By C. Vigo. School of the Visual Arts.
Several other regions were less tivity may be associated with persistent ADHD only buy generic haldol 1.5mg line. Consistent with these findings cheap haldol 10 mg on line, the natively, Ernst et al. These mice shift from the midbrain in childhood to the prefrontal cor- show learning impairments, impulsiveness, and hyperactiv- tex in adults. Metabolic mapping studies suggest that their behavioral Anterior cingulate cortex, lying on the medial surface deficits are associated with lower 2-deoxyglucose uptake in of the frontal lobe, has strong connections to dorsolateral the left striatum and the frontal and parietal cortex (61). In contrast to sion tomography, single photon emission tomography, controls, the adults with ADHD failed to activate the ante- functional magnetic resonance imaging, or electroencephal- rior cingulate cortex. The most consistent findings were hypoactivity of kin et al. The neurochemical basis of brain dysfunction in ADHD found gender differences in lateralization (63), future stud- was studied by Dougherty et al. They measured DAT ies will need to assess gender differences and to determine density by single photon emission computed tomography how they may be related to the male predominance of the with the radiopharmaceutical iodine 123–labeled altropane. Their findings were consistent with the catecholamine hy- 582 Neuropsychopharmacology: The Fifth Generation of Progress TABLE 43. FUNCTIONAL NEUROIMAGING STUDIES OF ADHD Study Diagnosis Method Findings Lou et al. Taken together, the brain imaging anomalies and malformations of the posterior fossa were studies fit well with the idea that dysfunction in frontosub- more common among patients with ADHD compared with cortical pathways occurs in ADHD. How- with the report of a father and son, both having methyl- ever, given that several other studies showed partial agenesis phenidate-responsive ADHD secondary to frontal lobe epi- of the corpus callosum or anomalies of the cerebellar vermis lepsy (68). Notably, the frontosubcortical systems that con- (also formed before birth), it seems reasonable to conclude trol attention and motor behavior are rich in that at least some children with ADHD have a very early catecholamines, which have been implicated in ADHD by onset of brain abnormalities. In a novel approach to assessing brain regions implicated in ADHD, Herskovits et al. Compared with head-injured children who did not develop Figure 43. To address this issue, Nopoulos et diagnosis is valid. These studies leave no doubt that ADHD Chapter 43: Pathophysiology of ADHD 583 Faraone et al. These investigators reasoned that cases that remit before adolescence could have a smaller genetic component to their disorder than persistent cases. Evidence supporting this hy- pothesis derives from several studies. In a prospective follow- A up study, Biederman et al. Thus, these data suggest that children with persistent ADHD have a more familial form of ADHD than those whose ADHD remits by adoles- cence. The 57% rate of ADHD among children of adults with ADHD was much higher than the more modest 15% risk for ADHD in sib- lings of referred children with this disorder. These findings were consistent with a prior study by Manshadi et al. C They studied the siblings of 22 alcoholic adult psychiatric patients who met DSM-III criteria for ADD, residual type. The authors compared these patients with 20 patients A: ADHD in siblings. Forty- one percent of the siblings of the adult ADD probands were diagnosed with ADHD compared with 0% of the non- ADHD comparison siblings. Moreover, studies of more distant relatives are In another retrospective study, Biederman et al. These investigators found that the relatives of adoles- The Harvard/Massachusetts General Hospital (Boston) cent probands had higher rates of ADHD compared with ADHD family project studied two independent samples of the relatives of child probands. Thus, a prospective study of children with attention-deficit disorder (ADD) as defined children and retrospective studies of adolescents and adults by the DSM-III (74) and ADHD as defined by the DSM- suggested that, when ADHD persists into adolescence and III-R (77). These data show that (a) ADHD and major adulthood, it is highly familial. Thus, stratification by conduct and bipolar disorders may Twin and Adoption Studies cleave the universe of children with ADHD into more famil- ially homogeneous subgroups. In contrast, major depression Although family studies provide much useful information, may be a nonspecific manifestation of different ADHD they cannot disentangle genetic from environmental sources subforms. In a sample of 132 ADHD sib-pair families, of transmission. To do so, we must turn to twin and adop- Smalley et al.
Pathophysiologic mechanisms in the pathogene- 49:104–124 haldol 10 mg line. Progressive cortical Am J Psychiatry 1997;154:1016–1018 buy 5 mg haldol with mastercard. GREEN Increasingly, neurocognitive paradigms are used to study This view changed rapidly with the advent of in vivo patients with schizophrenia. With such paradigms, the cog- techniques of brain imaging. First, it became evident that nitive abnormalities in schizophrenia are characterized by the lateral cerebral ventricles of patients with schizophrenia means of experimental and clinical tests. These techniques are larger than those of controls on computed tomography have indicated that some types of cognitive impairment are (96). Second, functional brain imaging suggested that the not only reliably present in schizophrenia, but are also cen- frontal lobe blood flow or metabolism of schizophrenic pa- tral and enduring features of the disease. Moreover, it was shown that one type of revision of the one published in 1995, focuses on certain cognitive impairment, poor performance on the Wisconsin recent advances in characterizing the precise nature of cogni- Card Sorting Test (WCST), is directly linked to impaired tive impairments in schizophrenia, on understanding the activation of the prefrontal cortex in regional cerebral blood implications of these for treatment given the course and flow (106). It was within this context that a series of studies relationship to outcome of these variables, and on novel in which broad neuropsychological test batteries were used applications of neurocognitive approaches to the genetics demonstrated that patients with chronic schizophrenia of schizophrenia. In the original clinical descriptions of reinterpretation of the original neuropsychological studies; schizophrenia made by Kraepelin (64), he commented, it was increasingly realized that patients with schizophrenia 'Mental efficiency is always diminished to a considerable perform in the range typically found in brain-damaged pop- degree. From this perspective, types of readiness information and imperative stimuli. Hunt schizophrenia is viewed as a disease of cortex in which infor- and Cofer (54) noted the intellectual quotient (IQ) of mation processing dysfunction is an obligatory concomi- schizophrenic patients to be lower than that of normal con- tant. However, the increasing influence of psychodynamic We examine certain crucial, conceptually driven issues theory tended to minimize the significance of the cognitive that derive from this view: What is the course of global deficits of schizophrenia. It was thought that the deficits cognitive impairment in schizophrenia? What is the charac- displayed on formal psychologic testing were secondary to ter of neurocognitive impairments in schizophrenia? What impaired motivation or cooperation, gross breakdowns in is the relevance of traits like neurocognitive impairment to reality testing, or disordered thought processes. We conclude this chapter by noting that neurocognitive impairments may be of prognostic significance in schizo- Terry E. Goldberg: Clinical Brain Disorders Branch, National Institute phrenia because of the importance of such functions in pro- of Mental Health, National Institutes of Health, Bethesda, Maryland. Green: Department of Psychiatry and Biobehavioral Sciences, viding orientation to and encoding relevant environmental University of California School of Medicine, Los Angeles, California. In measures for 1- to 2-year periods, little change was evident. It is possible the effects observed were secondary to the interaction between com- promised cognitive reserve in schizophrenia and normal COURSE aging; it is also possible that high doses of neuroleptics and long-term institutionalization had a significant effect on Several contrasting views of the course of cognitive function daily living skills and some cognitive functions. One view suggests that cognitive In contradistinction to these findings, Goldstein and deficits become progressively worse throughout the long du- Zubin (41) found no differences in performance on the ration of the illness. A second view suggests that cognitive deficits, chronic schizophrenia. The study design allowed comparison ning the premorbid and morbid periods, Schwartzman and over an extremely wide range of duration of illness (patients Douglas (92) found a significant decrement in the perfor- ranged in age from 18 to 70 years). In addition, each cohort mance of schizophrenic patients tested on an army intelli- was matched on a measure of premorbid intellectual ability, gence examination (standard deviation of nearly 0. No significant differences between age similar to controls in the premorbid period. Thus, over five decades of illness, no progression minority of patients had marked cognitive limitations from was noted. A synthesis of these results suggests that in the early on (see ref. This is not say that subtle premorbid modal patient, a sharp decline in cognitive ability, including deficits do not exist in the majority of patients. Recent pop- general intellectual efficiency, occurs around the time of the ulation-based studies have demonstrated attenuations in in- onset of clinical symptoms ( 3 to 5 years), which is fol- telligence measures in schizophrenic patients-to-be (13,16), lowed by an arrest in deterioration and a long period of in addition to delays in the attainment of some early devel- impaired but stable cognitive function. This view of the natural history of schizophrenia is con- Studies of patients during their first episode of schizo- sistent with a neurodevelopmental perspective (107) in that phrenia substantiate the view that marked cognitive abnor- a prenatal lesion remains silent for years before manifesting malities are present at the very onset of the illness. In several itself in overt symptomatology and cognitive impairment. Both groups of patients of the more striking morbid phenomena, a state of weak performed poorly on a wide range of tests, including tests mindedness will be developed which usually changes slowly assessing memory, executive functioning, and attentional and insignificantly. However, we examine three functions in detail because a clinical global rating of functioning. However, when pa- (a) evidence has been found of differential impairments, Chapter 48: Neurocognitive Functioning in Patients with Schizophrenia 659 especially in the cognitive domains related to frontal system cues), several other studies have not found differences be- executive and attentional systems and medial temporal yond general slowing (35).
Neurocritical care units have developed to coordinate the management of critically ill neurological patients in a single specialized unit order haldol 10 mg online, which includes many clinical domains haldol 5mg with amex. Care is provided by a multidisciplinary team trained to recognize and deal with the unique aspects of the neurological disease processes, as several treatable neurological disorders are characterized by imminent risk of severe and irreversible neurological injury or death if treatment is delayed. Some diseases need immediate action, so admission to the NICU is the best solution when there is: 14 | Critical Care in Neurology 1) Impaired level of consciousness. In the Neurocritical Care unit, patients with primary neurological diseases such as myasthenia gravis, Guillain-Barré syndrome, status epilepticus, and stroke have a better outcome than those patients with secondary neurological diseases. So, we can conclude that these specialized units have greater experience in the anticipation, early recognition, and management of potentially fatal complications. Early identification of patients at risk of life threatening neurological illness in order to manage them properly and to prevent further deterioration is the role of general assessment of new patients in a neurological emergency. The neurologic screening examination in the emergency settings focuses primarily on identifying acute, potentially life- threatening processes, and secondarily on identifying disorders that require other opinions, of other specialists. The importance of urgent neurologic assessment comes from recent advances in the management of neurologic disorders needing timely intervention like thrombolysis in acute ischemic Assessment of Patients in Neurological Emergency | 15 stroke, anticonvulsants for nonconvulsive and subtle generalized status epilepticus, and plasmapheresis for Guillain-Barré, etc. It is obvious that interventions can be time-sensitive and can significantly reduce morbidity and mortality. A comprehensive neurologic screening assessment can be accomplished within minutes if performed in an organized and systematic manner (Goldberg 1987). Neurologic screening assessment includes six major components of the neurologic exam, namely: 1) Mental status 2) Cranial nerve exam 3) Motor exam 4) Reflexes 5) Sensory exam 6) Evaluation of coordination and balance. Based on the chief findings of the screening assessment, further evaluation or investigations can be then decided upon. History A careful history is the first step to successful diagnosis, and then intervention. For example, an alert patient with a headache associated with neck pain that started after a car accident might help direct the examination and radiographic imaging to focus on cervical spine injury or neck vessels (carotid or vertebral artery) dissection, while the same patient not in a car accident may direct your attention to a spontaneous subarachnoid hemorrhage. Dramatic or acute onset of neurologic events suggests a vascular insult and mandates immediate attention and intervention. A full mental status exam is not necessary in the patient who is conscious, awake, oriented, and conversant; on the contrary it must be fully investigated in patients with altered mental status. Sometimes, we can find no change in mental status; at that point careful consideration should be given to concerns of family. A systematic approach to the assessment of mental status is helpful in detecting acute as well as any chronic disease, such as delirious state in a demented patient (Lewis 1995). The CAM (confusion assessment method) score was developed to assist in diagnosing delirium in different contexts. CAM assesses four components: acute onset, inattention, disorganized thinking or an altered level of consciousness with a fluctuating course. Cranial nerve (CN) exam Cranial Nerves II - VIII function testing are of utmost value in the neurologic assessment in an emergency setting (Monkhouse 2006). Cranial Nerves II – Optic nerve assessment involves visual acuity and fields, along with a fundus exam and a swinging flashlight test. Visual field exam using the confrontation method is rapid and reliable. Assessment of Patients in Neurological Emergency | 17 Assessment of the optic disc, retinal arteries, and retinal veins can be done by a fundus exam, to discover papilledema, flame hemorrhages or sheathing. Cranial Nerves III, IV, VI – CN III innervates the extraocular muscles for primarily adduction and vertical gaze. CN III function is tested in conjunction with IV, which aids in internal depression via the superior oblique, and VI, which controls abduction via the lateral rectus. Extraocular muscle function is tested for diplopia, which requires binocular vision and thus will resolve when one eye is occluded. Marked nystagmus on lateral gaze or any nystagmus on vertical gaze is abnormal; vertical nystagmus is seen in brainstem lesions or intoxication, while pendular nystagmus is generally a congenital condition. The pupillary light reflex is mediated via the parasympathetic nerve fibers running on the outside of CN III. In the swinging flashlight test a light is shone from one eye to the other; when the light is shone directly into a normal eye, both eyes constrict via the direct and the consensual light response. Asymmetry in pupils of less than 1 mm is not significant. Significant difference in pupil size suggests nerve compression due to aneurysms or due to cerebral herniation, in patients with altered mental status. Bilateral pupillary dilation is seen with prolonged anoxia or due to drugs (anticholinergics), while bilateral pupillary constriction is seen with pontine hemorrhage or as the result of drugs (e. Cranial Nerve V – Individual branch testing of the trigeminal nerve is unnecessary, as central nervous system lesions affecting CN V usually involve all three branches. Cranial Nerve VII – The facial nerve innervates motor function to the face, and sensory function to the ear canal, as well as to the anterior two-thirds of the tongue. Central lesions cause contralateral weakness of the face muscles below the eyes. Cranial Nerve VIII – The acoustic nerve has a vestibular and a cochlear component.
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