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Capgras syndrome must be distinguished from purely perceptual or hallucinatory disturbances fungus dandruff order fluconazole 100 mg visa, and from generalized disturbance of cognition fungus gnats treatment purchase fluconazole 50mg visa. That is fungus plague inc purchase fluconazole 200mg amex, in order to be properly and convincingly diagnosed as a delusion fungus species order 400mg fluconazole with mastercard, the disturbance must involve a mistaken belief (not merely a misperception) and must be persistent (not a transitory effect of confusion) zeasorb antifungal treatment buy fluconazole 100 mg with amex. For example fungus gnats new zealand fluconazole 200mg with visa, in autoscopy, the patient experiences a second self, as in the subjective doubles variant of Capgras. However, the phenomena differ in that the double is actually seen in autoscopy, rather than believed to be active elsewhere, as in subjective doubles. The prosopagnosic person may fail to recognize his wife, whereas the Capgras patient will insist that the present person is an imposter and that the ``real' wife is somewhere else. Patients in confusional states or dementia may express strange beliefs, but the beliefs typically change from hour to hour and do not persist once the confusion resolves. Patients with Capgras syndrome are usually described as forthcoming and cooperative. Although they insist that their delusional beliefs are true, they often admit to puzzlement or bemusement regarding aspects of the delusion. Rather than escalate their defenses by becoming hostile, they are more likely to confabulate an explanation. For example, a patient with a delusion of duplication (Malloy, 1991) was asked how she could have two sets of children with identical names. She appeared momentarily puzzled and then stated, ``My husband was in the Navy, and we moved around a lot; it was hard to keep that straight. Several researchers have found that about 25% of Alzheimer patients display delusions involving misidentification of people. C Natural History, Prognostic Factors, Outcomes About 58% of Capgras patients who receive adequate neurodiagnostic workups are found to display primary psychiatric disorder, uncomplicated by demonstrable neurologic disease (Dohn & Crews, 1986). Although psychological factors can be important in the production of delusions, a critical review of the literature by Malloy and Richardson (1994) demonstrated that delusions can also result from identifiable neurologic disease, from generalized disturbances to focal lesions. They found that Capgras and its variants have been reported in association with a variety of systemic diseases and diffuse neurologic disorders. In terms of focal lesions such as tumors and stroke, that review demonstrated that the right hemisphere or bilateral lesions were invariably found on neuroimaging, with no exclusively left-hemisphere lesions. Neuropsychological testing documented spatial, executive, and nonverbal memory problems, consistent with the right frontotemporal localization on neuroimaging studies. Neuropsychology and Psychology of Capgras Syndrome Epidemiology Dohn and Crews (1986) observed that Capgras syndrome was frequently overlooked in psychiatric patients and Capgras and its variants represent either underidentification or overidentification of the object of the delusion (Vie, 1930). Thus, in Capgras syndrome, the patient 486 C Capgras Syndrome mistakenly perceives the person as unfamiliar due to underidentification. In Fregoli syndrome, on the other hand, the patient misperceives diverse persons as the same person due to overidentification. Feinberg and Shapiro (1989) emphasized the importance of the right temporal lobe in producing misidentification delusions. They reviewed the evidence from stimulation and seizure studies indicating that the right temporal lobe plays an important role in producing the experience of familiarity. Cutting (1991) has put forth a similar argument regarding the role of the right hemisphere in identification. Crucial factors in the persistence of delusions may be the length of time the perceptual distortion continues, and the ability of the patient to correct the misperception on the basis of new information. Frontal lesions may impact on the latter self-corrective function, making it impossible to resolve conflicting information, resulting in unconcern and confabulation when the conflicts are confronted (Joseph, 1986). Alexander, Stuss, and Benson (1979) were the first to report a Capgras delusion clearly related to a specific neurologic structural lesion, involving the right hemisphere with predominantly frontal and temporal lobe damage. They noted the importance of frontal damage in Capgras, both in terms of the inability to resolve conflicts, and confabulation of a second persona. Psychodynamic or functional interpretations for the development of delusions are not incompatible with this neuropsychological explanation. Treatment In degenerative dementia, duplication delusions are usually transitory phenomena, occurring in the early-to-middle stages and disappearing when cognitive deficits become severe. In other etiologies such as cerebrovascular disease, they often occur acutely and persist for many months or years. For example, Santiago, Stoker, Beigel, Yost, and Spencer (1987) reported resolution of Capgras following treatment of underlying thyroid disease. Spontaneous resolution of Capgras delusions has also been reported (Ruff & Volpe, 1981). On the other hand, Joseph (1987) described a patient whose chronic psychosis and intermittent psychotic misidentification of the Capgras and intermetamorphosis types were refractory to neuroleptic treatment. Upon administration of a trial of clorazepate, complete remission of psychotic symptoms was achieved for the first time in 19 years, but these recurred when the patient discontinued her clorazepate. The effectiveness of psychological interventions may vary with the type of delusion, and the degree to which neurologic factors are involved. Unfortunately, there has been no systematic treatment follow-up research, and data are limited to uncontrolled case studies. Evaluation Careful clinical interview with both patient and family members will help to elicit evidence of Capgras delusions. In the course of family disputes and initial evaluations, patients may learn to minimize or deny their delusions. The literature is replete with case reports positing a psychodynamic explanation for Capgras, but with no workup to rule out neurologic etiology. Since Capgras is commonly associated with neurologic illness; full workup including neuroimaging and neuropsychological testing is essential. Neuropsychological testing often reveals deficits in frontal/executive and visuospatial functions (Malloy & Richardson, 1994). Delusional misidentification and the role of the right hemisphere in the appreciation of identity. Delusional misidentification of the Capgras and intermetamorphosis types responding to clorazepate. Environmental reduplication associated with right frontal and parietal lobe injury. C 487 Brand Name Tegretol, Carbatrol Class Anticonvulsant C Proposed Mechanism(s) of Action Carbamazepine is a use-dependent blocker of voltagesensitive sodium channels, it interacts with the open channel conformation of voltage-sensitive sodium channels, it interacts at alpha pore-forming subunit of voltage-sensitive sodium channels, and inhibits release of glutamate. Off Label Use Glossopharyngeal neuralgia, bipolar disorder, psychosis, schizophrenia, and personality disorders. Generic Name Carbamazepine 488 C Carbon Monoxide Poisoning Additional Information Drug Interaction Effects. With increased awareness of its potential dangers, the majority of these exposures can be prevented. Natural History, Prognostic Factors, Outcomes Compared to normal oxyhemoglobin. Acute exposure to lower concentrations of carbon monoxide will result in a slowly developing hypoxia that triggers peripheral vasodilation. Paradoxically, when there is a slow increase in carboxyhemoglobin saturation, compensatory changes in respiratory rate may lag. Thus, the symptoms of dizziness, weakness, headache, and nausea will precede fainting. Once unconscious, increased respiration and tachycardia will be followed by convulsions and coma, and death will ensue as the carboxyhemoglobin climbs and remains above 50% saturation. Chronic exposure to low concentrations of carbon monoxide can occur in heavy smokers as well as in individuals whose occupations involve protracted exposure to exhaust fumes. The binding of carbon monoxide to hemoglobin is fully dissociable though these individuals may manifest carboxyhemoglobin saturation at 10%, which is 20-fold higher than normal. Symptoms associated with chronic exposure include headache, fatigue, nausea, difficulty in concentrating, and impaired memory (Kao & Nanagas, 2005). When inhaled into the lungs, it readily competes with oxygen for binding sites on hemoglobin. The affinity of carbon monoxide binding to hemoglobin is more than 200-fold greater than that of oxygen. Acute carbon monoxide poisoning, for example, following exposure to automobile exhaust (which generates about 5% to 7% carbon monoxide) will rapidly saturate the hemoglobin and cause death within minutes with virtually no prior symptoms. Use of this battery in an emergency room setting allows for the early detection of cerebral impairment in the exposed individuals. Epidemiology Exposure to low concentrations of carbon monoxide consequent to the operation of faulty furnaces or gas-powered engines is the leading cause of accidental poisoning in the United States. Exposure to high concentrations of carbon monoxide is the most common form of intentional poisoning in the United States. These neurological signs reflect extensive damage to the basal ganglia and white matter of the brain with a demyelination that spares the neuronal axons. Neuroimaging scans will most likely appear normal 24 h after exposure; lesions may begin to appear 2 weeks later. Functional changes associated with these later-appearing lesions are variable but attempts have been made to relate these to the severity of the initial exposure. Acute exposure resulting in carboxyhemoglobin saturation of 25% or more will result in later onset cognitive impairments in as many as 50% of the patients. The cognitive deficits include agnosia, aphasia, and apraxia as well as impaired memory, impaired executive function, and a general decrease in intellect. C Carboxyhemoglobinemia Carbon Monoxide Poisoning Cardiac Ultrasound Echocardiogram Career Counseling for Individuals with Disabilities Vocational Counseling Treatment Effective treatment entails removal from the source of the carbon monoxide and providing oxygen; when breathing air, the half-life of carboxyhemoglobin is about 5 h and this time can be reduced to 1. Indeed, supplementation with oxygen immediately after exposure remains as the most effective strategy for reducing the severity of the later-appearing neural and functional consequences following carbon monoxide poisoning (Prockop & Chichkova, 2007). Neuroimaging, cognitive and neurobehavioral outcomes following carbon monoxide poisoning. Angio Definition Angiography is the evaluation of the blood vessels of the central nervous system and associated 490 C Carotid Artery cervicocerebral vasculature applying radiography to the simultaneous injection of intravascular contrast media. Femoral or axillary nonselective approaches can be used to catheterize the aortic arch or selective means employed to catheterize the carotid artery. Some of the disease entities studied include ischemic cerebrovascular disease, aneurysms, vascular malformations, neoplasms, and brain injuries. Arterial dissections develop when blood is extravasated within the arterial wall itself narrowing the arterial lumen. The carotid artery between C2 and the base of the skull is frequently a target for the formation of a pseudoaneurysm. After anesthesia, the surgeon clamps the carotid artery proximal and distal to the stenosis temporarily. The surgeon may place a shunt proximal to the clamp to reroute blood to the brain. After it is removed, the artery is sutured together, the clamps are removed, and any bleeding is stopped. Current Knowledge Can be part of the evaluation process of patients with cerebrovascular disease. Cross References Angioma Glioma Hemangioma Hemiplegia Current Knowledge the arch of the aorta gives off three branches: the innominate, the left common carotid, and the left subclavian. The innominate artery, also known as the brachiocephalic artery, gives rise to the right subclavian artery and the right common carotid artery. The common carotid arteries bilaterally split into internal and external carotid arteries. The right and left internal carotid arteries, along with the vertebral arteries, branches of the subclavian artery, are the major blood vessels supplying the brain. As plaque builds in the carotid artery, atherosclerosis, or hardening of arteries, develops. Carotid stenosis, or narrowing of the carotid artery, may also develop and is most common at the origin of the internal carotid artery or less commonly, at the distal common carotid artery. Case Coordination C 491 If the stenosis is severe, it may result in decreased perfusion of brain tissue, and consequently ischemia. Another mechanism by which ischemia can develop is by the development of a thrombus over the plaque. When this occurs, an embolus may break off and may result in the occlusion of a vessel distally. A stroke may develop if the brain is deprived of its blood supply, resulting in a sudden loss of neurologic function. This type of imaging bounces high-frequency sound waves off blood vessels and the blood within the lumen to determine blood flow and any abnormalities within the vessels themselves. This helps identify any areas of poor blood flow and determine the degree of stenosis. In addition, other risk factors that may cause further damage to the vessels, such as smoking, diabetes, hypertension, and hypercholesterolemia, should be treated medically. During this procedure, a catheter is inserted through the groin and is guided until it reached the site of stenosis. After the location of the catheter is confirmed, a balloon inflates and attaches a metal-mesh stent into the artery.
It is tempting to equate facilitation with neural excitation anti fungal gel safe fluconazole 50mg, though this is often not the case lawn antifungal buy fluconazole 400 mg otc. While facilitation often involves increased excitation in brain areas required for focused attention to the task antifungal herbal tea buy fluconazole 100mg online, facilitation may also occur as a by-product of the inhibition of unrelated areas antifungal rinse for mouth purchase fluconazole 400 mg online. Accordingly fungus plastic buy 200mg fluconazole visa, facilitation is an essential process underlying attention that may occur as the by-product of the interaction of neural inhibition and activation that typically occur simultaneously and involve complex interactions across brain systems antifungal powder cvs purchase fluconazole 100mg otc. Facial recognition test in the elderly: Norms, reliability and premorbid estimate. At an elementary level, neural facilitation occurs when there is an increase in post-synaptic potential resulting from the occurrence of a second stimulus shortly after the first. This process contributes to sensitization and is ultimately linked to the formation of a conditioned response. In the context of attention, facilitation occurs when focus is enhanced by the occurrence of some preexisting conditions or stimuli. For example, when a target Cross References Enhancement Inhibition Selective Attention Fake Bad Scale F 1013 References and Readings Ghatan, P. Factor invariance of the Kaufman Adolescent and adult intelligence test across male and female samples. Exploratory and confirmatory factor analysis: Understanding concepts and applications. For example, factor analysis might be applied to a set of test items in order to determine if different items might be organized into subtests. In conducting a factor analysis, the researcher must make decisions about the type of rotation used (orthogonal or oblique), the number of factors to extracted, the criteria for considering a factor loading as being meaningful, and finally the nature of the obtained factors. In exploratory factor analysis, decisions are made regarding the above-mentioned categories, and the resulting factor structure is interpreted. In confirmatory factor analysis, a specific factor structure, either on the basis of prior research with a separate sample or on the basis of theory, is evaluated as to its fit to the data. Confirmatory factor analysis is therefore an evaluation of a model and allows a statistical test of the similarity of different factor structure models to each other. It was intended to be sensitive to personal injury exaggeration and was constructed on a ``rational content basis. Studies differ as to the appropriate cutoff score (>22) for labeling someone a ``somatic malingerer. Subsequent studies have found cutoff scores of 22, 23, and others to show good specificity and sensitivity. It showed the largest effect size followed by Subtle-Obvious, Dissimulation, F-K, and the F scale. The construct validity of the Lees-Haley Fake Bad Scale: Does this scale measure somatic malingering and feigned emotional distress American Academy of Clinical Neuropsychology Consensus Psychometric Data this scale consists of 43 items: 18 of them are cued in the ``true' direction and 25 items are cued in the ``false' False Memory Conference Statement on the neuropsychological assessment of effort, response bias, and malingering. F 1015 toward faking bad raise questions regarding the validity of data, and are typically evaluated in conjunction with other symptom validity tests. In addition to traditional validity scales (L, F, F-back, and K), misrepresentation of symptoms can be assessed via the Weiner and Harmon Obvious and Subtle Subscales, Lachar and Wrobel Critical Items, the F minus K Index (Gough Dissimulation Index), and the Fake Bad Scale (Lees-Haley, Smith, Williams, & Dunn, 1996). Reasons for faking bad can include making a ``plea for help,' having a catastrophizing style, and/or being motivated by secondary gain issues. Reasons for underreporting include seeking to deny problems, desiring to appear psychologically healthy, and/or attempting to obtain some outcome (Greene, 1991). Within the context of neuropsychological evaluation, these tendencies are examined in conjunction with other information from the evaluation. A profile suggestive of efforts to faking good may indicate poor awareness of difficulties, which may be verified by a comprehensive clinical interview. False memory is not the same as confabulation, which is often spontaneously generated and the result of mental illness or brain injury. Vulnerability to false memory changes as a function of age, with young children more susceptible to false memory implantation and older adults more likely to create false memories. However, people of all ages are susceptible to false memories, suggesting that distortion of memory is a byproduct of normal memory processes. In a common paradigm for studying false memory, adults memorize a list of words. In another example, when shown a picture of a traffic accident that does not contain a blue car, for example, individuals often recall seeing a blue car if the experimenter suggests that the accident involved a blue car. This research has serious implications, for example for eyewitness testimony and accusations of abuse based upon repressed memories. There are numerous cases of individuals who have had false memories of severe abuse implanted, often by well-meaning psychologists during recovered memory therapy. Additionally, police investigators could easily (and unintentionally) implant a false memory in witnesses by suggesting that the witnesses saw the defendant at the crime scene. Implantation of false memory can even cause an innocent individual to accept culpability for a crime. However, when another person claims to have seen them perform the act, the accused will often end up signing a confession, and even create details consistent with the belief that they committed the act. Clinicians and detectives may exert some pressure on clients to recall past memories, and social pressure to give the expected information is very strong. In addition, when people have trouble remembering, a clinician or police investigator may explicitly encourage memory construction by imagining the events, and may neglect to encourage clients or witnesses to think about whether their memories are real or not. This is a highly controversial topic of research, as all recovered memories (or eye witness testimonies) are certainly not false. In fact, there is evidence in children that false memories are only likely to be implanted if they involve events that are plausible. Cross References Confabulation Intrusion Errors References and Readings Balota, D. Sensitivity is the extent to which an instrument is able to detect impairment in individuals who are demonstrating any symptoms of the impairment. A false negative suggests that an instrument may not be sensitive enough to capture the impairment. A false negative error can result from various factors, such as administration of a test that lacks sensitivity (the ability to detect the specified impairment), human error in administration, or transient states of the impairment itself, such as in delirium. Neuropsychologists and test developers attempt to Family Adjustment F 1017 reduce the chances of committing a false negative error by increasing the sensitivity of the test and verifying that test administrators are strictly adhering to standardized administration rules. Specificity is the extent to which an instrument is able to exclude individuals who do not demonstrate the impairment. In clinical practice, this can lead to the overidentification of a disorder in individuals who do not legitimately demonstrate evidence of the disorder. A false-positive error can occur in the case of poor construct validity for a test, such that the underlying construct is not well operationalized in the assessment measure. For example, a clinician may mistakenly provide a diagnosis of mild mental retardation for a child who presents with severe attentional difficulties. Perhaps, the child would demonstrate a higher level of general ability if the attention problems were better controlled. The stressor, A, constitutes an event capable of producing change and hardships in the family. For example, following a stroke or a traumatic brain injury, caregivers typically experience stress, role changes, and social and financial burdens (Dorsey & Vaca, 1998; Kreutzer, Serio, & Bergquist, 1994; Nabors, Seacat, & Rosenthal, 2002). The resulting adjustment is a combination of the financial and psychological resources of the caregiver or family and the interpretation of the stressor (McCubbin & Patterson, 1983). Education, careful discharge planning, and professional advice about the need to care for oneself are useful prophylactic measures. Cross References Family Burden Family-Centred Care Family Therapy References and Readings Dorsey, M. Cross References Family Needs Questionnaire Family Therapy References and Readings Burgess, E. The cost of care index: A case management tool for screening informal care providers. Although the chronic nature of neurobehavioral, emotional, and psychosocial disruption following brain injury is well-documented, often only short-term professional assistance and treatment are available to patients and family members, leaving them to manage these significant difficulties alone (Kolakowsky-Hayner, Miner, & Kreutzer, 2001). Questionnaire items represent commonly reported needs experienced by family members of traumatic injury survivors. Family members rate needs in terms of their perceived importance, on a scale with values ranging from 1 (not important) to 4 (very important), and the extent to which the perceived need is being met (yes, partially, no). Clinical Uses Originally developed to assess needs of family members of persons with brain injury (Kreutzer et al. Family needs after traumatic brain injury: A factor analytic study of the Family Needs Questionnaire. Assessing need for social support in parents of children with Autism and Down Syndrome. Given that many individuals sustaining traumatic injuries are young and most survivors have relatively normal life expectancy, family care providers often experience extensive and chronic needs. Needs of family caregivers caring for stroke patients: Based on the rehabilitation treatment phase and the treatment setting. A preliminary study of acute family needs after spinal cord injury: Analysis and implications. Current Knowledge the international movement toward patient-centered care and shared decision-making often necessitates meetings with patients and their families and/or caretakers to facilitate optimal care and planning. Increases in family team discussions have been linked to increased patient and family satisfaction and better health outcomes (Halm, Goering & Smith, 2003; Rotman-Pikielny, Rabin, & Amoyal, 2007). Historical Background In 1956, in an effort to mitigate patient relapse, Gregory Bateson and colleges employed family therapy to treat individuals with schizophrenia. Since then, the benefits of family therapy have been lauded for decreasing symptoms of depression and anxiety in persons with neuropsychological diagnoses (Laroi, 2003) (Morris, 2001; Sinnakaruppan, Downey, & Morrison, 2005; Singer, Glang, & Nixon, 1994), reducing burden, increasing life satisfaction (Rogers, Strode, Norell, Short, Dyck, et al. F Cross References Interdisciplinary Team Rehabilitation Patient-Family Education Recommendation References and Readings Halm, M. Participation of family members in ward rounds: Attitude of medical staff, patients and relatives. Drawing on this theory, family therapists approach families as an interconnected system wherein the whole is greater than the sum of the parts. Changes within the family system affecting patterns of interaction, roles, or family membership are thought to reverberate throughout the family and affect individual family members. Instead of conceptualizing problems as residing within an individual, family therapists focus on how problems are maintained by patterns of communication and interaction. Positive feedback loops consist of energy being added to the family that is thought to create change, whereas with negative feedback loops, new information is not added to the family, and homeostasis is maintained. Sessions focus on family level intervention and can be held with or without the identified patient present. Neurological conditions and resulting disability often have profound effects on family members and family functioning. Generally, family therapy is meant to alleviate symptoms expressed by the identified patient and maintained by the family system. Further, a clinician can assist the family in understanding how problematic cycles of anger and blame get in the way of reaching their goals. The therapist can also teach the family new skills to enhance communication and problem-solving. Finally, to address aggressive behavior, family level interventions have been developed including assertiveness training and behavior management (McKinlay & Hickox, 1988). Efficacy Information Only a handful of studies have documented the efficacy of family therapy for neuropsychological disorders. Singer, Glang, and Nixon (1994) found that support groups focusing on stress management and coping skills reduced anxiety and depression in families of neurologically injured children. Sinnakaruppan, Downey, and Morrison (2005) found that family support groups reduced anxiety for the caregiver as well as the patient; the later also displayed reduced depression. Treatment Participants Family therapy is often used in inpatient and outpatient settings to help families of patients with stroke, brain injury, and other neurological disorders. Therapy is appropriate for virtually all families experiencing grief, loss, confusion, anger, frustration, and helplessness related to the neuropsychological diagnosis of a family member. Therapists address a variety of themes common in families after neuropsychological diagnoses and brain injury including psychoeducation; manifestation of denial, anger, guilt, and blame; overprotectiveness; and aggression (Kreutzer, Zasler, Camplair, & Leininger, 1990). Education about brain injury has been found to be an essential service for family members (Leske, 1986). The family systems approach to treating families of persons with brain injury: A potential collaboration between family therapist and brain injury professional. Psychological distress in carers of head injured individuals: the provision of written information. Adapting multiple-family group treatment for brain and spinal cord injury intervention development and preliminary outcomes. A comparison of two psychosocial interventions for parents of children with acquired brain injury: An exploratory study. Head injury and family carers: A pilot study to investigate and innovative communitybased educational programme for family carers and patients.
That inattention neglect is more commonly associated with right hemisphere injury might also account for the asymmetries of anosognosia fungus gnats perlite effective 200mg fluconazole. Studies from our laboratory have revealed when undergoing selective right hemisphere anesthesia antifungal diet order fluconazole 100mg amex, during the time these patients demonstrate shoulder weakness their shoulder proprioception is intact antifungal bath soap 100 mg fluconazole with mastercard. To learn if this disorder could be related to neglect fungus gnat grubs cheap 200 mg fluconazole with amex, spatial or personal fungal infection purchase fluconazole 400 mg overnight delivery, we brought their hemiplegic left forelimb over to the right Anosognosia A 181 side of their body and to their right visual field antifungal nail polish walmart discount fluconazole 100mg fast delivery. To make certain subjects see their hand, we wrote a number on their hand and subjects were able to read these numbers. Despite these strategies many, but not all, patients still denied weakness of that hand. In support of this postulate, several investigators have reported dissociations between the presence of spatial neglect and anosognosia. While patients with personal neglect might be unaware of the parts of their body, patients with asomatognosia do not feel or claim that certain body parts belong to them. Like spatial and personal neglect, asomatognosia is more commonly associated with right than left hemisphere lesions. If patients with right hemisphere injury do not believe their left arm-hand belongs to them, they will not recognize their own weakness. We found that there were some patients who had anosognosia who also had asomatognosia, but only a small proportion. As mentioned, in few patients when their arm could be visualized in the right visual field left hemisphere, they did recognize their weakness. In these cases, we cannot be sure if their anosognosia was induced by a failure in feedback or a disconnection. However, as mentioned above this procedure only helps a small minority of patients. Limb amputation is often associated with a perception that the limb is still present and this perception is thought to be related to the continued presence of a brain representation of that missing phantom limb. When patients with a hemiparesis are asked to move a limb, many often perceive that the paretic limb is moving, and this phantom movement in combination with impaired feedback might account for anosognosia. During selective hemispheric anesthesia (Wada test), we had blindfolded subjects with left hemiplegia attempt to raise their paretic left arm and we then asked them to raise their right (non-paretic) arm to the same level as they perceived left arm. Some of the patients we tested did raise their right arm, suggesting that they had phantom movements, but we found no significant relationship between phantom movements and anosognosia. Patients with right hemisphere lesions often demonstrate contralesional limb akinesia also called motor neglect. Many of these patients do not attempt to spontaneously move their akinetic arm and while less common some do not even attempt to move this arm to command. Patients with limb akinesia might not discover that they are weak because they do not attempt to move this left arm. If they do not attempt to move this arm, they will not experience a dissociation between their expectations and performance, and it is this dissociation that alerts people that there is a problem. Providing external motivation such as suggestions or commands might entice patients to attempt a movement and with these commands some patients do discover their weakness. Electromyographic studies have also provided evidence in support of this akinesia hypothesis. Based on the above discussion it appears that several mechanisms might contribute to the presence of anosognosia for hemiplegia. Amnesic patients with medial temporal lesions are often aware 182 A Anosognosia of their disability and patients with damage to the basal forebrain and to the medial thalamus are often unaware of their memory deficit. The reason for this dichotomy is not fully known, but the dorsomedial thalamic nucleus is heavily connected with the frontal lobes and damage to this dorsomedial nucleus induces frontal dysfunction. Frontal lobe dysfunction is often associated with impaired recall but not recognition, suggesting that the problem is not with the consolidation of memories, but rather retrieval. The patients with amnesia from a thalamic or basal forebrain injury, more often confabulate memories than do those with medial temporal lobe damage. These patients often deny their blindness, confabulate responses, and are unaware they are blind, anosognosic. Perhaps since these patients have intact visual imagery and cannot receive visual input, this imagery is mistaken for online input. These aphasic patients might have focused their attention on what they were attempting to say rather than how they said it. Future Directions Anosognosia, the failure to recognize a disease or a disability, might delay treatment, interfere with rehabilitation, and put people in danger. Patients might be anosognosic for a variety of neurological disorders such as weakness, sensory loss, personal and spatial neglect, memory loss, and aphasia. There appears to be a variety of mechanism that might account for anosognosia including psychological denial, impaired and false feedback, alterations of the body schema, failures to test systems, and to initiate behaviors. In addition to continuing to define and test possible mechanisms, effective treatments for these disorders are needed. For example, we saw a patient, who when speaking jargon, became angry when he was not understood. To be aware that an error has been made, a person needs to have a normal representation of the targeted behavior. Blindheit nach beiderseitiger Gehirnerkrankung mit Verlust der Orienterung in Raume. Therefore, it appears that the action of glutamate on these cells is the putative mechanism mediating cell death in this region of the hippocampus and helps explain many of the signs and symptoms associated with anoxia (Bonner & Bonner, 1991). A Signs and Symptoms Anoxia often results in impairments in memory, executive, and motor function. This is likely due to the fact that anoxia is associated with damage to limbic and subcortical regions, in addition to the frontal lobes and the cerebellum (Golden, Zillmer, & Spiers, 1992). Presenting symptoms may also include impairments in awareness and affect as well as confabulatory behavior. Anoxia associated with cardiac arrest may include amnesia, in addition to bibrachial paresis, cortical blindness, and visual agnosia. Carbon monoxide poisoning may be associated with affective disturbances as well as cortical and anoxia induced dysfunction (Aminoff, Simon, & Greenberg, 2005). Synonyms Oxygen deficiency; Severe hypoxia Definition Anoxia refers to a hypoxia. In contrast to anoxia, hypoxia refers to a reduction in oxygenation, rather than a complete loss of oxygenation (Zillmer & Spiers, 2001). Cross References Carbon Monoxide Poisoning Glutamate Hippocampus References and Readings Aminoff, M. Etiology Anoxia can result from a number of conditions including cardiac arrest, carbon monoxide poisoning, stroke, brain injury, and complications due to anesthesia. Antagonist Receptor Spectrum Medical, Neuropsychological, and Psychological Symptoms Infarctions in the territory of this artery are associated with a variety of clinical signs and symptoms involving gait, limb sensation, abulia, lack of spontaneous activity, urinary incontinence, frontal and memory impairments, in addition to emotional dysregulation (apathy) (Brust, 1995). Innervated areas also include the medial-orbital surface of the frontal lobe, frontal pole, and a small strip of the lateral surface of the cerebral hemisphere along the superior border (Ropper, Brown, Adams, & Victor, 2005). Its cell characteristics are agranular, and therefore are distinct from the cortex. At that time, the role of the frontal lobes in emotion and behavioral control were recognized, and frontal lobotomy was experimented with as a means of treating a variety of psychiatric conditions, including severe depression and schizophrenia. While frontal lobotomy resulted in a reduction in agitation and other severe psychiatric symptoms, surgical removal of the frontal lobe caused severe cognitive dysfunction. Given that the orbital frontal region was considered to be particularly important for the control of impulses and emotional regulation, subsequent psychosurgical approaches typically restricted ablation to these areas, often through leukotomy. Unfortunately, patients undergoing this procedure often exhibited marked personality change, with flattening of affect, apathy, and other undesirable effects. A third generation of psychosurgical procedures ensued with efforts to target brain areas more selectively. Beginning in the late 1950s, cingulotomy was developed as an alternative to frontal ablation. There was also some evidence that it was helpful for patients with severe chronic depression, though the basis for these effects may relate to reductions in emotional tension, obsessive thought processes, and other depression-associated problems. Postsurgery patients tended not to experience significant memory, language, or visual change. Subsequent controlled studies indicated that while these functions are largely spared following cingulotomy, there are alterations in some attention-related functions, most notably attentional focus, intention, and response selection and control (Cohen et al. These changes correspond with reductions in emotional tension and distress, and also a tendency for reduced self-initiation of behavior (Cohen et al. It has also been implicated in A 186 A Anterior Cingulate System processing new motor programs, working memory, and mismatch detection. This probably reflects the fact that it plays an increased role when tasks require motivation and drive to complete and where there is demand for attentional effort and focus. Neuroimaging studies have begun to point to its role in a variety of behavior problems, such as obesity and inactivity. Cross References Apathy Executive Function Intention Psychosurgery References and Readings Ballentine, H. Habituation and sensitization of the orienting response following bilateral anterior cingulotomy. Alteration of intention and self-initiated action associated with bilateral anterior cingulotomy. However, these changes are usually part of a much more global pattern of brain abnormality. It also tends to be associated with obsessive rumination and preoccupation with internal states and signals, such as pain and impulses to seek reward. Damage to this area would, therefore, particularly interfere with cholinergic activation of structures and circuits implicated in memory within the medial temporal lobe (Schnider & Landis, 1995). The subcallosal perforating artery has, in fact, been implicated in and may mediate personality changes and memory impairments. Relationships between recovery of executive function and temporal gradients in retrograde amnesia have been reported, with improvements in executive function accompanied by parallel improvements in the severity of retrograde amnesia. Improvement in the recall of complex visual-spatial information and an enhanced ability to benefit from an executive learning strategy have also been reported with little improvement on traditional measures of memory or executive function (Diamond, DeLuca, & Kelley, 1997a). Recovery from neuropsychological disturbances is generally poorer in patients with ventral frontal lesion compared to those with basal forebrain and striate lesions. Comparisons of clipping versus endovascular embolization procedures have shown that, in a number of studies, clipped patients have more severe cognitive impairments than embolization patients and that 33% of clipped patients had impairments in memory and executive functioning (Chan, Ho, & Poon, 2002). Generally, the severity of cognitive impairment has predictive value for functional status particularly with respect to levels of required supervision at discharge (Saciri & Kos, 2002). Some work suggests that recovery of executive function and not short- and long-term memory may, in fact, be the best predictor of the ability to return to work (DeLuca & Diamond, 1995). Neuropsychological and Psychological Outcomes Neuropsychological It is generally concluded that verbal intellectual skills, language functions, visuo-spatial skills, and attention/ concentration are within normal limits or only mildly impaired, although complex concentration appears to be reduced. More severe impairments are seen in delayed versus immediate memory and in executive function (DeLuca & Diamond, 1995). Impairments in spatiotemporal discrimination appear similar to other populations with frontal lobe dysfunction (Schacter, 1987). Procedural memory on serial reaction time and mirror-reading tasks also appears to be preserved. The key difference between provoked and spontaneous confabulation is that in spontaneous confabulation the confabulation guides actions. Recovery from confabulation appears to parallel improvement in temporal context confusion, and recovery can occur in the absence of significant improvement on traditional tests of memory and executive function. Levels of productive employment are generally reduced and many patients show clinically significant posttraumatic stress symptomatology (see Table 1 for a list of neuropsychological and psychological impairments). In some cases, modification of existing assessment tools can be an effective way to enhance the assessment process. Moreover, encoding and recall were improved by using an executive organizational strategy, in addition to identifying patients who were more likely to benefit from such an intervention (Diamond, DeLuca, & Kelly, 1997a; Prignatano & DeLuca, 1999). Neuropsychological deficits in patients with an anterior communicating artery syndrome: A multiple case study. Neuropsychological sequelae of patients treated with microsurgical clipping or endovascular embolization for anterior communicating artery aneurysm. Cerebral aneurysms and arteriovenous malformations: Implications for rehabilitation. Autonomic and recognition indices of aware and unaware memory in amnesics and healthy subjects. Executive and memory impairment in patients with anterior communicating artery aneurysm. Verbal learning in anterior communicating artery aneurysm and multiple sclerosis patients: Performance on the California verbal learning test. Impaired delay eyeblink classical conditioning in individuals with anterograde amnesia resulting from anterior communicating artery aneurysm.
Table 1 lists different types of dysarthria and the corresponding level of nervous system involvement and describes features of speech impairment associated with each type of dysarthria fungus ants purchase 100 mg fluconazole overnight delivery. Definition Dynamic assessment refers to an interactive approach to conducting assessments antifungal zinc oxide cheap fluconazole 50mg overnight delivery, focusing on the ability of the examinee to respond to an intervention fungus gnats dryer sheets fluconazole 400 mg without a prescription. As an alternative to a more traditional assessment approach fungus deck buy 150mg fluconazole amex, within dynamic assessment antifungal yeast infection pills generic fluconazole 400mg on-line, the evaluator conducts a pre-test fungal lung infection order fluconazole 400mg with visa, imposes an intervention, and then conducts a post-test. Epidemiology Dysarthria is a subset of a larger group of communication disorders referred to as motor speech disorders. Therefore, epidemiology of dysarthria is best represented by the epidemiology of the References and Readings Haywood, H. Table 1 Types and characteristics of dysarthria and associated level of nervous system involvement Type of dysarthria Level of nervous system damage Lower motor neuron: Damage to the cranial or spinal nerves including the nuclei, axons, or neuromuscular junctions that make up the motor units Primary characteristics Muscle weakness, hypotonia, diminished reflexes, atrophy, fasciculations. Speech may be characterized by imprecise consonants, hypernasality, breathy phonation, reduced breath support, and abnormal prosody. Levels of the speech mechanism may be independently impaired by individual damage to cranial nerves such as breathy phonation from a vocal cord paralysis or distorted tongue tip articulation due to hypoglossal nerve damage Spasticity and weakness in the speech muscles results in harsh, strained-strangled phonation, low-pitch, short phrases, imprecise articulation, hypernasality, slow rate, abnormal prosody with monopitch and monoloudness, excess and equal stress Primarily a disorder of articulation resulting from weakness and incooordination of speech; imprecise consonants, irregular articulatory breakdowns, harsh vocal quality in some patients. Often symptoms are mild, temporary, and resolve spontaneously or with minimal intervention Muscular discoordination resulting in ``drunken-like' speech, with imprecise articulation and irregular articulatory breakdowns, distorted vowels, prolonged phonemes, slow rate, abnormal prosody, and harsh vocal quality Reduced range and force of movement as well as rigidity; slow individual but also fast repetitive speech movements. Hypophonia or reduced loudness, repeated phonemes, palilalia, rapid or ``blurred' speech, short rushes of speech, variable rate often increased, reduced amplitude of articulation, abnormal prosody and reduced facial expression. Slow speech initiation Involuntary movements interfere with normal control of speech. Abnormal movements are often evident in other parts of the body and the larger physical movements of the body impact the motor control of each level of the speech mechanism. Unexpected inhalations and exhalations, irregular articulatory breakdowns, abnormal prosody, voice tremor, spasms, strained, harsh voice, abnormal prosody, voice stoppages, excess loudness, and hypernasality may be present Any combination of the characteristics of the six types of dysarthrias listed above. Brain stem strokes, for example, may cause spastic dysarthria Unilateral damage to the upper motor neurons. Etiologies include: cerebellar tumors, cerebellar atrophy or degenerative diseases of the cerebellum Subcortical, basal ganglia control circuits; Extrapyramidal system involvement Parkinsonism is the most common cause of hypokinetic dysarthria Hypokinetic Hyperkinetic Subcortical, basal ganglia control circuits; often of unknown etiology. May be medication-related (tardive dyskinesia); etiologies include: fast movement disorders such as tremors, chorea, myoclonus, athetosis, dystonia Mixed Neurological damage to more than one level of the nervous system. Duffy (1995) cited a review of the distribution of acquired communication disorders at the Mayo Clinic between 1987 and 1990 and found that 34. When dysarthria co-occurs with aphasia, impaired cognition, language, and even personality changes may be present. Speech is one of the critical skills that enable an individual to function independently. When an individual loses the ability to communicate effectively, they often are deemed unsafe to live independently or to make decisions autonomously. D Evaluation Natural History, Prognostic Factors, Outcomes An influential classification system based on perceptual judgments of dysarthria, reflecting neuromuscular condition and probable neuroanatomic origin, emerged from the Mayo Clinic studies (Darley, Aronson, & Brown, 1969a, b). These authors described distinctive speech patterns for the various types of dysarthria resulting from lesions in different regions of the nervous system. The onset, progression, and prognosis for dysarthria vary depending on the type and severity of the etiology and the level(s) of nervous system involvement causing the dysarthria. As one can predict, dysarthria resulting from an etiology that has a predicted pattern of neuromuscular recovery has a better prognoses than a dysarthria that is caused by a degenerative neuromuscular disease. The goals of the motor speech evaluation include: (a) To describe the characteristics of speech (b) To differentially diagnose the type of dysarthria (c) To confirm the presence of neurologic disease and the level of nervous system involvement (d) To determine the severity of the speech impairment (e) To determine the presence of other neurologic communication disorders (f) To determine prognosis for recovery (g) To define an intervention plan the components of the motor speech exam include: gathering of a thorough history of the onset and progression of the symptoms, identifying salient speech features and confirmatory signs. After gathering relevant history of the speech symptoms and observing and measuring motor speech behaviors, the data are analyzed. The collection and analysis of data from the history and motor speech exam lead to diagnosis and recommendations. The motor speech exam examines the symmetry, strength, speed, range, steadiness, tone, and accuracy of neuromuscular features of speech. The anatomic structures and physiologic functions of each level of the motor speech system are examined in isolation and in coordination with the rest of the system in contextual speech tasks. The oral mechanism and motor speech exam consists of studying the structures and functions of respiration, phonation, articulation, resonance, and prosody. Examples of confirmatory signs are suck and gag reflexes; tongue Neuropsychology and Psychology of Dysarthria Dysarthria is a motor speech impairment caused by a neurologic disease or disorder, which may present with 908 D Dyscalculia wiggle or rapid lateral movements of the tongue; cough and glottal attack, which indicates whether the vocal folds adduct; presence of fasciculations on the chin or tongue; and/or evidence of atrophy of the tongue. Uninhibited laughter or crying represent frontal lobe release signs of pseudobulbar affect and are indicative of bilateral upper motor neuron damage. Treatment Therapeutic intervention for dysarthria addresses the speech impairment, taking into account the underlying neuropathological substrates of the dysarthria. Therapy may focus on one or more levels of the motor speech system simultaneously or sequentially. For example, hypokinetic dysarthria is characterized by impaired articulation, phonation, and prosody. For example, for the patient with hypophonia of hypokinetic dysarthria who is unable to be heard and understood, therapeutic strategies may focus on increasing vocal loudness, as well as articulation and prosody. In addition to working in structured, controlled linguistic contexts, therapeutic tasks are planned in more naturalistic environments, outside of the clinic to facilitate carryover and generalization. Recruitment of significant others to facilitate carryover of new behaviors for effective communication is critical. For more severely impaired patients or those whose dysarthria is part of a degenerative neurologic process, the use of alternative and augmentative communication systems may be beneficial; including, voice amplification devices, palatal prosthesis, or electronic communication devices. For some dysarthrias, surgical or pharmacologic interventions are available and more effective than behavioral intervention. For example, the treatment of choice for adductor spasmodic dysphonia is Botox injection. Pharmacologic intervention may be beneficial for some hyperkinesias such as tics, chorea, and tremor. In the broad sense, dyscalculia pertains to a difficulty in learning, understanding, and completing math problems. Others have suggested that dyscalculia is a specific subtype of a math disorder, involving lack of skills in executing math calculations, brought about by deficits in writing, reading, understanding, and language abilities. Cross References Anarthria Aphasia Apraxia Neuropsychology and Psychology of Dyscalculia (Syndrome/Illness) the field of neuropsychology and neuro imaging is moving closer to the understanding of math ability and Dysconjugate Gaze D 909 dyscalculia. Neuropsychologists postulate that the dyscalculia is fundamentally a genetically determined disorder or basic numeration (von Aster & Shalev, 2007). Recent studies have found different subtypes of the disorder, including those involving dissociations between exact calculation and the ability to approximate and number quantities (Stanescu-Cosson et al. Additionally, the literature suggests that there is a connection between finger counting and calculation and math processing (Kaufmann, 2008). Cross References Acalculia Learning Learning Disability D References and Readings American Psychiatric Association. Education and neuroscience: Evidence, theory and practical application [Special issue]. Understanding dissociations in dyscalculia: a brain imaging study of the impact of number size on the cerebral networks for exact and approximate calculation. Depending on the developmental level of the child and level of mathematics, treatment may vary in form. Much of the remediation of math disorders is conducted in the school by special educators. Thus, they require individually tailored learning instruction which will work on their particular areas of deficit. That is, they may be visual learners and learn mathematical concepts best by using manipulatives to represent quantities or concepts. Additionally, treatment has taken the form of working on tracking and math automaticity. Several new neuropsychological studies are investigating the part executive dysfunctions, such as memory and planning, play in the deficit so as to create viable interventions to correct the difficulties. However, a great deal of treatment with math disorders involves understanding the area of deficit, Synonyms Strabismus Definition Dysconjugate gaze is a failure of the eyes to turn together in the same direction. Current Knowledge Vision Normal coordinated movements of the eyes produces conjugate gaze, in which the eyes are aligned for binocular 3-dimensional vision. With the visual axis of each eye fixated on a different 910 D Dysdiadochokinesia Walsh, F. However, if the image from the weaker eye is suppressed by higher cortical centers, there is only one image with loss of visual acuity (or a blurred image). It may result from a congenital condition affecting the central nervous system, such as cerebral palsy or polymicrogyria; from an acquired condition affecting the central nervous system such as stroke, multiple sclerosis, or traumatic brain injury; or from conditions affecting the peripheral nervous system impacting oculomotor control such as lateral gaze palsy. Pathology may also result from displacement of an eye from its normal position in the eye sockets, such as in proptosis or forward eye displacement. Synonyms Ataxia; Dysmetria Definition Dysdiadochokinesia refers to the inability to perform rapid alternating movements in a controlled, coordinated fashion. It causes a lack of rhythmicity in the performance of movements that require rhythmic alterations in the direction of a movement. Function Dysconjugate gaze may result in disturbances of function requiring integration of accurate 3-dimensional vision with other motor-sensory systems, such as dysmetria with motor targeting systems, and balance deficits with the vestibular system. It arises within the supratentorial cortex and is almost always associated with partial complex seizures. It may appear cystic and show one of three characteristics, including a specific glioneuronal element, nodular component, or association with cortical dysplasia. However, since they occur primarily in infants, their effects on cognition are unpredictable, although their clinical symptoms, mainly intractable localization-related seizures, are notable. This index primarily measures behavioral difficulties associated with executive functioning such as impulsivity, inhibition control, monitoring, and planning. The test is a 20-item self-report questionnaire focusing on potential deficits in emotional/personality, motivational, behavioral, and cognitive. D Cross References Behavioral Assessment Behavioral Assessment of the Dysexecutive Syndrome Dysexecutive Syndrome Cross References Brain Tumor Neoplasms Oligoastrocytoma Oligodendroglioma References and Readings Alderman, N. A comparison of the validity of self-report measures amongst people with acquired brain injury: A preliminary study of the usefulness of EuroQol-5D. Dysexecutive symptoms among a non-clinical sample: A study with the use of the dysexecutive questionnaire. Fractionation of the dysexecutive syndrome in a heterogeneous neurological sample: Comparing the dysexecutive questionnaire and the brock adaptive functioning questionnaire. Ecological assessment of the dysexecutive syndrome using execution of a cooking task. Initial development of a work-related assessment of dysexecutive syndrome: the complex task performance assessment. Dysexecutive syndrome can result from many causes, including head trauma, tumors, degenerative diseases, and cerebrovascular disease, as well as in several psychiatric conditions, including schizophrenia, attention deficit disorder, and antisocial personality disorder. These tests measure attention, spatial tasks, tests of planning and set-shifting, and temporal judgments. Dyslexia is at its core, a problem with phonological processing, that is, getting to the elemental sounds of spoken language, affecting both spoken and written language (Shaywitz, 1996, 2003). Recent evidence provides empiric support for defining dyslexia as an unexpected difficulty in reading (Ferrer, Shaywitz, Holahan, Marchione, & Shaywitz, 2010). Furthermore, longitudinal data indicate that in typical readers, intelligence and reading track together and are dynamically linked. In contrast, in dyslexic readers, intelligence and reading are quite separate and are not dynamically linked. Dyslexia D 913 much lower level of reading than expected for a person of that level intelligence, education, or professional status. Thus, in dyslexia, a highly intelligent person may read at a level above average but below that expected, based on his/her intelligence, education, or accomplishments. These new findings provide an explanation for the ``unexpected' nature of developmental dyslexia and the long-sought empirical evidence for the seeming paradox involving cognition and reading in individuals with developmental dyslexia. In the Connecticut Longitudinal Study sample survey, in which each participant was individually assessed, 17. D Natural History, Prognostic Factors, and Outcomes Data from the Connecticut Longitudinal Study indicate the persistence and chronicity of reading problems, refuting the notion, long and tightly held, that reading difficulties are outgrown or somehow reflect a developmental lag (Francis, Shaywitz, Stuebing, Shaywitz, & Fletcher, 1996). While persistent, it is important to keep in mind that the expression of the reading difficulty may change with time, so that difficulties with reading accuracy, especially in very bright children, often evolve into relatively accurate, but not fluent reading. Current evidence suggests that the etiology of dyslexia is best conceptualized within a multifactorial model, with multiple genetic and environmental risk and protective factors leading to dyslexia. This conceptualization recognizes that dyslexia is both familial and Categorization Dyslexia is a member of the family of learning disabilities; in fact, dyslexia is the most common and most comprehensively studied of the learning disabilities, affecting 80% of all individuals identified as learning-disabled (Lerner, 1989). Rather, dyslexia is best explained by multiple genes, each contributing a small amount of the variance. Neuropsychology and Psychology of Dyslexia Print emerged from the language system, the relationship between print and spoken language perhaps best captured by the statement, ``Writing is not language, but merely a way of recording [spoken] language by visible marks' (Bloomfield, 1933). Of the several theories suggested, an explanation reflecting what is known about the relationship between spoken and written language, the phonological model has received the most support. Results from large- and well-studied populations with reading disability confirm that in young school-age children (Stanovich & Siegel, 1994) and in adolescents (Shaywitz et al.
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According to the dopamine hypothesis fungus hydrangea leaves fluconazole 50 mg amex, the psychotic symptoms emerge from an excess of dopamine activity in the mesolimbic system and the negative symptoms from a deficit of dopamine in the mesocortical system fungus gnats hydro buy 150mg fluconazole overnight delivery. The two systems are thought to interact such that the hypoactive prefrontal neurons enhance dopamine neurotransmission in the mesolimbic system (Iversen et al anti fungal bacterial cream discount fluconazole 100 mg mastercard. In support of the dopamine hypothesis is the observation that chronic abuse of dopamine agonists antifungal over the counter purchase fluconazole 100mg without prescription. Definition Dyskinesias are abnormal fungus predator animal prey order fluconazole 200 mg without a prescription, involuntary flowing movements that likely result from an inappropriate response to levodopa administration fungus soap buy fluconazole 100mg without prescription. They are felt to occur when the postsynaptic dopamine receptors are downregulated over time, resulting in an abnormal postsynaptic response. Dyskinesias are typically related to peak levodopa plasma levels or to a relative change in the plasma levodopa level. As the disease progresses, the dose required for symptomatic control approaches that which induces intolerable dyskinesias, thus narrowing the therapeutic window and limiting medical therapy. The Doppler effect is familiar to most of us since it accounts for the change in pitch of a sound, such as an ambulance siren, as it speeds past an observer. Continued advances in Doppler technology such as electronically steered, phased array transducer systems and the application of sophisticated signal processing, and display techniques has allowed for sophisticated analysis of ultrasound echoes and has advanced new medical applications of this technology in a wide variety of clinical diagnostic applications (Sloan et al. Clinical Applications of Doppler Ultrasonograpy in Cerebrovascular Disease Carotid Doppler is commonly used to evaluate for carotid artery stenosis in a suspected cerebrovascular disease. Evaluation of the carotid arteries using Carotid Doppler ultrasonography has the advantage in that it is noninvasive and safe while the gold standard carotid angiography, requires the injection of a contrast medium. A common clinical application of Carotid Doppler ultrasound is in the screening of patients for clinically significant stenosis in the carotid arteries, which can be a risk factor for stroke. Patients with significant stenosis may be candidates for carotid arteriogram and surgical intervention. Transcranial Doppler is also noninvasive and can be performed at the bedside, repeated as needed or used for continuous monitoring (Taylor, Holland, & Doppler, 1990). Report of the therapeutics and technology assessment subcommittee of the American Academy of Neurology. Synonyms Sensory nerve roots Definition Nerve fibers entering the spinal cord that carry somatosensory data such as pain, temperature, pressure, touch, state of muscular contraction, and related information. These fibers originate from various types of nerve endings in the skin, muscles and joints of the trunk, extremities, and back and top of the head and travel to the spinal cord in the nerve bundles collectively referred to as the spinal or peripheral nerves. The latter consist not only of sensory fibers travelling toward the cord, but also motor fibers exiting the cord and heading toward muscles. As these peripheral nerves reach the vertebral column, the afferent or sensory fibers split off from the exiting efferent or motor fibers and enter the cord dorsally (posteriorly) at the dorsolateral sulcus. This short segment between where the peripheral nerve divides into its sensory and motor components and these afferent fibers enter the cord is known as the dorsal nerve root. The term ``ganglion' refers to a collection of cell bodies outside the central nervous system. In the majority of cases an axon exits the cell body at one point (axon hillock) and the dendritic processes are attached at one (bipolar) or more (multipolar) sites on the same cell body. There is a single short extension off the axonal process that goes to the cell body. Just before the dorsal nerve roots (which represent a collection of individual sensory Anterior horn cells Dorsal (sensory) nerve root Dorsal root ganglion Peripheral nerve (mixed) Ventral (motor) nerve root Dorsal Nerve Roots. Figure 1 Dorsal and ventral roots, entering and exiting the spinal cord and combining to form a peripheral nerve Dorsal Visual Pathway D 887 nerve fibers) enter the spinal cord their axons give off these unipolar branches to their individual cell bodies. Thus, each dorsal nerve root has a very visible bulb-like enlargement just outside the cord which represents a collection of these cell bodies which are known as the dorsal root ganglia. A similar ganglion is readily seen just outside the pons in association with the sensory portion of the trigeminal nerve. Mishkin and Ungerleider (1982) provided the first empirical evidence for this intuition, by showing that monkeys with inferior temporal cortex lesions had problems recognizing objects by their shape (what), while monkeys with parietal lobe lesions had problems in processing the location of objects in space (where). These findings provided evidence for anatomically and functionally distinct visual pathways: a ``what' or ``ventral' pathway involved in recognition that originates in primary visual cortex and projects into the inferior temporal lobe, and a ``where' or ``dorsal' pathway that from primary visual cortex projects into the dorsal posterior parietal cortex. Historical Background Starting from the 1960s, scientists had intuitions that the visual system could be divided into two separate the anatomical substrates of the dorsal visual pathway were initially identified in the macaque brain with inputs originating in V1 and then proceeding to the inferior parietal area, located approximately between the superior temporal sulcus and the intraparietal sulcus (Mishkin & Ungerleider, 1982; Mishkin, Ungerleider, & Macko, 1983). In the human brain, the dorsal stream originates in the primary visual cortex and terminates in the superior parietal lobule (see Creem & Proffitt, 2001, for a review). Milner and Goodale have proposed that the dorsal stream uses information about the location, orientation, and size of an object in egocentric coordinates to allow the observer to perform goal-oriented actions (cf. Damage to components of the dorsal visual pathway can result in deficits in goal-directed behavior and/or in visuo-spatial performance. These disorders are caused by damage to the posterior parietal cortex (Perenin & Vighetto, 1988). Patients with optic ataxia have difficulties in reaching and grasping objects, despite showing no impairment in object recognition (Perenin & 888 D Dorsolateral Frontal System Mishkin, M. Contribution of striate inputs to the visuospatial functions of parieto-preoccipital cortex in monkeys. Fewer cases have been documented regarding impaired performance on visuo-spatial tasks, such as judging distances. These cases have been associated with large lesions in the posterior parietal lobe, usually rightlateralized (Newcomb & Ratcliff, 1989). A third neurological disorder associated with the parietal lobe damage is neglect syndrome. Neglect patients show an inability to process information, attend, and orient to the side of space that is contralateral to the damaged lobe. Unlike optic ataxia patients, neglect patients usually have damage in the inferior portion of the parietal lobe. This dissociation in symptoms between the two syndromes has supported a functional distinction between the superior and inferior parietal lobes, with the superior parietal lobe being primarily involved in action-oriented spatial processing, and the inferior parietal lobe being responsible for more generic deficits in processing a specific portion of the surrounding environment (cf. Architectonically, it is composed of granular neurons distinct from the pyramidal cells of the adjacent motor cortex. It is also part of a cortical-subcortical system involving the dorsomedial thalamic nucleus and basal ganglia (Cummings, 1993). There are direct connections to the dorsolateral head of the caudate nucleus, the lateral aspect of the dorsomedial globus pallidus, and rostrolateral substantia nigra. Separate neural pathways for the visual analysis of object shape in perception and prehension. Dorsolateral Frontal System D 889 the dorsal globus pallidus and ventromedial subthalamic nucleus, with thalamic relays in the parvo- and magnocellular portions of the ventral anterior nucleus and the mediodorsal nucleus (Saint-Cyr, 2002). Using ideas stemming from connectionist theories, each of these domains is a part of a wider network of sensory, motor, and limbic areas (Goldman-Rakic, 2002). This theory uses evidence from the parietal and temporal visual streams that contends that the parietal lobe (dorsal stream) processes spatial information (where: the relation of objects across coordinates), while the temporal lobe (ventral stream) processes nonspatial (what: as in a visual image or object) information. Several animal and human studies have supported this model (McLaughlin, 2009; Petrides, 1994, 2000). Lesions of the dorsolateral cortex cause apathy and difficulty maintaining new goals. Wisconsin Card Sorting Test performance in obsessive-compulsive disorder: no evidence for involvement of dorsolateral prefrontal cortex. Regional brain changes in bipolar I depression: a functional magnetic resonance imaging study. Dorsolateral and dorsomedial prefrontal gray matter density changes associated with bipolar depression. Object and spatial visual working memory activate separate neural systems in human cortex. Normal development of prefrontal cortex from birth to young adulthood: cognitive functions, anatomy, and biochemistry. Investigating a network model of word generation with positron emission tomography. The functional neuroanatomy of symptom dimensions in schizophrenia: a qualitative and quantitative review of a persistent question. Elevated striatal and decreased dorsolateral prefrontal cortical activity in response to emotional stimuli in euthymic bipolar disorder: no associations with psychotropic medication load. The functional neuroanatomy of depression: distinct roles for ventromedial and dorsolateral prefrontal cortex. Cooperation of the anterior cingulate cortex and dorsolateral prefrontal cortex for attention shifting. The mid-ventrolateral prefrontal cortex: insights into its role in memory retrieval. Dorsolateral prefrontal cortex activity predicts responsiveness to cognitive-behavioral therapy in schizophrenia. Differential contributions of lateral prefrontal cortex regions to visual memory processes. Dissociable roles of mid-dorsolateral prefrontal and anterior inferotemporal cortex in visual working memory. Shifting set about task switching: behavioral and neural evidence for distinct forms of cognitive flexibility. Figural fluency: differential impairment in patients with left versus right frontal lobe lesions. Neurobehavioral consequences of neurosurgical treatments and focal lesions of frontal-subcortical circuits. Dorsolateral prefrontal and anterior cingulate cortex volumetric abnormalities in adults with attention-deficit/ hyperactivity disorder identified by magnetic resonance imaging. Dissociation of neural systems mediating shifts in behavioral response and cognitive set. Fractionation and localization of distinct frontal lobe processes: evidence from focal lesions in humans. The major symptom dimensions of obsessive-compulsive disorder are mediated by partially distinct neural systems. Dorsomedial Nucleus of the Thalamus Mediodorsal Nucleus of Thalamus monkeys, though its role in man is still not entirely clear. V6 receives input from primary visual cortical areas and contains white matter pathways that are highly myelinated, providing for fast transmission of visual information. V6 neurons are particularly responsive to the orientation of visual contours and direction of the movement of visual patterns. Topographically, these neurons provide a representation of the entire visual field, which together with their responsiveness to low spatial frequency information makes them particularly well tuned to gross spatial information. Accordingly, V6 may contribute to the sense of self-orientation relative to the spatial cortex. V6 has projections to frontal lobes, which appear to influence the control of arm movement in reaching for objects. Each of the first six cards contains an odd number of randomly arranged dots Dot Counting Test D 893 (ungrouped), while the final six cards show an even number of dots (one more than each corresponding card from the first six) arranged in an organized pattern (grouped). The task requires examinees to count the dots as quickly as possible by the fastest means possible. It is expected that cooperative examinees will count grouped dots more quickly and accurately than ungrouped dots. Therefore, suspect effort is identified when the number of errors is higher for the grouped dots condition, or when the time taken to count grouped dots is equal to or more than that required to count the ungrouped dots (Lezak, Howieson, & Loring, 2004). The first procedure involved the administration of only the six cards of ungrouped dots, and the second procedure involved all 12 cards with the cards of ungrouped dots being presented before the cards with grouped dots. Frederick (1997) included instructions that participants should not count out loud or use their fingers to count, which would most likely slow down the speed of counting. For instance, Frederick, Sarafaty, Johnston, and Powel (1994) used a comparison of counting times for the grouped and ungrouped dots. Paul, Franzen, Cohen, and Fremouw (1992) suggested scoring the number of counting errors. Rose, Hall, and Szalda-Petree (1998) proposed counting the number of deviations from linearity for ungrouped and grouped dots. Frederick (1997) suggested a scoring method that transformed counting times and errors into a single score. Failure on the test has been defined as mean grouped dot counting time less than mean ungrouped counting time (Lezak, 1995) or greater than three errors (Martin, Hayes, & Gouvier, 1996); or ungrouped time greater than 180 s or grouped time greater than 130 s (Paul et al. This finding probably explains why their data have greater group classification rates than did prior studies that did not combine those variables. The initial series of validity studies compared performance of community volunteers to simulators, patients diagnosed with brain disorders, and psychiatric inpatients. It was one of the few tests developed by Rey (see Frederick, 2002) to assess poor effort. Rey originally designed his effort measures in response to 894 D Double Simultaneous Stimulation tests in identifying simulated mild head injury. An investigation into the reliability and validity of two tests used in the detection of dissimulation.