the posterior cerebral and superior cerebellar arteries, the basal vein, and the trochlear nerve. The interpeduncular cistern lies in the midline between the cerebral peduncles and contains the oculomotor nerves, the bifurcation of the basilar artery, and the origins of the superior cerebellar and posterior cerebral arteries; anterior to it is the chiasmatic cistern, which surrounds the optic chiasm and the pituitary stalk. The portion of the subarachnoid space extending from the foramen magnum to the dorsum sellae is collectively termed the posterior cistern. It is mainly absorbed through the arachnoid villi (arachnoid granulations, pacchionian corpuscles), which are most abundant along the superior sagittal sinus but are also found at spinal levels.

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Additional interosseous ligaments are the pisohamate and pisometacarpal ligaments medications used to treat bipolar discount generic pepcid uk, which symptoms zika virus buy generic pepcid 40mg on line, together with the fibrous capsule medications ending in zine buy pepcid 40 mg low cost, connect the pisiform with the palmar surface of the triquetral bone treatment 5th toe fracture order 20 mg pepcid mastercard. These ligaments also connect the pisiform with the hamate and the base of the 5th the ulna is part of the elbow joint, relatively fixed at the ulnohumeral joint. The radius has a greater degree of movement than the ulna due to its rotational component. Adduction or abduction of the ulna leads to reciprocal repositioning of the hand; for example, when the ulna abducts, the radius glides distally, forcing the wrist into increased adduction. The reverse occurs during ulna adduction, which automatically creates an abducted wrist. When pronation of the hand occurs, the distal radius crosses over the ulna as the distal end moves anteriorly and medially; toward the end of pronation, the radial head glides posteriorly (dorsally) on the carpal bones. When supination occurs, the distal radius crosses back over the ulna as the distal end moves posteriorly (laterally); at the extreme of supination, the radial head glides anteriorly. Palpation exercise the practitioner supports the flexed elbow so that the thumb is resting on the radial head. At the same time, the other 13 Shoulder, arm and hand 503 hand grasps the forearm just proximal to the wrist and alternately pronates and supinates it. The movements described above are felt for near the end of full pronation (radial head glides posteriorly) and supination (radial head glides anteriorly). Posterior radial head dysfunction is common following a fall forward onto the palm of an outstretched hand, whereas an anterior radial head dysfunction is common following a fall backward onto the palm of the outstretched hand of the extended arm. Both active and passive range of motion tests may be used to assess limits of movement of the wrist joint. Bilateral comparison is possible, performing action on each side simultaneously in most cases. Minor restriction ­ for example, in gliding potential ­ is commonly the only symptom of dysfunction in this area. Passive bilateral comparison of minor gliding motions is an accurate means of identifying sites of dysfunction. Dysfunction of the ulnohumeral joint is commonly the primary feature, with radioulnar dysfunction being secondary, seldom primary, in elbow dysfunction. Any dysfunctional state of any joint in the arm will cause adaptive demands on all other joints of the arm, leading to compensatory problems. If elbow flexion is restricted after all ulnohumeral features have been treated and if inflammation is absent, the Box 13. The notes on this topic, as set out below, are largely based on her years of research and findings. In contrast to generalized dystonia, which may affect the entire body, focal dystonias present in the context of performing a specific motor task usually with only one part of the body. When patients attempt to perform that target task, they experience involuntary co-contractions of flexor and extensor muscles (Altenmueller 1988). When that happens the ability to perform finely graded and sequenced movements is disrupted and replaced by crude, uncontrolled movements (Rosenbaum & Jankovic 1988). Although the disorder is typically painless, some patients may have painful spasms and others can experience increased sensitivity or a sense of dullness or even numbness of the affected limb. In the majority of cases, repetitive movements performed in the workplace seem to be a major risk factor for this disorder (Hochberg et al 1990). The evidence for microtrauma from repetitive overuse of the upper limb is convincing. Rest, antiinflammatory medications, change in biomechanics and good ergonomics are usually effective treatment modalities. Unfortunately, some individuals must continue to work despite their symptoms and rest is a limited option in such cases. Thus, the repetitive strain injury becomes chronic with degenerative changes found in tendons and muscles (Barbe et al 2003), restricting soft tissues and joint mobility (Barr & Barbe 2002), together with compression of peripheral nerves (Stock 1991). In some cases of cumulative trauma, chronic neuropathic pain develops (Viikari-Juntura & Silverstein 1999). In other cases fatigue and clumsiness of the hand is reported, often associated with a tremor (Fernandez-Alvarez et al 2003). There is increasing evidence of degradation of the somatosensory representation of the hand in patients with dystonic hand movements. If the origin is aberrant learning with degradation of the cortical hand representation in the brain, treatment should include learning-based training strategies to reorganize the brain (Sanger & Merzenich 2000). Examination During the musculoskeletal examination the patient may complain of weakness but the muscles are usually strong unless there are signs of clear peripheral nerve compression with secondary atrophy. However, there may be an imbalance in strength, with the extrinsic muscles unusually strong compared to the intrinsic muscles (Byl et al 1996). Poor posture is common (forward head and protracted shoulders) and there may also be end-range limitations in finger spread, forearm rotation or shoulder external rotation (Wilson et al 1993). However, some individuals do note a worsening of normal physiological tremors, uncontrollable excitability and possibly some dullness in the pads of the fingers when placed on the target surface. These patients may also perform poorly on tasks demanding cortical sensory discrimination. Performing artists often report having achieved a new high level of performance using new techniques or a new instrument, suddenly followed by involuntary, abnormal end-range postures of the fingers, making normal musical performance impossible (Altenmuller 2003). It is hypothesized that dystonia, particularly focal dystonia of the neck, is genetic (Ozelius et al 1997). In both general and focal dystonia, there is also strong evidence of an imbalance of inhibitory and excitatory pathways in the globus pallidus/substantia nigra (Black et al 1998). Some researchers report hand dystonia could result from cortical motor dysfunction (Toro et al 2000), degradation in the sensory thalamus (Lenz & Byl 1999) or disruption in cortical sensory activation, somatosensory representation or spatial perception (Tinazzi et al 2003). Other researchers report abnormal gating of somatosensory inputs (Murase et al 2000), abnormal presynaptic desynchronization of movement, abnormal muscle spindle afferent firing (Toro et al 2000) or disruption of inhibition in the spinal cord (Chen et al 1995). Botulinum toxin injections or baclofen can decrease the severity of dystonic cramping by interfering with neural signals to the muscle (van Hilten et al 2000). Surgery such as nerve decompression at the elbow or wrist may be helpful (Charness et al 1996). Surgical release of tight retinaculum or fascia has been tried with limited success. Surgical implantation of deep brain stimulators is sometimes used for patients with focal hand dystonia. None of these medication or surgical approaches actually targets the defined somatosensory degradation. Conservative exercise strategies based on the principles of neuroplasticity have been tried as alternatives, or supplementary, to medications and surgery. Some of these learning approaches include constraint-induced therapy (also called sensory motor retuning) (Candia et al 2003), sensitivity training (Tubiana 2003), conditioning techniques (Liversedge 1960), kinematic training (Mai & Marguardt 1994), immobilization (Priori et al 2001) and learning-based sensorimotor training (Byl et al 2000). While some limited research has been carried out on these techniques, none has been confirmed by randomized clinical trials. People who successfully rehabilitate are those who can stop the activities that lead to the abnormal movements, integrate healthy, stress-free, normal biomechanics into functional hand use, create a positive, supportive environment, manage stress, use good ergonomics, engage in wellness and fitness activities, and can carry out a learning-based sensorimotor training program to reorganize the somatosensory maps of the hand. Byl & Melnick (1997) proposed the sensorimotor learning hypothesis as one etiology of work-related focal hand dystonia. This suggests that repetitive use, simultaneous firing, coupling of multiple sensory signals and voluntary coactivation of muscles lead to a degradation of the sensory cortical representation of the hand and disruption in sensorimotor feedback (Xerri et al 1999). If the sensorimotor and the neural circuitry connecting the deep cortical nuclei, basal ganglia and thalamus are unstable, then a focal or a general dystonia could develop, depending on the extent of the imbalance across multiple sensory and motor systems (Sanger & Merzenich 2000). Based on the sensorimotor learning hypothesis integrated into the computational model, appropriate treatment must help to redifferentiate cortical and subcortical representations. Pathological connections must be uncoupled and 13 Shoulder, arm and hand 505 30° 40­45° 15° A 55° 85° B 85° C Figure 13. Active and passive range of motion testing for the wrist should show: Assessment tips flexion (85°) extension (85°) ulnar deviation (45°) radial deviation (15°). Kaltenborn (1989) states that if a passive movement and an active movement in the same direction produce painful symptoms, this suggests an osseous problem. If, however, a passive movement in one direction and an active movement in the opposite direction produce symptoms (pain, for example), this suggests a soft tissue problem. Stabilizing the proximal wrist with one hand and covering the clenched fist with the other, the practitioner attempts to extend the wrist against resistance. This evaluates strength of extensor carpi radialis longus and brevis and extensor carpi ulnaris.

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