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By: J. Sivert, M.B.A., M.D.
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Samples that have preinjury data antibiotic xifaxan side effects buy trozocina paypal, such as athlete samples antibiotics meat trozocina 500 mg with amex, differ in several important respects from emergency department populations (see previous Cognitive Sequelae section) with respect to being young infection 7 weeks after surgery discount 250mg trozocina fast delivery, healthy virus y antivirus order trozocina once a day, motivated to minimize symptoms, and perhaps exerting less effort on preseason testing so as to minimize any apparent effects of a concussion during the season. Age at time of injury appears to play a role in terms of both symptoms and neuropsychological function (Dikmen et al. Intuitively, it would seem that repetitive injuries would be associated with persistent symptoms, and certainly studies of contact athletes suggest that for some groups this holds true (McKee et al. Furthermore, it seems that novel or more difficult cognitive tasks, or tasks performed under mild degrees of physiological stress, can negatively influence the performance of patients with mild injury (Ewing et al. It is possible that specific genetic profiles contribute to response to neurotrauma and cognitive outcomes (see Chapter 3, Genetic Factors, in this volume; see also McAllister et al. A theme in the literature is that compensation seeking plays a role in adverse outcome. Some of the studies on this topic are drawn from largely medicolegal referral practices. Other studies have failed to confirm any significant linkage between compensation or litigation and frequency or severity of postconcussive symptoms either prior to or after settlement (Keshavan et al. For example, Rutherford (1989) reported on a series of patients with mild brain injury involved in litigation. In this sample, over 40% of those involved in litigation had no symptoms at the time of their medical-legal evaluation approximately 1 year after the injury. Approximately onethird of those who had symptoms at that time did not have 252 Textbook of Traumatic Brain Injury norms obtained from populations with known severe neurological disorders, suggest a negative response bias (Iverson and Binder 2000; Meyers et al. Poor effort was associated with poor neurocognitive performance, lower educational attainment, and change in work status but not litigation. However, there are numerous reasons that may account for apparent poor effort or negative response bias on tests of cognitive function, and malingering should not be immediately assumed. Inconsistent performance must be interpreted within the context of such factors as fatigue, medication effects, and medical or comorbid psychiatric conditions. With respect to the latter, somatoform disorders, depression, and factitious disorders need to be sorted out. Performance variation under various different conditions or worsening of symptoms in the context of heightened stress such as adversarial litigation is "normal" and should not be construed as evidence of malingering or of "real injury" not being present. Related to this, some have suggested that the expectation of symptoms might play a role in outcome (Mittenberg et al. However, if one expects something to happen and then it does, this in no way should suggest that the symptoms are not physiologically based. By this argument, because one might expect pain from hitting oneself with a hammer, the pain experienced is caused by that expectation rather than the stimulation of pain fibers brought about by crushed tissue and related hemorrhaging and edema. Thus, for many patients, improvement can occur before medical-legal evaluation, during the interval between evaluation and settlement, and may remain long after compensation issues have been settled. Litigation and compensation proceedings are frequently highly adversarial, prolonged ordeals, and it would be naive to expect that this kind of psychosocial stress would not affect symptom presentation. Even this early in the process, those involved in litigation were experiencing significantly more anxiety and social dysfunction and had poorer outcomes on the Glasgow Outcome Scale and the Rivermead Head Injury Follow-Up Questionnaire (Crawford et al. Rees (2003) suggested that these issues may well cause sufficient stress to the hypothalamicpituitary-adrenal axis to prolong or maintain symptoms. Of interest, this was true in studies that looked at measures of effort as well as those that did not. Unfortunately, many seem to conclude from these associations that the interest in being compensated for an injury causes the symptoms, an assertion that does not follow from a simple association. Other motivational factors may also play a role in functional level and cognitive performance. A variety of tests have been developed to help with the assessment of effort (for discussion, see Iverson and Binder 2000). Anxiety disorders Symptoms consistent with anxiety often endorsed, but may not be more frequent than in general population (Schoenhuber and Gentilini 1988). Full return to work and low levels of postconcussive symptoms 6 months after injury were the primary outcome variables. The presence of these disorders can serve to accentuate or increase the degree of distress associated with lingering symptoms, and successful treatment of comorbid conditions can result in significant reduction of postconcussive symptoms (Fann et al. However, Merskey and Woodforde (1972), in their study of 27 patients with mild brain injury, found that 7 patients had "endogenous" depression, 9 others had a mixture of anxiety and depression, and another 4 had "reactive" depression in combination with a variety of other behavioral problems. Many postconcussive symptoms such as subjective slowing, irritability, fatigue, and sleep disturbance can be consistent with a depressive syndrome, even when patients may not endorse explicit items such as "depressed mood. In this sample, early depressive symptoms did not predict subsequent injury difficulties, whereas early and current injury difficulties did predict depressive symptoms. The conflicts in Iraq and Afghanistan have spurred an interest in the relationship between psychological and biomechanical trauma, particularly in military populations. Quite commonly, patients have both personality changes secondary to their injury and a manic syndrome (Zwil et al. The latter can present as a periodic worsening of the irritability and impulsivity characteristic of the former. This periodicity may be mistaken for an integral part of the personality changes and may account for the lower frequency of mania diagnosed in these patients (Hale 1982; Stewart and Hemsath 1988). Psychosis Psychotic syndromes similar in presentation to those seen in schizophrenia and the affective disorders do occur subsequent to brain injury (see Chapter 11, Psychotic Disorders, in this volume; see also Harrison et al.
However antibiotic h pylori buy trozocina paypal, despite anecdotal clinical experience in the psychopharmacological management of behavioral complications in neuropsychiatric settings infection 5 years before and after eyelid surgery cheap trozocina line, there remains a dearth of evidencebased data supporting the use of a particular antipsychotic medication or class antibiotics for chest acne generic trozocina 500mg line. Information largely comes from case reports and extrapolation from studies in other populations of patients with brain damage antibiotics for bladder infection nitrofurantoin purchase trozocina 500mg line. Given these caveats, many experts advise that neuroleptics should be used specifically for psychotic symptoms and not for agitation only. In light of this paucity of evidencebased data, the following general guidelines are offered. In general, care should be taken in administering neuroleptics, as animal studies suggest that dopamine antagonists (antipsychotic medications) can impede recovery after brain injury (Feeney et al. Problems with motor function, gait, arousal, and speed of information processing are common in brain-injured patients and may be exacerbated by the sedation, psychomotor slowing, parkinsonism, and anticholinergic side effects of neuroleptics. The clinician must be wary of medications with significant sedative and anticholinergic properties. Therefore, among typical neuroleptics, high-potency antipsychotic medications such as haloperidol may produce fewer of these side effects than lowpotency antipsychotics such as chlorpromazine. McAllister (1998) suggested that augmenting the effects of one medication by using a second low-dose agent with a different method of action is a way to address the problem of sensitivity to side effects in these patients. Clozapine is a candidate for the treatment of posttraumatic psychosis in that it yields a low incidence of extrapyramidal symptoms and tardive dyskinesia. However, clozapine can lead to seizures and other adverse events, such as sedation and dizziness, for which brain-injured patients may have greater vulnerability. Additionally, there are risks of agranulocytosis (minimized with weekly blood draws), tachycardia, orthostatic hypotension, hypersalivation, and weight gain. There is a complex interrelationship in terms of vulnerability, causality, and pathophysiology between brain injury and posttraumatic psychosis. Diagnosis of posttraumatic psychosis-specifically the distinction between a primary psychotic disorder and one attributable to the preceding brain injury-is limited by methods for direct ascertainment of causality. The current diagnostic approach must include a careful and detailed history that takes into account premorbid history and risk factors along with clinical presentation and, to the extent possible, diagnostic studies. Subpopulations at particular risk for posttraumatic psychosis must be kept in mind. Current treatment of posttraumatic psychosis is largely based on anecdotal clinical observations and extrapolation from management of other neurological conditions, highlighting the need for randomized controlled studies in this area. However, clear distinction between these two diagnoses is often confounded by uncertainty in causality and temporal association. These include posttraumatic amnesia, posttraumatic mood disorders, and medication/drug intoxication or withdrawal. In general, neuroleptics should be used specifically for psychotic symptoms and not for agitation only. Whatever medication is chosen, dosing should be "low and slow," typically starting with one-third to one-half of the usual dose. New York, Oxford University Press, 1994 197 National Institutes of Health Consensus Development Panel on Rehabilitation of Persons With Traumatic Brain Injury: Consensus conference: rehabilitation of persons with traumatic brain injury. Considerable attention and ongoing research investigations are focused in this area. The majority of individuals who experience a mild brain injury will experience transient symptoms such as mental confusion, headache, fatigue, and dizziness. Typically, these symptoms gradually remit over the course of a few seconds to minutes in the mildest cases and up to a few months in the most serious of mild injuries. However, other factors may cause a deviation from this typical uncomplicated course of recovery. Symptoms included in this syndrome occur in the areas of physical, cognitive, and emotional functioning. Both the circumstances at the specific time of the injury and general environmental factors in the deployed setting are potentially influential in the recovery process (see Chapter 26, Traumatic Brain Injury in the Context of War).
Mendez (1995) found that amateur versus professional status of the participant accounted for the largest amount of variance in cognitive functioning antimicrobial essential oils order trozocina cheap, with greater negative impact on professionals bacteria 4 buy generic trozocina 250 mg on line, particularly when professionals had neuroimaging evidence of neurological injury antimicrobial activity of xanthium strumarium trozocina 100 mg visa. Amateur boxers antibiotics for acne problems generic trozocina 500mg overnight delivery, in contrast, demonstrated neuropsychological functioning similar to that of other amateur athletes. A review article examining amateur boxers (Butler 1994) also indicated no consistent evidence of neuropsychological deficiency apart from decreased, though not impaired, nondominant-hand fine motor coordination, which may reflect mild peripheral nerve damage rather than central nervous system injury. The authors noted that only a few of the boxers demonstrated severe neuropsychological impairment. Other researchers investigated the relationship between neuropsychological testing and functional neuroimaging in amateur boxers (Kemp et al. Potential selection bias and the lack of appropriate comparison control groups are issues in boxing research. As recently as the mid-1980s, it was commonly believed that neurological and neurocognitive deficits in boxers were artifacts of prior substance abuse, poor education, and poor training (American Medical Association Council on Scientific Affairs 1983). The authors found abnormalities on at least two of the assessments for the majority of boxers. The 430 Textbook of Traumatic Brain Injury active players in their 20s and 30s collected during a relatively brief span of 6 years. In support of this position, a large-scale study of collegiate football players found that a history of previous concussions was associated with slower recovery of neurological function (Guskiewicz et al. Notably, this study also found a threefold greater risk of future concussions for players with a past history of three concussions versus those with no concussion history, which may be indicative of increased vulnerability following recurrent injuries. In terms of the association between concussion history and risk of developing long-term neurocognitive impairment, a study of retired professional football players found that those with three or more reported concussions had a fivefold prevalence of having a diagnosis of mild cognitive impairment and threefold prevalence of self-reported significant memory problems as compared with retirees reporting no significant concussion history (Guskiewicz et al. Multiple studies have indicated that the rate of concussion in football is as high as 5% of all acquired injuries (DeLee and Farney 1992; Karpakka 1993), and it is often the case that football players receive "dings" or "see stars" only to have the symptoms ignored or minimized to facilitate return to play (Magnes 1990). Results showed that concussed players had mild neurocognitive deficits or failed to show expected practice effects on cognitive testing compared with control subjects, primarily on measures of sustained attention and visuomotor speed. Preseason neuropsychological assessment and subsequent postinjury evaluation of participants, including 4 players with documented concussions, revealed sub-baseline performance on measures of information processing speed and verbal fluency, as well as a lack of expected improvement from practice effects. Further, the authors cited prior research that found no higher frequency of cognitive or memory impairment among players reporting three or more concussions as compared with players who had two or fewer (Pellman et al. Studies of brain injury risk in soccer have been complicated by questions of head injury from heading the ball, and findings have been mixed in this area (Putukian et al. Current consensus is that there are insufficient published data to support recommendations against the allowance of heading the ball or mandating the use of protective headgear for soccer players (Guskiewicz et al. Head injuries in soccer are most frequently the result of head-to-head, head-to-ground, and elbow-to-head contact (Andersen et al. Another study using neuroimaging found cerebral atrophy in one-third of a sample of retired soccer players, and approximately 80% demonstrated deficient performance on measures of attention, concentration, memory, and judgment in comparison with age-matched control subjects (Sortland and Tysvaer 1989). These early findings were not consistently replicated in subsequent research (Haglund and Eriksson 1993). More recent investigations found no evidence of impaired neurocognitive functioning among collegiate soccer players as compared with nonsoccer athletes and student nonathletes (Guskiewicz et al. These findings retained significance after correcting for education, concussions unrelated to soccer, number of treatments with general anesthesia, and alcohol use. Potential factors that might account for the variability of findings are differences in inclusion criteria from study to study, a reduction over time in the composition and make of soccer balls (in relation to ball-to-head injury) reducing potential mass on impact (Jordan et al. Failures to account for preexisting learning disorders and non-soccerrelated concussion are other potential sources of confound. Differences between early and more recent research may also be related to gradual improvement in measuring concussion history. Cantu grading: severity of concussion Grade 1 (mild) 2 (moderate) 3 (severe) Loss of consciousness None <5 minutes 5 minutes Duration of posttraumatic amnesia <30 minutes or 30 minutes but <24 hours or 24 hours Source. Although well over 20 other systems exist for grading concussion severity, the Cantu and American Academy of Neurology practice parameters severity scales have been among the most widely used. The cumulative aspects of multiple concussions have also been considered in classification and management. Overall, despite the fact that some systems are encountered more frequently than others in practice, there does not seem to be a single overall concussion classification system used in the management of sport-related head injury. American Academy of Neurology practice parameters for concussion severity Grade 1 (mild) 2 (moderate) 3 (severe) Symptoms Transient confusion; symptoms or mental status abnormalities on examination resolve in <15 minutes Transient confusion; symptoms or mental status abnormalities on examination last >15 minutes - Loss of consciousness None None Any loss of consciousness, either brief (seconds) or prolonged (minutes) Source. Cantu guidelines for return to play after concussion Grade 1 (mild) First concussion Return to play if asymptomatic for 1 week Return to play after asymptomatic for 1 week Minimum 1 month out; may return to play if asymptomatic for 1 week Second concussion Return to play in 2 weeks if asymptomatic at that time for 1 week Minimum 1 month out; may return to play if asymptomatic for 1 week; consider terminating season Terminate season; may return to play next season if asymptomatic Third concussion Terminate season; may return to play next season if asymptomatic Terminate season; may return to play next season if asymptomatic 2 (moderate) 3 (severe) Note. Asymptomatic means no headache, dizziness, or impaired orientation, concentration, or memory during rest or exertion. Sideline Assessment In addition to the player, personnel such as team physicians, teammates, athletic trainers, and coaches play a role in observing and identifying when a possible concussive event has occurred. Once identified, the player should receive a sideline assessment involving both gross neurological assessment and brief neurocognitive screening. Verification of a concussion using sideline assessment should lead to removal of the athlete from competition and instigation of return-to-play criteria, which may involve additional brief or more comprehensive neuropsychological assessment. The 2008 Zurich statement also includes a copy of the updated Sport Concussion Assessment Tool, which combines key elements of multiple concussion measures (Maddocks et al. Individual differences or vulnerabilities are likely an important moderating factor in such cases, including a history of learning disabilities, attention deficit disorders, or previous head injuries. No athlete should be returned to play under any circumstances if he or she reports current neurological or postconcussive symptoms.
Despite these pre~autions antibiotic resistance of bacteria order genuine trozocina on line, painful instability of the distal ulnar stump can occur 600 mg antibiotic buy generic trozocina 250mg line. The caput ulnae syndrome in rheumatoid arthritis: a study of the morphology antibiotic chart cheap trozocina 250mg with visa, abnormal anatomy and clinical picture infection fighting foods generic 500 mg trozocina with visa. The SauvC-Kapandji procedure for posttraumatic disorders of the distal radio-ulnar joint. Kapandji-Sauve procedure fur chronic disorders of the distal radioulnar joint with special regard to the long-term results. Amount of ulnar resection is a predictive factor for ulnar instability problems after the SauveKapandji procedure: a retrospective study of 44 patients followed fur 1-13 years. The SauvC-Kapandji procedure for posttraumatic wrist disorders: further experience. Modified SauvC-Kapandji procedure for disorders of the distal radioulnar joint in patients with rheumatoid arthritis. Fujita S, Masada I<, Takeuchi E, et al Modified Sauve-Kapandji procedure for disorders of the distal radioulnar joint in patients with rheumatoid arthritis. A soft tissue tube should surround the pseudarthrosis site to connect and stabilize the proximal and distal ulnar segments. Tlu: SauvC-Kapandji procedure for posttraumatic disorders of the distal radioulnar joint. Modification of the SauvC-Kapandji procedure with exrensor carpi ulnaris renodesis. Functional ouocome of en bloc excision and osreoarticular allograft replacement with the SauveKapandji procedure for Campanacci grade 3 giant-cell tumor of the distal radius. The SauvC-Kapandji procedure for reconstruction of the rheumatoid distal radioulnar joint. Closed rupture of a finger exrensor following the SauvC-Kapandji procedure: a case report. Chapter 93 f Ulnar Head Implant Arthroplasty -t-~ Cari Cordell and Randy R. When the distal ulna has been res~ted and the forearm is rotated under such a compressive load. These patients present with pain on stress loading of the upper extremity, weakness in grip strength, decreased forearm rotation, and difficulty with lifting. The first prosthesis used was a silicone cap designed to provide a soft end to the ulnar stump. Newer designs aim to restore the ulnar head using a metallic prosthesis to articulate with the sigmoid notch. The forearm rests on the x-ray cassette and the radiograph is then taken with the beam aligned in the coronal plane, creating a posteroanterior view of the neutral forearm. This procedure is indicated when the disease process, typically arthritis, is limited to the distal ulnar articular surface. Contraindication& include instability of the distal ulna, excessive ulnar positive variance, and degeneration at the sigmoid notch. The articulating two-piece prosthesis has the theoretical advantage of less radius erosion from articulation with the pyrocarbon head. When implanted, the prosthesis preserves the ulnar styloid and attachment of the triangular fibrocartilage complex (fight). With mild instability, repair of the soft tissue envelope is adequate to restore stability. An eccentric-shaped metallic head has been designed to more closely approximate the shape of the normal head. However, biomechanical studies have demonstrated normal tracking patterns of the distal ulna around the radius, closely simulating the normal joint, even with the use of spherical heads. An adequate soft tissue envelope is essential to prevent subluxation of a complete ulnar head replacement. Thus, an essential part of the surgical technique is reconstructing the capsuloligamentous envelope surrounding the ulnar prosthesis. Other contraindication& include previous open fracture, infection in or around the joint, skeletal immaturity, and known sensitivity to the implant materials. The radial component consists of a plate with a polyethylene-lined metal sphere affixed to the interosseous surface of the radius. The ulnar stem has a protruding peg that is captured and rotates within the polyethylene liner. The components include (a) radial plate with socket, (b) polyethylene ball, (c) hemi-socket with screws, and (d) ulnar stem with peg. Divide the extensor retinaculum over the fourth compartment and reflect it ulnarly. Retract the two slips of the extensor digiti minimi tendon and elevate a large ulnar-based triquetra! Resect the articular portion of the ulnar head using a customized jig specific to the implant system to be used. Ream the ulnar medullary canal and place a trial prosthesis of the appropriate size. Obtain intraoperative radiographs to confirm correct sizing of head and ulnar variance. Obtain intraoperative radiographs to evaluate the size of the ulnar head and the ulnar variance. Remove the trial implant by gently applying anteriorly directed pressure on the distal ulna to dislodge the ulnar head from the sigmoid notch.
In its narrowest sense antibiotic resistance agriculture buy 100mg trozocina fast delivery, psychosis is currently defined as the presence of delusions or hallucinations infection rate order 500 mg trozocina free shipping, without insight that the hallucinations are pathological in nature infection en la garganta cheap trozocina 100mg mastercard. This definition of psychosis is used for psychosis due to a general medical condition virus 68 california purchase trozocina 250mg overnight delivery. A broader sense of psychosis is drawn from the positive symptoms of schizophrenia, which extend beyond delusions and hallucinations to encompass disorganized speech and grossly disorganized or catatonic behavior. The conundrum in the diagnosis of posttraumatic psychosis is the ability to distinguish between a primary psychotic disorder and a psychotic disorder that is caused by a prior brain injury. This distinction is further complicated by emerging data suggesting complex interactions between brain injury and risk for development of schizophrenia. On the basis of a review of literature from 1978 to 2006, the American Neuropsychiatric Association concluded that "the issue of a temporal versus causal relationship [for posttraumatic psychosis] is not possible to resolve in the absence of a clearer understanding of the pathophysiological mechanism underlying posttraumatic psychosis and a reliable means of distinguishing this process from that underlying idiopathic psychosis" (Kim et al. Nonetheless, there is evidence that posttraumatic psychosis frequently resembles a primary mental disorder, such as schizophrenia, and in those instances may be better accounted for by a primary psychotic disorder. Third, schizophrenia and other primary psychotic disorders are complex heterogeneous illnesses that arise from the interaction of multiple etiologies, including genes, obstetric complications, and other exposures. It is interesting that having relatives with schizophrenia increases Clinical Features Characteristic Presentation On the basis of an amalgamation of several reports including a review by Davison and Bagley (1969), Zhang and Sachdev (2003) suggested the following profile for individuals with posttraumatic psychosis. Patients with posttraumatic psychosis are typically young male (but see caveats above in discussion of gender as a risk factor); there are typically prodromal symptoms. In contrast, thought disorder and negative symptoms that are prototypical of schizophrenia are typically described as less common, if not entirely absent (Fujii and Ahmed 2001; Sachdev et al. For example, there are case reports of Lilliputian hallucinations (in which objects, people, or animals seem smaller than they would be in real life) occurring in individuals with previous brain trauma (Cohen et al. Cognition Elements of cognition are impaired in posttraumatic psychosis, but there is no clear consensus as to whether posttraumatic psychosis can be differentiated from primary psychotic disorders by the extent of impairment. In one sample of schizophrenia patients, those with a history of childhood brain trauma that required hospitalization had poorer scholastic performance as children (Gureje et al. Poor insight complicates compliance with treatment recommendations for both psychotic and brain-injured patients. A similar overlap between populations with psychosis and a history of brain injury is seen in the deficits on formal neuropsychological testing. Poor performance on tests of executive function is common in both brain-injured patients and patients with schizophrenia (reviewed in Johnson-Selfridge and Zalewski 2001). Both schizophrenia patients and braininjured patients also show deficits in explicit memory as well as decrements in volume of the hippocampus, the part of the brain thought to be responsible for explicit memory. Notably, in both groups of patients, the extent of memory deficit is associated with the degree of volume reduction of the hippocampus (Gur et al. Remarkably, these subjects were not selected for clinical evaluation because of any evident psychopathology but were chosen for neuropsychological testing in the hope of appealing for clemency when their executions were imminent. These death row inmates had repetitive episodes of brain trauma beginning in childhood that were quite dramatic, including severe physical abuse, falling from heights, getting hit by and run over by cars, and getting hit with baseball bats. Notably, reported rates of prior child abuse are 52% (20/38) of patients with first-episode psychosis (Greenfield et al. Family History/Genetic Vulnerability Early studies suggested that brain trauma could contribute to schizophrenia either directly or through an interaction with latent vulnerability and that these two pathways yielded different symptom patterns. For example, Shapiro (1939) evaluated 2,000 cases of dementia praecox (schizophrenia) in residents of a large public hospital and found that "a large number. In a reexamination of a database of 722 probands with schizophrenia, the diagnosis of schizophrenia was confirmed in a subsample of 660, and the prevalence of schizophrenia in the parents and siblings of these 660 probands was examined. It was found that the risk for schizophrenia was particularly low in siblings of probands whose onset of illness occurred within a year of major brain trauma (Kendler and Zerbin-Rudin 1996). Overall, the preponderance of brain injuries sustained in the Iraq/Afghanistan conflict are mild (Schwab et al. Given the large number of troops who serve in these present-day conflicts, clinicians will need to be increasingly aware of this potential risk factor as servicemen and servicewomen return to the civilian population. Studies have shown that homeless persons have an elevated prevalence of schizophrenia that ranges between 13. For example, studies of white matter using diffusion tensor imaging have implicated a relationship between white matter deficits and both positive (Skelly et al. It has been hypothesized that these abnormalities result from disruptions in connections between different parts of the brain and that the inability to filter out stimuli can lead to sensory flooding by irrelevant information. Common deficits in sensory gating may also implicate abnormal connectivity between various parts of the brain in both conditions. Primary Sites of Lesion Brain trauma frequently leads to injury of the frontal and temporal cortices. Psychosis resulting from other neurological conditions, such as metachromatic leukodystrophy and cerebrovascular disease, usually involves pathology in the frontal cortex and temporolimbic areas. In epilepsy, visual hallucinations have been found to result from seizure foci in the temporal lobes or orbitofrontal regions, and delusions of passivity ("Forces are acting upon me," "I am being controlled") have been linked to left temporal lobe seizure foci. Also, deficits in frontal lobe function are a widespread finding in schizophrenia; in particular, it has been hypothesized that attendant working memory deficits (holding on to information while attending to other tasks) may be a key pathophysiological feature of this disease. Clinical Evaluation A thorough assessment of the patient with posttraumatic psychosis is an essential prerequisite to the prescription of any treatment (Arciniegas et al. Premorbid history and current medication treatment are important because they can influence neuropsychiatric symptoms (Arciniegas et al. As noted earlier, there are important states to rule out, specifically delirium, before one makes a diagnosis of posttraumatic psychosis. It should be determined whether there are autonomic nervous system abnormalities, a waxing and waning mental status, or an inability to orient on mental status exam. If patients are delirious, medications should be carefully evaluated and serum levels obtained.
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