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Psychiatric disturbance and aphasia Benson and Geschwind (1971) and Benson (1973) summarise the common forms of reaction that may be seen in aphasic patients blood pressure 39 year old male furosemide 100mg overnight delivery. Indeed the absence of distress among such patients is usually indicative of widespread cerebral damage and consequent impairment of general intellectual ability blood pressure specialist order 100mg furosemide overnight delivery. Both frustration and depression are con- sidered to indicate a more favourable prognosis for recovery with therapy prehypertension fatigue buy furosemide 100mg without prescription, representing as they do an awareness of the speech difficulties arteria zygomaticoorbitalis discount furosemide 100 mg. On the other hand, angry negativism with hostile responses and refusal to participate in treament can sometimes emerge and seriously complicate rehabilitation. Such patients often act as though they believe their own speech to be normal and as though they feel that people around them fail to speak normally. Agitation and sometimes severe paranoid reactions may ensue, with suspicions that others are talking about them, plotting against them or deliberately using unintelligible jargon to prevent them from understanding. Aphasia is frequently followed by calamitous alterations in lifestyle and economic status, along with disruption of simple pleasures such as conversation, reading or watching television. Social and family status are often undermined, irrespective of the presence of other handicaps such as hemiparesis, likewise confidence in sexual functioning. The distinction between the language disorder seen in certain schizophrenic and manic patients and the phenomena of aphasia due to brain damage needs to be very carefully distinguished. This can only be done by careful attention to the form of language output and by comprehensive tests of language function. Linguists who have studied schizophrenic speech have reached different conclusions, some arguing for a distinct disorder of language and others that such speech can be classified within the standard aphasia rubric. In one study that used speech transcripts from patients with schizophrenic thought disorder and (mostly) fluent aphasias, clinicians were poor at distinguishing the two (Faber et al. Any sudden onset of speech disorder must therefore always dictate Neuropsychology in Relation to Psychiatry 57 caution, even in the established chronic schizophrenic patient. The length of verbal responses to openended questions was considerably shorter among the aphasics, and these did not show the bizarre reiterative themes frequently encountered among the schizophrenics. Vagueness of response arose from word-finding difficulties in the aphasic patients but was apparently attributable to shifts of attention in the schizophrenics. In a recent and fine-grained application of an aphasiological approach to schizophrenic thought disorder, Oh et al. They found that some of the abnormalities observed in the speech of patients with schizophrenia, including syntactic errors, may be accounted for by their general cognitive impairment. This implies that deficits in attention and concentration or working memory are at the root of such problems and that higher-level problems of discourse planning reflect problems with planning generally. Of particular interest was the finding that the thought-disordered group, even those with preserved cognitive functioning, showed most impairment at the level of semantics in their expressive speech. This was in contrast to high levels of visual confrontation naming and ability to comprehend complex material, for example `. Attempts to recount fairy tales elicited disorganised and tangential speech that lacked a global semantic structure, presumably because of the open-ended, unconstrained nature of these tasks. In line with the main locus of impairment as being at the semantic level, Rodriguez-Ferrera et al. They were less sensitive to linguistic (syntactic, semantic and pragmatic) violations because they were apparently unable to use linguistic context to form an overall semantic representation needed to process speech online. Reduced or slowed speech may reflect depressed mood and psychomotor retardation generally, as well as part of the negative schizophrenia syndrome. Parkinsonism, either idiopathic or secondary to antipsychotic medication, may cause a similar clinical picture. Again, one might argue whether poverty of speech is truly a language disorder or a higher-level problem of initiation and planning. The verbal fluency test may be used to quantify reduced speech in terms of a psychometric deficit. The patient can be asked to generate as many words as possible in a minute beginning with a given letter (F, A or S). This can be contrasted with semantic fluency in which the patient is asked to produce as many words as possible from a given category. Conversion disorders It is only on rare occasions that difficulty arises in distinguishing between psychogenic and organic disturbances of language function.

The ratio of N-acetylaspartate to creatine blood pressure medication isn't working purchase 40 mg furosemide mastercard, which is indicative of neuronal arrhythmia normal buy cheap furosemide 40 mg on-line, not axonal prehypertension and chronic kidney disease purchase furosemide 40 mg with amex, health pulse pressure endocarditis purchase furosemide 100 mg free shipping, did not differ between groups. This suggests that solvent exposure leads to changes in cerebral white matter and not gray matter, at least in the regions studied by these authors. No measures of cognitive function were administered and while each subject underwent a psychiatric examination, no objective measures of behavior or emotional status were reported. We have also published a study that highlights changes in cerebral white matter in workers with a history of exposure to solvents [18]. Thirty-one railroad workers with at least 10 years of exposure to solvents were compared to 31 age-, education-, and intelligence-matched healthy control subjects. The volume of the corpus callosum was smaller in the railroad workers, and this was not a product of health status or psychiatric symptoms. The area of difference was restricted to the genu of the corpus callosum and not the body or the splenium. In addition, smaller corpus callosum volume was associated with a greater degree of exposure to solvents. Finally, the volume of corpus callosum correlated with cognitive measures of frontal lobe function, such that smaller volume of the genu was associated with worse performance. This is consistent with the hypothesis that solvents selectively affect cerebral white matter due to their lipophilic nature. However, this does not rule out changes in gray matter following solvent exposure as this has not been well studied to date. For example, there have been no imaging studies to date reporting solventrelated changes in the hippocampus. In fact, one might hypothesize that the changes in white matter will lead to gray matter degeneration, but this remains to be empirically tested. One could also argue that gray matter changes have led to the degradation of the white matter. Consistent with the hypothesis that solvents affect frontal lobe functions, there is one small pilot functional imaging study that demonstrated differences in frontal lobe activation during working memory [25]. Specifically, on two different tasks of working memory, six individuals with a history of solvent exposure were studied with O15 water positron-emission tomography. Although they performed the tasks at the same level as controls, exposed subjects activated different areas in the frontal cortex on both tasks. The findings were interpreted as indicating that since the frontal cortex was dysfunctional, solvent-exposed subjects had to compensate by recruiting additional cortex to complete the working memory tasks. However, the findings from these studies should be considered preliminary and replication with different solvent-exposed 482 M. This is highlighted by a recent study that used a combination of imaging modalities to examine the effects of solvent exposure [26]. White matter differences were not found, but there were methodological differences compared to previous studies. This points to the need for more study on the neuroanatomical substrates of solvent-related cognitive changes. In summary, exposure to organic solvents can lead to changes in cognition and result in depression and anxiety. These symptoms are not experienced by all who are exposed and symptoms can remit for some if exposure is terminated. However, some individuals will experience permanent deficits, which may be exacerbated by age. There is emerging evidence from neuroimaging that solvents affect the white matter of the brain and that the frontal lobes may be particularly affected. In addition, the cognitive deficits associated with solvent exposure may have a primary frontal focus. However, further research is needed to replicate, clarify, and extend these findings. Lead accumulates in soft bone, and thus previous cumulative exposure can be determined from bone studies with some reliability. Symptoms can also be acute or chronic, including neurological symptoms such as ataxia and peripheral neuropathy.

Resolution of confusion blood pressure of 150/90 purchase furosemide 40 mg otc, drowsiness hypertension lifestyle modification 40 mg furosemide with amex, apathy and even coma have followed lowering of intracranial pressure blood pressure medication can you stop generic furosemide 40 mg on-line, either by decompression or dexamethasone blood pressure chart based on height and weight discount 40 mg furosemide free shipping. After long-continued elevation of pressure there may be extensive parenchymal damage resulting from such factors, and the mental impairments will then remain even after the pressure is lowered. Focal effects in the region of the tumour may also be aggravated by increased pressure, as seen for example when dysphasic symptoms recede as the pressure is lowered. Even when intracranial pressure is not raised, there are likely to be other important factors at work leading to the appearance of mental symptoms. Of these, localised cerebral oedema in the neighbourhood of the tumour is clearly of special importance. Psychiatric sequelae of meningiomas were found to correlate with the extent of peritumoral oedema rather than the size of the tumour itself (Lampl et al. The pathophysiological mechanism implicated in the appearance of psychiatric symptoms in the context of cerebral oedema could be attributed to the disruption of intracerebral pathways rather than the single pressure effect per se. Psychotic symptoms Hallucinations may occur in any modality, commonly as part of an epileptic disturbance but also without evidence of paroxysmal activity. Occipital tumours are associated with simple visual hallucinations; temporal lobe tumours with more complex formed visual and auditory hallucinations, also gustatory and olfactory hallucinations; and parietal lobe tumours with localised tactile and kinaesthetic hallucinations. Circumscribed frontal lobe tumours may sometimes produce visual, auditory or even gustatory hallucinations, presumably through effects on the neighbouring temporal lobe. Medial frontal lesions can also discharge directly to the temporal lobe and produce hallucinations and other phenomena by this means. Peduncular hallucinosis caused by brainstem compression has been described in a variety of posterior fossa tumours (Roser et al. Visual perseveration (palinopsia) and auditory perseveration (palinacousis) in the context of ictal activity have been reported in a patient with a left temporoparietal astrocytoma (Auzou et al. Any form of delusional illness may accompany cerebral tumour, either early or late in its evolution. Depressive, Nature of the tumour It seems likely that the rapidity of growth of a tumour is one of the most important factors determining the incidence and 286 Chapter 5 Location of the tumour the importance of tumour location in relation to mental symptoms has been much debated. Many observations concerning special regional effects can be offset by negative findings. Bleuler (1951), reviewing 600 unselected tumours from the Zurich neurosurgical clinic, suggested that the psychopathological picture was in fact very uniform; 83% of his patients showed mental symptoms, but there were no significant differences according to the site of the tumour. The latter embraced more than memory defects alone, also including widespread cognitive disturbances, emotional instability and impairment of personality. However, it seems likely that local effects may be seen, for example focal cognitive deficits with parietal tumours and focal amnesic syndromes with diencephalic tumours. When considering more than such relatively elementary symptoms, it becomes harder to demonstrate the role of focal cerebral disorder in the pictures that result. Thus disturbances of affect and personality cannot be tied convincingly to tumours in specific parts of the brain, and psychotic illness appears to be largely determined by other factors. Frontal and temporal lobe tumours show a somewhat higher frequency of mental disturbances than do tumours of the parietal or occipital lobes (Keschner et al. The observation that symptoms were more frequent with malignant tumours than benign (Busch 1940) may be explained by rate of tumour growth. This might also be one of the reasons why gliomas have repeatedly been found to produce a higher incidence of mental disturbance than meningiomas. Metastatic tumours with several deposits scattered throughout the brain have proven to be associated with a larger prevalence of mental disturbance than any variety of primary intracerebral tumour (Keschner et al. Frontal lobe tumours Frontal lobe tumours are notorious for their ability to present under guises that may lead to the mistaken diagnosis of a primary dementing illness. This is partly due to the paucity of striking neurological signs accompanying frontal lesions, and partly to the frequency with which mental disturbances appear from an early stage. When considering the effects of frontal lobe tumours it is useful to remember the clinical syndromes that may be observed following orbitofrontal lesions compared with lesions affecting dorsolateral prefrontal lobe or anterior cingulate (Cummings 1993). Sachs (1950), in a large series of patients with meningiomas, found eight who presented with dementia before any symptoms indicative of tumour had appeared, and in six the tumours were frontal in location.

The Parkinson Study Group (1999) and the French Clozapine Parkinson Study Group (1999) performed randomised controlled trials which showed that clozapine was safe and effective at doses very much smaller than those used in the treatment of schizophrenia blood pressure chart jnc generic 100mg furosemide mastercard. The drawback in using clozapine is the risk of agranulocytosis blood pressure 3rd trimester discount 40mg furosemide mastercard, necessitating frequent blood tests hypertension pamphlet order furosemide 100 mg overnight delivery. There is a single case report of clozapineinduced aplastic anaemia in a psychotic parkinsonian patient (Ziegenbein et al hypertension blurred vision generic furosemide 100 mg free shipping. In a small case series performed by Bergman and Lerner (2002) it appeared safe and effective, although Cummings (2000) has observed worsening of parkinsonian motor signs in dementia with Lewy bodies. The drug was relatively well tolerated, although nausea was a dose-limiting side effect. Closely associated is the proposition that psychological influences may be important in the development of the disorder. None of the observations in this area can be regarded as well founded, but neither can it be said that they have been decisively disproved. Sands (1942) and Booth (1948) championed the view that persons of a particular psychological make-up were at special risk of developing the disorder. Premorbid histories showed the patients to have been exemplary citizens, successful in their undertakings and externally calm, undemonstrative and stable. Close acquaintance, however, revealed a subjective state of tension that was suppressed and concealed from outsiders. With the development of parkinsonism a decompensation could often be observed, exposing the inner turmoil in the form of complaints, demands and self-centred behaviour. Sands suggested that the habitual suppression of emotion, doubtless involving intense physiological activity in many parts of the brain, may have led in some way to the degenerative changes responsible for the disease. Booth (1948) developed such concepts further in a clinical study of 66 patients supplemented with Rorschach protocols. He concluded that the personality structure had been more decisive for the development of parkinsonism than the immediately obvious pathogenic mechanism; the latter had merely served to precipitate or actualise the disorder. Features stressed by Booth included a habitual impulse to action and a striving for success, independence and authority. Tension was prone to arise between this and the equally strong drive towards social conformity. Regarding their success in life, he found this to be usually the result neither of great intelligence nor of unusual vitality, but attributable to aggressive perseverance and Movement Disorders 771 instinctive social conformity. An externally virtuous and docile disposition concealed hostile and sadistic impulses of unusual strength. Such a character structure would be vulnerable to frustration in a number of ways. Booth saw the major symptoms of parkinsonism as reflecting the original personality and its conflicts, rigidity for example being the product of a balance between overcoming obstacles and submission to restrictive influences, and the parkinsonian posture being related to unconscious hostility. Psychotherapy, in conjunction with antiparkinsonian medication, was claimed to meet with success in alleviating the symptoms. Smythies (1967) compared 40 consecutive patients referred for surgery with control groups on a questionnaire relating to childhood disturbance, premorbid neurotic symptoms and life adjustment. No excess of premorbid emotional disability could be discerned, and no unusual difficulties in life adjustment antedating the illness. However, Pollock and Hornabrook (1966) were impressed with the high proportion of teetotallers among their large unselected series of parkinsonian patients, and found that many lacked hobbies and showed narrow intellectual horizons. Both patient groups were significantly more likely to be introverted, rigid, pedantic and selfreproachful than the controls, confirming previous impressions of personality. However, the similarity between the parkinsonian and tremor patients suggested that such traits were merely the product of chronic disability. The affected members tended to describe themselves as more nervous, quiet, serious and introspective, whereas their co-twins were more outgoing and lighthearted. These differences in personality sometimes dated well back into adolescence and early adult life. It seemed possible therefore that neuro- chemical differences between the twins might have existed from early in their lives, or that there had been some error of fetal development in the member destined for the disease. The only possible association that has emerged is that affected twins have smoked less often and less heavily than their co-twins (Ward et al.

Apart from slight effacement of the cerebral sulci blood pressure monitor amazon cheap furosemide 100 mg amex, there is little distortion of the brain architecture heart attack during sex 40mg furosemide fast delivery. A man of 64 had a 4-week history of behaving strangely at work blood pressure rates chart order furosemide 100mg online, seeming oblivious of questions and unable to focus his attention hypertension thyroid furosemide 40 mg visa. At home, he would sit in the same place for hours at a time, once wound a clock for 3 hours on end, and once lathered his face for 2 hours. He sat staring ahead oblivious of his surroundings, or with his eyes closed picking aimlessly at the bed clothes. He proved to have a glioblastoma practically confined to the genu of the corpus callosum (Alpers 1936). Early on there are subtle cognitive and emotional changes, which are then followed by deficits in sustained attention, memory retrieval, visuospatial skills and frontal lobe function but with sparing of language for example. Personality changes may also be an early feature, similar in all respects to those seen with frontal lobe tumours. In his comprehensive review, Elliott (1969) suggests that the combination of delusions and stupor can come to resemble schizophrenia closely. A large part of the mental disturbance is probably due to the tendency for tumours of the corpus callosum to involve adjacent structures. Almost all involve the third ventricle and diencephalon at some stage, which presumably accounts for the somnolence, akinesis and stupor which ultimately appear. In part this may be ascribed to the paroxysmal phenomena occasioned by temporal lobe epilepsy. Apart from features particular to temporal lobe epilepsy, there does not seem to be any form of mental disturbance specific enough to be of localising value. Non-dominant temporal lobe tumours can be clinically silent until they are very large, whereas tumours on the dominant side tend to produce the greater cognitive 290 Chapter 5 disturbances in both verbal and non-verbal functions (Bingley 1958). Often the symptoms of temporal lobe tumours are akin to those of frontal lobe tumours, for example slowing and aspontaneity of speech and movement are seen in both. Memory disturbances may likewise feature prominently, including occasional cases that present with a florid Korsakoff syndrome or pure amnesia (Umemura et al. Impairment of semantic memory with preservation of autobiographical memory has been reported in a meningioma. Axial T2 image shows an extensive area of T2 hyperintensity in the right temporal lobe. Paroxysms of anxiety or anger have been described, and occasional cases have presented with mania or hypomania. Exacerbation of mania, previously stabilised pharmacologically, has been described in a patient with a right temporal lobe astrocytoma (Sokolski & Denson 2003). In their review, Gupta and Kumar (2004) reported personality changes with left frontal and left temporal meningiomas. However, there does not appear to be a form of personality change specific for temporal lobe tumours. A change towards facetiousness, foolish joking and childish behaviour may be indistinguishable from that seen in frontal lesions, and has been reported to be just as common. Strobos (1953) observed marked personality alterations in 7 of 62 patients with temporal lobe tumours, including psychopathic and paranoid trends, hypochondriasis and extreme irritability. Occasionally, patients with temporal lobe tumours develop psychotic illnesses resembling schizophrenia, which may be the initial manifestation. Such cases are rare, but were drawn together in a review of the literature by Davison and Bagley (1969). There was insufficient information to indicate whether such patients had been genetically predisposed to schizophrenia, or whether temporal lobe pathology might have played a more direct aetiological role. Some isolated clinical examples rather strongly suggest that the temporal lobe pathology may itself be responsible: see following case vignettes. Cerebral Tumours 291 A 53-year-old woman with a previous sociable and outgoing personality was admitted to hospital after attacking her husband with a knife. She felt persecuted by her family, believing that they were attempting to harm her and that her son was turned into a dog. On examination, her speech was incoherent and she displayed bizarre facial mannerisms and sudden unpredictable behaviour.

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