Background {#Sec1}
==========

This review, written for the psychiatrist as much as for the malariologist, serves as an introduction to what by modern perspectives may be viewed as surprising areas of common interest. The disciplines of psychiatry and malariology were united briefly in the early to mid twentieth century in the historical practice of malariotherapy, in which patients were intentionally inoculated with malaria for its presumed therapeutic neuropsychiatric effects. Although this practice has long fallen out of favour and although the two disciplines have subsequently diverged, insights from malariotherapy and more broadly the field of malariology have continued to make important contributions to psychiatry in the modern era.

Untreated or delayed treatment of malignant *Plasmodium falciparum* malaria infection may result in coma. This cerebral complication of malaria is implicated particularly with lasting cognitive deficits that owing to the high prevalence of disease worldwide may contribute significantly to the global burden of psychiatric morbidity \[[@CR1]\]. Yet similarly, anti-malarial drugs, particularly of the quinine-like class of quinolines commonly used in treatment and prevention of disease, are also increasingly recognized to exert potentially chronic psychiatric adverse effects that may also contribute to this global burden of morbidity \[[@CR2]\].

This review, inspired by an earlier seminal work \[[@CR3]\], synthesizes over a century of critical literature from psychiatry and malariology---ranging from anecdotal historical observations to evidence from modern randomized controlled trials---to explore the evolving understanding of the psychiatric effects of malaria and of anti-malarial drugs. In this review, the evolution of psychiatric effects attributed to malaria is described, from the historical perspective in which a broad range of symptoms were attributed to the disease, to the current understanding of the more limited psychiatric effects of cerebral malaria (CM) and post-malaria syndromes. Next, malariotherapy and its historical role in psychiatry are described. Lastly, the psychiatric effects of anti-malarial drugs, particularly of the quinoline class, are reviewed, including a discussion regarding the potential confounding effect that these may have had on symptoms historically associated with malaria.

Psychiatric effects of malaria {#Sec2}
------------------------------

Although early descriptions of the psychiatric effects of malaria first appeared in the ancient medical literature of Hippocrates and Galen \[[@CR4], [@CR5]\], it was only many centuries later that descriptions of these effects became relatively common. Such descriptions grew particularly detailed in the aftermath of World War I (WWI), where malaria, epidemic on the Macedonian front between 1916 and 1918, was unexpectedly found to be the leading cause of psychiatric disorders among soldiers of the Allied powers fighting there \[[@CR6]\].

Detailed reports in the literature from this era described a seemingly bewildering set of psychiatric effects attributed to both severe and mild forms of the disease. Early reports had described dreamlike states \[[@CR7]\], anterograde amnesia, difficulties with concentration, disorientation, and forgetfulness \[[@CR8]\], confusional psychosis, dementia, "melancholia", and mania \[[@CR9]\] emerging in patients recovering from severe malaria. During this era, mild chronic or intermittent malaria infection had also become associated with symptoms of "neurasthenia", including depression, irritability, anxiety, and insomnia \[[@CR10]\]. In subsequent years, even more severe symptoms such as confusion \[[@CR11]\], intermittent psychoses, and delirium were also commonly attributed to those with mild forms of malaria \[[@CR12]\].

This literature even warned of the potential for missed diagnoses of malaria prior to the onset of malarial fever among psychiatric patients admitted for care and thought to be suffering from delirium and psychoses \[[@CR13]\]. Many such patients were diagnosed with malaria only some time later at the onset of fever, or when their symptoms progressed to coma. These reports described a common prodrome of hallucinations, anxiety, crying, violence, agitation, and a dreamy and confusional state \[[@CR13]\].

So common and diverse became the psychiatric effects attributed to both severe and mild forms of malaria during the post-WWI era, that an entire textbook, well received by psychiatrists at the time \[[@CR14]\], was published with chapters featuring case reports of malarial psychoses, "dementia praecox", confusional and delusional insanity, mania, "melancholia", delirium, and dementia attributable to the disease. As noted by the author in his preface, "very few known syndromes are absent from the list apparently arising from malarial infection" \[[@CR15]\].

By World War II (WWII), growing US and allied military experience, particularly in the South Pacific, had identified similar psychiatric effects associated with malaria. Reports from US military clinicians noted a characteristically confusional form of psychosis, as well as persecutory, grandiose, bizarre delusions, and symptoms of anxiety, depression, and mania associated with both severe and mild forms of the disease \[[@CR16], [@CR17]\]. Yet others had begun to challenge the true association of many of these symptoms with malaria, noting "too great a tendency to blame malaria for many of these symptoms" \[[@CR16]\], with the temporal association of certain of these symptoms suggesting to other authors a toxic process \[[@CR16]\].

Despite such growing suspicions, the psychiatric effects of malaria were still considered "more common than are generally known" \[[@CR4]\], and a military journal editorial noted that malaria should be considered "associated with protean mental states" \[[@CR18]\]. Psychiatric symptoms also remained clearly associated in the literature of the era with even the mild chronic and relapsing forms of disease, with a case report describing psychosis developing weeks prior to the onset of fevers from the generally benign *Plasmodium vivax* malaria \[[@CR17]\].

Reports from among soldiers of the Vietnam War era similarly described mostly transient cases of psychosis, and impaired memory and concentration generally following admission for treatment for malaria \[[@CR19]\], often lagging admission by some days, and typically without evidence of such symptoms while previously febrile \[[@CR20]\]. Neuropsychological testing of certain of these patients both soon after their acute illness and following their recovery identified common patterns of deficits, particularly in tests of recent memory, visual organization, psychomotor speed, and visual motor integration \[[@CR21], [@CR22]\]. Decades later, follow-up of malaria patients from the Vietnam War demonstrated lasting changes in personality, depression, and symptoms of partial seizure \[[@CR23]\], as well as deficits on tests of memory, and other evidence of chronic cognitive dysfunction on neuropsychological testing \[[@CR24]\].

In more recent studies of broadly defined malaria infections, acute malaria among children \[[@CR25]\], and multiple recurrent malaria infections have been associated with adverse effects on short-term cognitive performance \[[@CR26]\]. Similarly, in recent reviews, among chronic psychiatric effects, the most common and strongest evidence exists for a risk of chronic cognitive impairment following successful malaria treatment \[[@CR27]--[@CR30]\]. Additional retrospective studies have attributed a risk of subclinical depressive and anxiety symptoms \[[@CR31]\], as well as altered executive functioning \[[@CR32]\], particularly following severe malaria infection.

Cerebral malaria {#Sec3}
----------------

Unlike past usage of the term, which had been significantly broader in scope \[[@CR33]\], and had included presentations that had involved organic mental syndrome and even acute personality change \[[@CR21]\], the modern strict definition of CM has gradually evolved to require alterations in consciousness for diagnosis \[[@CR34], [@CR35]\]. This modern definition of CM, which was developed for research purposes \[[@CR36]\], and which is considered a diagnosis of exclusion \[[@CR37]\], specifically limits use of the term to a patient with coma occurring in the presence of malignant *P. falciparum* malaria parasitaemia \[[@CR38]\]. The strong and highly sensitive and specific association of such clinically-defined CM with objective signs, including malaria retinopathy, has significantly improved diagnostic reliability \[[@CR39], [@CR40]\], particularly among children in tropical countries who are primarily affected by the disorder.

Unlike historical definitions, the modern definition of CM is primarily described as an acute neurological disorder and is notably less associated in the literature with acute psychiatric symptoms \[[@CR33], [@CR41]\]. Some authors have questioned its acute association with psychosis \[[@CR42]\], although early case reports \[[@CR43]\] and reviews \[[@CR44]\] through the 1990s continued to describe self-limiting acute psychosis occurring following treatment for CM.

Prospective follow-up of patients specifically with CM are limited, but small studies of children find increased risk of cognitive deficit \[[@CR45]\] lasting through 2 years of follow-up \[[@CR46]\]. In children surviving CM confirmed by retinopathy, certain measures of retinopathy were associated with chronic deficits in attention and cognitive ability \[[@CR40]\]. A prospective study of children with a spectrum of severe malaria including CM also found sub-acute behavioural problems and decreased attention \[[@CR47]\].

Retrospective studies of children with CM also report long-term impairments in cognition and executive functioning \[[@CR48]\] as well as developmental and cognitive impairments including in speech, language, and memory \[[@CR49]--[@CR51]\], with seizure during acute infection emerging as a strong risk factor \[[@CR52]\]. Small retrospective studies in adults have also shown chronic impairments in verbal learning and abstract reasoning \[[@CR53]\].

With the rise in diagnostic specificity of malaria disorders, investigators have been able to distinguish chronic sequelae of treated CM from those of other complications of malaria, including severe malarial anaemia (SMA) without coma. Consistent with the findings in other anemic disorders, children under 5 years of age with SMA have also been found to suffer long-term cognitive impairment \[[@CR54]\].

Post-malaria syndromes {#Sec4}
----------------------

With the evolution of the definition of CM requiring neurological signs during acute *P. falciparum* parasitaemia for diagnosis, three additional disorders have been defined to describe cases in which neuropsychiatric sequelae become manifest primarily following treatment and resolution of acute malaria infection, independent of the severity of prior disease, including occasionally occurring following illness from benign *P. vivax* infection. One disorder has been referred to as delayed cerebellar ataxia (DCA) \[[@CR55]\], or in some cases as related delayed cerebellar syndromes \[[@CR56], [@CR57]\]. A later somewhat distinct disorder has been referred to as post-malaria neurological syndrome (PMNS) \[[@CR58]\] while a related disorder of acute disseminated encephalomyelitis (ADEM) has been defined which is diagnosed with the aid of neuroimaging studies. Although disagreement has been raised as to whether certain of these constitute unique disorders \[[@CR59]\], they appear to differ from each other and from the modern disorder of CM in regards to the latency, frequency, and type of reported psychiatric findings.

Although psychiatric symptoms are only rarely associated with delayed cerebellar syndromes in the literature, when reported, these have included giddiness \[[@CR56]\], alterations in attention \[[@CR60]\], and word-finding difficulties \[[@CR61]\].

Similarly, in cases of ADEM, although neurological findings tend to predominate, psychiatric symptoms including alterations in sensorium \[[@CR62]\], confusion \[[@CR63]\], disorientation \[[@CR64]\], and language difficulties have been reported \[[@CR65]\].

In contrast to ADEM and the delayed cerebellar syndromes, psychiatric symptoms have been far more commonly reported with PMNS, to include the broader range of symptoms historically associated with malaria infections, including anxiety \[[@CR66]\], temporospatial disorientation \[[@CR67]\], difficulties with word-finding \[[@CR68]\], acute confusion \[[@CR69]\], mood changes, \[[@CR70]\], psychosis with hallucinations, persecutory delusions, and mania \[[@CR58]\], and disturbances in behaviour \[[@CR71]\].

Malariotherapy of psychiatric disease {#Sec5}
-------------------------------------

Ancient knowledge of the psychiatric effects of malaria included accounts describing reductions in aggressiveness among the mentally ill after bouts of malaria \[[@CR72]\]. In the early twentieth century, growing awareness of the reported psychiatric effects of malaria, and recognition that febrile illness had proven therapeutic in the treatment of neurosyphillis \[[@CR73]\]---a debilitating and epidemic condition then known as "general paresis" for which no effective treatments were then available \[[@CR74]\]---prompted the first formal experimentation with the practice of malariotherapy.

According to the first published description of the practice \[[@CR75]\], for which its author would subsequently win the Nobel Prize in medicine \[[@CR76]--[@CR78]\], neurosyphillis patients were intentionally inoculated with blood-stage benign forms of malaria, allowing upwards of ten cycles, or paroxysms, of intermittent fever prior to treatment of the infection with available anti-malarial drugs \[[@CR75]\].

Early case reports of this technique described common and pronounced improvements in psychiatric symptoms including reduced irritability, aggression, mania, psychosis, confusion, amnesia, and disorientation following such fever treatment \[[@CR75], [@CR79]--[@CR84]\]. Complete cures, later categorized as remissions by some authors \[[@CR85], [@CR86]\], were initially reported in up to a third of patients. Partial cures were reported in about a half \[[@CR87]\], although subsequent reports claimed somewhat greater risks and more mixed success rates \[[@CR86], [@CR88]--[@CR93]\]. Intriguingly, following the termination of fever paroxysms by treatment with available anti-malarial drugs, a distinct mental state described as "paraphrenic" or late psychosis was occasionally described with transient confusional, delusional, incoherent, hallucinatory, and manic-depressive features \[[@CR94]\].

So common became the practice of malariotherapy soon after its introduction that concerns of autochthonous spread of malaria led to health ministries establishing standard guidelines for the practice \[[@CR95]\], including the enforcement of vector controls in the vicinity of patients \[[@CR96], [@CR97]\]. Although mosquito inoculation, rather than blood-stage inoculation, had been recognized as associated with a risk of malaria relapse \[[@CR98]\], and to thus pose an increased risk of autochthonous spread, the growing popularity of malariotherapy for the treatment of non-syphilitic psychiatric patients \[[@CR99]\], together with concerns regarding cross-contamination with *Treponema pallidum*, led to increasing use of direct mosquito inoculation for the purpose \[[@CR85], [@CR100], [@CR101]\].

Subsequent experience would demonstrate that the results of treatment of other psychiatric disorders (including chronic "dementia praecox" or schizophrenia, as well as manic-depressive psychosis) were mixed and perceived as less successful \[[@CR73], [@CR94]\] and with the development of effective antibiotics for treatment of neurosyphillis, the practice of malariotherapy gradually fell into disuse.

Psychiatric effects of anti-malarial drugs {#Sec6}
------------------------------------------

Although many classes of drug have wide clinical applications as anti-malarials and also are known to cause psychiatric effects, the quinoline derivatives are unique in medical history for having been used ubiquitously to treat and prevent malaria, often to the exclusion of other classes of drug. For example, with few alternatives, prior to WWI, malaria was invariably treated and prevented with quinine, or occasionally with one of the other naturally occurring quinoline-based cinchona alkaloids \[[@CR102], [@CR103]\]. Similarly, in the aftermath of WWI and through WWII, the only other anti-malarials that came into reliable use were synthetic quinolines initially developed by German scientists \[[@CR102]\].

It was only in the decades following WWII, with the gradual development and deployment of drugs of alternative classes, to include proguanil and pyrimethamine \[[@CR102]\], the discovery of the anti-malarial activity of tetracyclines \[[@CR104], [@CR105]\], and recently, the isolation of naturally-occurring *qinghaosu* \[[@CR106]\], or artemisinin, from *Artemisia annua* \[[@CR107], [@CR108]\], that effective and widely used alternatives to the quinolines emerged both for prevention and treatment of disease.

While the quinolines have remained in common use through the present day, unlike these newer anti-malarial classes, the utility of certain members of the quinoline class in treating and preventing malaria has become progressively compromised through rising awareness of symptoms of idiosyncratic intoxication and central nervous system (CNS) toxicity associated with their use. Suggestive of a broad class effect spanning common structural variations, anti-malarial quinolines with psychiatric effects that are commonly described in the literature include the naturally occurring 4-quinolinemethanol cinchona alkaloids quinine and quinidine, whose use as anti-malarials predominated prior to WWII; the synthetic acridine derivative quinacrine (which may be considered a ring-substituted 4-aminoquinoline), whose use reached a peak during that war; the synthetic 4-aminoquinolines including chloroquine, whose use expanded widely following WWII; the synthetic 4-quinolinemethanol mefloquine, developed in the aftermath of the Vietnam War and whose use took the place of chloroquine throughout the 1980s and 1990s, and the synthetic 8-aminoquinolines, which have been used sporadically since their first development following WWI, but which are now being considered for expanded use in global malaria control efforts.

Quinine and the cinchona alkaloids {#Sec7}
----------------------------------

The earliest human experience with the quinolines dates to discovery of the naturally-occurring drug quinine, a 4-quinolinemethanol alkaloid first isolated from the bark of the *Cinchona* tree in the seventeenth century, together with the related cinchona alkaloid quinidine \[[@CR109]\]. Although reports from the early twentieth century noted that quinine could have significant psychiatric effects \[[@CR11]\], including causing depression, mania, irritability and personality change \[[@CR110]\], and that these might not be distinguished from those attributed to disease \[[@CR7]\], only relatively recently has it become clear that quinine, independent of malaria infection, may cause a serious toxic state marked by symptoms including delirium and confusion \[[@CR111], [@CR112]\].

In contrast, a broader range of psychiatric effects specifically due to quinidine have been widely reported in the literature, including mood change \[[@CR113]\], auditory hallucinations \[[@CR114], [@CR115]\], visual hallucinations and delusions \[[@CR115], [@CR116]\], paranoia \[[@CR116], [@CR117]\], confusion, and delirium \[[@CR116], [@CR118]\].

Quinacrine {#Sec8}
----------

Quinacrine, a derivative of acridine dye first synthesized in the early 1930s \[[@CR119]\], marketed initially under the names erion and atabrine \[[@CR120]\], then later also under the name Mepacrine \[[@CR121]\], may be considered a ring substituted 4-aminoquinoline. In early reports of its use, it was noted to induce "definite cases of delirium and mental disturbances" \[[@CR122]\], including symptoms of depression \[[@CR123]\], and delusional insanity. Case reports described acute personality and behavioural change, severe insomnia and anxiety described as an "impression of impending death" \[[@CR124]\], visual hallucinations, and cognitive dysfunction. One patient complained that "a large part of his brain was out of action" \[[@CR124]\], while another patient was described as manic, restless, disoriented, and suffering visual hallucinations that "snakes and fantastic animals were crawling on the floor" \[[@CR125]\].

Although early marketing materials for the drug acknowledged "mental disturbances which have been observed in a few instances during treatment" \[[@CR126]\], it was also emphasized that disorders of the nervous system, including sudden delirium and delusional insanity, were "not infrequent in the course of acute malarial fevers" \[[@CR126]\], and that it was "important to distinguish between those due to malaria itself and those which may be attributable to the drug" \[[@CR126]\].

With shortages of quinine during WWII, quinacrine was added to the US pharmacopoeia in 1942 \[[@CR127]\], and was quickly prioritized for military use both as treatment and as a suppressive prophylaxis throughout the war \[[@CR128]\]. Although studies of the acute toxicity of quinacrine had been planned during a wartime anti-malarial drug development effort \[[@CR129]\], these were soon deprioritized after they were declared to be of "minor importance" to military leadership \[[@CR130]\]. Although early studies in the UK had suggested that quinacrine caused "troublesome dreams" \[[@CR131]\], and independent studies in the US had noted slight increases in nervousness \[[@CR132]\], it was initially unclear whether such presumed toxic effects were actually due to quinacrine or merely to a contaminant \[[@CR128], [@CR133]\].

Towards the end of the war, however, sufficient experience had accumulated, including from rechallenge experiments, for wartime researchers to conclude that quinacrine use was definitely associated with a toxic psychosis distinct from the effects of malaria, often of abrupt onset \[[@CR134], [@CR135]\], described as including "mania, catatonia, and paranoid and hallucinatory states" \[[@CR136]\], and typically developing only several days after the start of treatment \[[@CR134]\]. Authors noted the psychosis was typically marked either by "excitement, hallucinations, and delusions" with an affect of "euphoria and expansiveness" \[[@CR137]\], or alternatively with "retardation, disorientation, and amnesia to recent events, together with confabulation" \[[@CR137]\], where affect was predominantly "one of bewilderment and fearfulness" \[[@CR137]\].

In controlled tests of intellectual functioning, a large proportion of subjects administered quinacrine were found to suffer significant subclinical impairment, and in two cases of psychosis that developed subsequently, tests of intellectual functioning had showed mild impairment prior to onset \[[@CR138]\]. The authors concluded that "among a large group" administered quinacrine, "some would show clinical confusion" \[[@CR139]\]. A separate controlled study conducted among healthy US military physicians clearly demonstrated quinacrine induced changes in the electroencephalograph \[[@CR140]\], accompanied by apprehension, restlessness, insomnia, "awakening dreams which at times were of frightening and nightmare quality" \[[@CR141]\], and symptoms of mania described as "an unusual push of activity" associated with "tension, irritability, and anxiety" \[[@CR142]\]. One subject experiencing panic attack and flight of ideas noted he "felt so bombarded by stimuli that he could not deal with them effectively" \[[@CR141]\]. The patient became very anxious, depressed, confused, and was thought to be suffering delirium, although his consciousness was in fact preserved \[[@CR141], [@CR142]\].

With the publication of such research findings initially restricted due to wartime considerations, official documents acknowledged only that "psychological disturbances occasionally appear" with use of quinacrine \[[@CR143]\], and that the drug could cause "mild excitement" and rarely, "acute maniacal psychoses" \[[@CR144]\]. Despite the imprecision of official reports, quinacrine was nonetheless recognized by numerous wartime physicians as a potential cause of psychiatric disorders \[[@CR145]\], and as the war ended and in subsequent years as restrictions were rescinded, numerous publications appeared describing psychiatric effects associated with the drug's use.

One ecological study linked an increase in a combat unit's rate of psychoses to their initiation of quinacrine for prophylaxis \[[@CR146]\]. A case report described a previously healthy soldier suffering three distinct episodes of mania, each occurring with recurrent use of quinacrine both for prophylaxis and treatment \[[@CR147]\]. Another detailed case report described a patient initially free of psychiatric history and thought to be suffering from cerebral malaria, who following 5 days of treatment with quinacrine developed excitement, talkativeness, and rambling, progressing to depression, impaired concentration, disorientation in time and place, anterograde and retrograde amnesia, and delusions. These symptoms lasted 2 weeks \[[@CR148]\]. One case series of those treated with quinacrine reported psychoses developing 0--10 days after the last day of malarial fever \[[@CR149]\]; another between 3--12 days following the start of quinacrine \[[@CR137]\]; while another reported an even wider latency of onset of 2--22 days, with a similarly wide range in time to satisfactory recovery of 1--30 days. Of significance, in at least four cases in the series, failure to recover and the development of chronic psychiatric disorders was noted \[[@CR135]\].

In the immediate postwar years, a few additional studies and case reports of psychiatric effects from quinacrine were also published \[[@CR150]\], including a series describing inappropriate sexual behaviour associated with psychoses \[[@CR151]\]. In a final published study of 31 previously healthy Army Medical Department officers who volunteered to take the drug experimentally at treatment doses \[[@CR152]\], 77 % suffered some form of mental disturbances: 71 % complained of abnormal, anxious and disturbing and rarely terrifying dreams; 58 % developed sleep disturbances, with loss of up to half of normal sleep, prompting sedative use to treat insomnia in two-fifths of these, or 26 % of the total; 39 % went on to develop severe psychic disturbances, of which a quarter, of 10 % of the total, suffered frank psychoses with delusions, hallucinations, and profound changes in mood, including mania; 35 % complained of tension; 32 % complained of restlessness, and 29 % depression. During an earlier phase of the trial when the drug had been administered at lower prophylactic dose rates, 29 % had noted mild complaints, most significantly abnormal dreams and sleep disturbances, which were deemed "the most reliable warning sign" of the development of "more severe reactions" \[[@CR152]\]. Intriguingly, it was reported that during earlier widespread use of the drug, such "minor toxic symptoms of restlessness, insomnia, and increased dreaming might frequently have passed unnoticed as a manifestation of malaria" \[[@CR152]\].

Chloroquine and other 4-aminoquinolines {#Sec9}
---------------------------------------

Chloroquine, a 4-aminoquinoline, was also first synthesized in the 1930s by German scientists, who named it resochin \[[@CR153], [@CR154]\]. Expecting a quinacrine-like effect in initial clinical testing, presumably owing to the drugs' structural similarities, its toxicity was described as being "so great in comparison to its effect" \[[@CR155]\], that the drug was deemed "too toxic for practical use in humans" \[[@CR153]\] and further German development was abandoned. The drug was rediscovered only during the subsequent US WWII drug development effort \[[@CR154]\], where it was initially referred to as SN-7618. Chloroquine was investigated during this WWII era effort only after the potential utility of a related 4-aminoquinoline, sontochin, later referred to as SN-6911, was noted following the Allied invasion of Tunisia, where it was found that the drug was undergoing clinical testing by Axis-affiliated French researchers \[[@CR153]\].

In the WWII era of US testing, sontochin was noted to induce acute confusional psychosis and nervousness at high doses \[[@CR156]\], and in postwar testing, was found to induce a wider variety of psychiatric symptoms, including anxiety, nervousness, a sensation of "being on edge", irascibility, and irritability at lower prophylactic dose rates \[[@CR157]\]. In contrast, during similar testing, chloroquine appeared to have only "minor toxic manifestations" \[[@CR158]\], and in published WWII era trials, appeared devoid of psychiatric effects. Considered more effective and less toxic than sontochin during the WWII development effort \[[@CR153]\], chloroquine was also considered "better" than quinacrine, and "much better" than quinine \[[@CR159]\], and by the early 1950s it had begun to replace both drugs for the treatment and prophylaxis of malaria \[[@CR160]--[@CR162]\].

With increasing use however, chloroquine came to be associated with similar idiosyncratic cases of toxicity as those noted previously with the cinchona alkaloids and with quinacrine and sontochin. These took the form of various psychiatric symptoms including sleep disturbances and insomnia \[[@CR163]--[@CR165]\], mood and personality change \[[@CR165], [@CR166]\], impulsivity, flight of ideas, and inappropriate behaviour \[[@CR165], [@CR167]\], persecutorial and paranoid delusions \[[@CR165], [@CR168]\], delusional misidentification \[[@CR169], [@CR170]\], depersonalization \[[@CR166]\], visual and auditory hallucinations \[[@CR165], [@CR171]\], and mania \[[@CR172], [@CR173]\]. Suicidality \[[@CR167]\] and completed suicide \[[@CR174]--[@CR176]\] were also not uncommonly reported. Although psychiatric symptoms from chloroquine have been noted to often resemble a brief psychotic or delusional disorder \[[@CR177]--[@CR179]\], on careful evaluation they are more likely to feature visual hallucinations, derealization, restlessness, agitation, and anxiety than other cases of psychosis \[[@CR180]\].

A case of severe psychosis with features of depersonalization and anxiety that developed under controlled research settings following chloroquine therapy for induced malaria was causally attributed by the researchers to the drug and not to malaria disease; following resolution of psychosis the patient experienced difficulties with concentration that lasted 4 months \[[@CR181]\]. A separate case of transient amnesia linked to the drug, \[[@CR182]\], and difficulties with concentration \[[@CR183]\], confusion \[[@CR184]\], delirium, and catatonia \[[@CR165], [@CR185]\] have also been reported.

Mefloquine {#Sec10}
----------

Mefloquine is a synthetic 4-quinolinemethanol analogue of quinine that was developed by the US military amid concerns of rising chloroquine resistance during the Vietnam War \[[@CR186]\] through a subsequent drug development effort similar to that of the earlier WWII era \[[@CR187]\] that spanned the 1960s--1980s \[[@CR188]\]. Although once commonly considered the drug of choice for treatment and prophylaxis of malaria and marketed under the trade name Lariam, use of mefloquine has been severely limited by awareness of significant idiosyncratic CNS toxicity \[[@CR189]\] which, as with quinacrine \[[@CR152]\], has been found to affect a sizeable minority of users at prophylactic dosages and a majority of users at treatment dosages \[[@CR189]\]. According to recent European product labelling \[[@CR190]\], very commonly reported psychiatric effects occurring in \>10 % of prophylactic users of mefloquine include abnormal dreams and insomnia, while commonly reported psychiatric effects occurring in 1--10 % of prophylactic users include anxiety and depression.

As with earlier generations of quinoline anti-malarials, and consistent with product label warnings of encephalopathy, case reports of psychiatric effects from mefloquine typically describe a complex and diverse range of effects on mood, personality, thought, cognition, sleep, and behaviour \[[@CR191]\]. These include asthenia \[[@CR192]\], melancholia \[[@CR193]\], anxiety \[[@CR194]\], phobias \[[@CR195], [@CR196]\], feelings of unrest \[[@CR197], [@CR198]\], paranoia \[[@CR199]\], increased self-esteem \[[@CR200], [@CR201]\], impaired judgment \[[@CR198]\], social disinhibition \[[@CR192], [@CR202]\], giddiness \[[@CR203]\], altered sexual libido \[[@CR204]\], manic behaviour and paranoid delusions or psychosis \[[@CR194], [@CR200], [@CR202], [@CR204]\], hyperreligiosity \[[@CR204]\], depersonalization \[[@CR192], [@CR198], [@CR205]\], concentration and cognitive problems \[[@CR197]\], problems with word finding \[[@CR201]\], disorientation \[[@CR193], [@CR198], [@CR206]\], symptoms of amnesia and confusion or disorientation \[[@CR192], [@CR193], [@CR203]\], sleep disorders \[[@CR207], [@CR208]\], severe nightmares, \[[@CR209]\] sleep paralysis and "flashbacks" \[[@CR201]\], suicidal ideation \[[@CR210]\], and suicide \[[@CR176], [@CR211]--[@CR213]\].

On initial presentation, individuals suffering from these diverse effects may appear to be suffering from a potentially wide range of psychiatric disorders that span the diagnostic nosology, to include anxiety, depressive, bipolar, psychotic, dissociative, personality, conversion, and factitious disorders \[[@CR189], [@CR191], [@CR198]\]. In particular, the psychiatric effects of mefloquine have been noted to potentially confound the diagnosis of a number of psychiatric disorders prevalent in military settings, including posttraumatic stress disorder \[[@CR189], [@CR214]\].

Severe and life-threatening psychiatric symptoms from mefloquine, including suicidal ideation and suicide, may be preceded by often subtle prodromal symptoms including even mild disturbances in sleep and dreaming \[[@CR215]\]. Although such symptoms have often previously been attributed to other causes and their critical significance overlooked even by influential authorities \[[@CR216]--[@CR218]\], both the European and US product labelling now explicitly direct the discontinuation of the drug at the onset of any psychiatric symptom \[[@CR190]\]. Even the earliest approved US mefloquine product insert appeared to echo the conclusions of prospective studies of quinacrine conducted decades earlier \[[@CR152]\] listing "anxiety, depression, restlessness or confusion" as potentially prodromal to a "more serious event" and requiring the drug's discontinuation \[[@CR190]\].

Similarly, while psychiatric symptoms from mefloquine were previously considered reversible and self-limiting, the US product label for mefloquine was recently updated to include a boxed warning (or "black box") that psychiatric effects from mefloquine could last years after use \[[@CR219]\]. A recent follow-up study has found a sizeable proportion of those previously reporting adverse events from the drug complain of long-term psychiatric symptoms including cognitive dysfunction years after use \[[@CR220]\]. Mefloquine has been convincingly linked to an increased risk of PMNS \[[@CR58], [@CR221]\], and a number of reviews have observed that certain psychiatric symptoms observed following malaria might plausibly be due to this and related quinoline anti-malarials \[[@CR36], [@CR44]\].

8-Aminoquinolines {#Sec11}
-----------------

The 8-aminoquinolines were among the first synthetic quinoline anti-malarials. Pamaquine (also known as plasmochin), developed by German scientists \[[@CR222], [@CR223]\], and in use since the 1920s \[[@CR224]\] was initially thought to be free of CNS toxicity, but a fatal case of fatal human toxicity, marked by symptoms of apprehension and restlessness, revealed evidence of extensive brain and brainstem neurotoxicity \[[@CR225]\]. By the late 1940s, other synthetic 8-aminoquinoline anti-malarials in common use prior to WWII, or introduced during the WWII drug development effort, had been linked to a severe neurotoxic syndrome \[[@CR226]--[@CR228]\], potentially masking more subtle psychiatric effects, such as previously reported mild psychosis \[[@CR229], [@CR230]\].

Primaquine, the only synthetic 8-aminoquinoline to safely emerge from the post-WWII era drug development program, although long considered safe and only rarely associated with psychiatric adverse effects \[[@CR231]\], has been linked to rare reports of confusion, amnesia, and depression \[[@CR232], [@CR233]\]. Similarly, symptoms reported with the experimental 8-aminoquinoline tafenoquine, originally developed by the US military and now in late-stage development \[[@CR234]\] and anticipated for use both as a replacement for mefloquine and primaquine \[[@CR235], [@CR236]\] and in mass drug administration campaigns for global malaria control \[[@CR234]\] have been described in randomized trials as similar to those of chloroquine \[[@CR237]\]. In a recent blinded trial, tafenoquine was found to cause a slightly higher incidence of psychiatric symptoms than mefloquine, including abnormal dreams, agitation, anxiety, amnesia, and paranoia \[[@CR238]\], with other reported symptoms including insomnia and depression \[[@CR239]\].

Other anti-malarials {#Sec12}
--------------------

In contrast to the quinoline class of anti-malarials, there is a paucity of data on the psychiatric effects of newer anti-malarial classes, including the tetracyclines, and artemisinins. What evidence does exists suggests these drugs cause a narrower range, and typically fewer and less extreme psychiatric symptoms than do the anti-malarial quinolines.

For example, in contrast to trials of tetracycline in combination with mefloquine \[[@CR240]\], early trials of tetracycline monotherapy for treatment of malaria reported no psychiatric adverse effects \[[@CR104]\]. Early trials of minocycline monotherapy for treatment and prophylaxis also reported no psychiatric adverse effects \[[@CR241]\]. Indeed, reviews of the use of tetracyclines \[[@CR242]\] and specifically doxycycline \[[@CR243]\] in malaria do not specifically mention adverse psychiatric effects, and one recent review suggested these are "nearly nonexistent" \[[@CR244]\]. Despite this, a number of studies comparing doxycycline to mefloquine report psychiatric symptoms such as insomnia and nightmares occurring, albeit less commonly than with mefloquine \[[@CR245], [@CR246]\]. Additionally, a recent case series has directed attention to the potential for rare anxiety and suicidality from doxycycline \[[@CR247]\].

In contrast, pyrimethamine, typically used in combination with sulfadoxine, appears to have few psychiatric effects. Recent reviews do not specifically mention adverse psychiatric effects from the drug \[[@CR248], [@CR249]\], although early observational studies suggested the combination presented a risk of insomnia and depression, although less commonly than from quinoline anti-malarials \[[@CR250]\]. A recent trial of sulfadoxine-pyrimethamine against mefloquine also noted sleep disturbance occurring with use of the drug, although similarly less commonly than with mefloquine \[[@CR251]\].

Likewise, the drug combination atovaquone-proguanil, commonly marketed under the trade name Malarone^®^, also appears to have few psychiatric effects. As with the other drugs mentioned in this section, recent reviews also do not specifically mention adverse psychiatric effects from the drug \[[@CR252]\]. Although one review suggested that atovaquone-proguanil is "the best tolerated of all antimalarial medications", psychiatric symptoms, particularly sleep disturbance and abnormal dreams, do occur with use of the drug, although again less commonly than with quinoline anti-malarials including mefloquine \[[@CR253]\] and chloroquine-proguanil \[[@CR254]\]. Additionally, and unlike as is the case with mefloquine \[[@CR190]\] and with quinacrine before it \[[@CR152]\], such psychiatric symptoms from atovaquone-proguanil are not considered prodromal or predictive of more serious neuropsychiatric adverse effects, and do not mandate discontinuation of the drug at their onset.

Lastly, and particularly given suggestive evidence of CNS toxicity from the artemisinins \[[@CR255]--[@CR259]\], psychiatric effects from anti-malarials of this class, including the semi-synthetic derivatives artemether, artesunate, and dihydroartemisinin, should be considered plausible in spite of a paucity of observational and experimental evidence of this effect. The ascertainment of psychiatric effects from the artemisinins is made particularly challenging both by their widespread use in the treatment of symptomatic malaria \[[@CR260], [@CR261]\], and by their ubiquitous combination with other anti-malarial drugs, including the quinoline drugs amodiaquine and piperaquine \[[@CR262]\], which are themselves not well studied for psychiatric effects. Although a recent systematic review found consistently higher rates of psychiatric effects, particularly sleep disturbances, with artemisinin-based combination therapies containing mefloquine than with those containing other drugs, these cited studies were not designed to assess the unique effects of artemisinins \[[@CR260]\], and no prospective studies have assessed the psychiatric effects of artemisinin monotherapy alone.

Conclusions {#Sec13}
===========

This review has demonstrated that malaria, regardless of its severity, has historically been associated in the literature with certain common psychiatric effects that resemble those now known to be caused by certain anti-malarial drugs. This review has also demonstrated that as awareness of the adverse psychiatric effects of anti-malarial drugs has grown in the modern era, the number of psychiatric effects commonly attributed in the literature to malaria, and particularly to less severe forms of the disease, has steadily decreased.

Earlier historical eras, when the psychiatric effects of malaria were considered far broader than they are today, coincided with a period of ubiquitous exposure to quinolines, both as prophylaxis and in subsequent treatment of disease. Similarly, more modern eras, in which the psychiatric effects of malaria have been generally considered to be more limited, have coincided with a period of more widespread use of alternative classes of anti-malarial drugs less commonly associated with psychiatric effects. This ecological trend suggests the distinct possibility that some psychiatric effects previously attributed to malaria may have been due in whole or in part to the effects of quinoline anti-malarials.

While malaria, and particularly in its modern definition of CM, is undoubtedly associated with a risk of cognitive impairment, the insights presented in this article should draw attention to the potentially significant confounding effects of anti-malarial exposure in the causal attribution of certain other psychiatric symptoms unique to malaria. This suggests a need to critically reevaluate the existing evidence base for the potential effects of such confounding.

The insights presented here should also underscore the importance both of designing future studies of the psychiatric effects of malaria to control for such confounding as much as is feasible, and also of more thoroughly assessing and characterizing those effects potentially attributable to anti-malarials, including those drugs currently under development and testing, and planned for use in global malaria control efforts, informed by knowledge of their common adverse psychiatric effects.

ADEM

:   acute disseminated encephalomyelitis

CM

:   cerebral malaria

CNS

:   central nervous system

DCA

:   delayed cerebellar ataxia

PMNS

:   post-malaria neurological syndrome

SMA

:   severe malarial anaemia

WWI

:   World War I

WWII

:   World War II

RLN drafted the manuscript. AMC critically revised the manuscript. Both authors read and approved the final manuscript.

Acknowledgements {#FPar1}
================

None.

Competing interests {#FPar2}
===================

Both authors report being retained as consultants and expert witnesses in legal cases involving claims of anti-malarial drug toxicity. Both authors report no other relevant financial or other competing interests.

Availability of data and materials {#FPar3}
==================================

Historical references cited by the authors are available upon request.

Consent for publication {#FPar4}
=======================

Not applicable.

Ethics approval and consent to publish {#FPar5}
======================================

This article is based on previously conducted studies and does not involve any new studies of human or animal subjects performed by any of the authors.

Funding {#FPar6}
=======

Both authors report no grant funding or other financial support to acknowledge.


Urinary tract stone disease (urolithiasis) is a common clinical disorder that frequently leads to hospitalization. The objective of this proposal is to advance the understanding of the pathogenesis of urolithiasis by determining the physical mechanisms through which important inhibitors that include small urinary molecules, such as magnesium and citrate that are currently used in the treatment of urinary tract stone disease and urinary macromolecules, such as osteopontin control the nucleation, growth, aggregation, and phase transformations of calcium oxalate (CaOx) precipitates. This objective will be accomplished by investigations focusing on 1). the mechanisms of modulation of CaOx nucleation and growth by small urinary molecules and urinary macromolecules, 2). the mechanisms by which urinary modulators affect the sequence of events during phase transformations of CaOx crystals and 3). the surface interactions and events underlying urinary protein modulation of CaOx aggregation. The proposed research will use in situ atomic force microscopy to follow the evolution of CaOx crystal surfaces and quantify the impact of growth modulators on the thermodynamic and kinetic factors controlling the dynamics of atomic steps on those surfaces. This work will lead to new insights that integrates an understanding of the specific stereochemical interactions on the crystal surface with the quantitative impact on kinetics and morphology. The atomic force microscopy measurements will be correlated with concurrently performed constant composition measurements of growth kinetics and contact angle measurements of interfacial energies. The knowledge derived from our studies will assist in the design of inhibitory molecules that are potentially useful in therapy of stone disease.


For Sale $700 cash or $760 shipped to you.Hello, this is a custom made weather enclosure made by myself here in Minnesota. Ive been making these since 2007 and have sold these throughout the snow belt states. I make a limited quantity of these per year for the X700 series garden tractors, so buy now Thanks for viewingModel MJX700 and MJX700-SThis weather enclosure fits the following John Deere ...

This Curtis cab was used for a few years on John Deere F935 and F932 front deck mowers, and has been stored inside whenever it wasnt being used. It has been over a decade since this was last used. The paint and glass are in good shape. It doesnt have doors. It may fit other similar models of mowers such as F910 F911 F912 F915 F925 F930 F932 F935 F1145, but I havent done any research to verify t...

1946 John Deere H for parts or restoration project. It has the electric start, head lights, hydraulic pump. The sheet metal is all good except front grills missing, fuel tanks solid, block and head good and block bored out to .030. Babbot on the rods are in good shape, the crank is good. There are 2 gears with teeth missing in the transmission, good rims and front tires. Everything is apart and...

John Deere 48 mower deck hanger parts, these are thehanger parts for where themower deck attaches in thefront of the deck to the lawntractor. These are from a 48mower deck on a John DeereGT 275 lawn tractor, may workon other models. $45No checks. No emails.Call .John Deere GT lawn tractors.John Deere LX lawn tractors.


Sharing Thoughts, Links and Insights to Cloud Computing and Social Networks. Try and bring some (at least mine) insight to this new frontier.

Friday, June 12, 2009

Four short links: 12 June 2009

New Media Challenges: Legal and Policy Considerations for Federal Use of Web 2.0 Technology (Center for American Progress) -- report on the issues around Web 2.0 use in Government, which include privacy, security, Public Records Act, advertising, etc. See also It's Not the Campaign Anymore: How the White House Is Using Web 2.0 Technology So Far from the same... http://ping.fm/2dE0C

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Functions

DSP_Lib CM0 LE.txt File Reference

Functions

Rebuild target DSP_Lib CM0 LE

compiling arm_abs_f32 c

compiling arm_abs_q7 c

compiling arm_abs_q15 c

compiling arm_abs_q31 c

compiling arm_add_f32 c

compiling arm_add_q7 c

compiling arm_add_q15 c

compiling arm_add_q31 c

compiling arm_dot_prod_f32 c

compiling arm_dot_prod_q7 c

compiling arm_dot_prod_q15 c

compiling arm_dot_prod_q31 c

compiling arm_mult_f32 c

compiling arm_mult_q7 c

compiling arm_mult_q15 c

compiling arm_mult_q31 c

compiling arm_negate_f32 c

compiling arm_negate_q7 c

compiling arm_negate_q15 c

compiling arm_negate_q31 c

compiling arm_offset_f32 c

compiling arm_offset_q7 c

compiling arm_offset_q15 c

compiling arm_offset_q31 c

compiling arm_scale_f32 c

compiling arm_scale_q7 c

compiling arm_scale_q15 c

compiling arm_scale_q31 c

compiling arm_shift_q7 c

compiling arm_shift_q15 c

compiling arm_shift_q31 c

compiling arm_sub_f32 c

compiling arm_sub_q7 c

compiling arm_sub_q15 c

compiling arm_sub_q31 c

compiling arm_cos_f32 c

compiling arm_cos_q15 c

compiling arm_cos_q31 c

compiling arm_sin_f32 c

compiling arm_sin_q15 c

compiling arm_sin_q31 c

compiling arm_sqrt_q15 c

compiling arm_sqrt_q31 c

compiling arm_cmplx_conj_f32 c

compiling arm_cmplx_conj_q15 c

compiling arm_cmplx_conj_q31 c

compiling

arm_cmplx_dot_prod_f32 c

compiling

arm_cmplx_dot_prod_q15 c

compiling

arm_cmplx_dot_prod_q31 c

compiling arm_cmplx_mag_f32 c

compiling arm_cmplx_mag_q15 c

compiling arm_cmplx_mag_q31 c

compiling

arm_cmplx_mag_squared_f32 c

compiling

arm_cmplx_mag_squared_q15 c

compiling

arm_cmplx_mag_squared_q31 c

compiling

arm_cmplx_mult_cmplx_f32 c

compiling

arm_cmplx_mult_cmplx_q15 c

compiling

arm_cmplx_mult_cmplx_q31 c

compiling

arm_cmplx_mult_real_f32 c

compiling

arm_cmplx_mult_real_q15 c

compiling

arm_cmplx_mult_real_q31 c

compiling

arm_biquad_cascade_df1_32x64_init_q31

c compiling

arm_biquad_cascade_df1_32x64_q31

c compiling

arm_biquad_cascade_df1_f32 c

compiling

arm_biquad_cascade_df1_fast_q15

c compiling

arm_biquad_cascade_df1_fast_q31

c compiling

arm_biquad_cascade_df1_init_f32

c compiling

arm_biquad_cascade_df1_init_q15

c compiling

arm_biquad_cascade_df1_init_q31

c compiling

arm_biquad_cascade_df1_q15 c

compiling

arm_biquad_cascade_df1_q31 c

compiling

arm_biquad_cascade_df2T_f32 c

compiling

arm_biquad_cascade_df2T_init_f32

c compiling arm_conv_f32 c

compiling arm_conv_fast_q15 c

compiling

arm_conv_fast_opt_q15 c

compiling arm_conv_fast_q31 c

compiling arm_conv_partial_f32

c compiling

arm_conv_partial_fast_q15 c

compiling

arm_conv_partial_fast_opt_q15

c compiling

arm_conv_partial_fast_q31 c

compiling arm_conv_partial_q7

c compiling

arm_conv_partial_opt_q7 c

compiling arm_conv_partial_q15

c compiling

arm_conv_partial_opt_q15 c

compiling arm_conv_partial_q31

c compiling arm_conv_q7 c

compiling arm_conv_opt_q7 c

compiling arm_conv_q15 c

compiling arm_conv_opt_q15 c

compiling arm_conv_q31 c

compiling arm_correlate_f32 c

compiling

arm_correlate_fast_q15 c

compiling

arm_correlate_fast_opt_q15 c

compiling

arm_correlate_fast_q31 c

compiling arm_correlate_q7 c

compiling arm_correlate_opt_q7

c compiling arm_correlate_q15

c compiling

arm_correlate_opt_q15 c

compiling arm_correlate_q31 c

compiling arm_fir_decimate_f32

c compiling

arm_fir_decimate_fast_q15 c

compiling

arm_fir_decimate_fast_q31 c

compiling

arm_fir_decimate_init_f32 c

compiling

arm_fir_decimate_init_q15 c

compiling

arm_fir_decimate_init_q31 c

compiling arm_fir_decimate_q15

c compiling

arm_fir_decimate_q31 c

compiling arm_fir_f32 c

compiling arm_fir_fast_q15 c

compiling arm_fir_fast_q31 c

compiling arm_fir_init_f32 c

compiling arm_fir_init_q7 c

compiling arm_fir_init_q15 c

compiling arm_fir_init_q31 c

compiling

arm_fir_interpolate_f32 c

compiling

arm_fir_interpolate_init_f32 c

compiling

arm_fir_interpolate_init_q15 c

compiling

arm_fir_interpolate_init_q31 c

compiling

arm_fir_interpolate_q15 c

compiling

arm_fir_interpolate_q31 c

compiling arm_fir_lattice_f32

c compiling

arm_fir_lattice_init_f32 c

compiling

arm_fir_lattice_init_q15 c

compiling

arm_fir_lattice_init_q31 c

compiling arm_fir_lattice_q15

c compiling

arm_fir_lattice_q31 c

compiling arm_fir_q7 c

compiling arm_fir_q15 c

compiling arm_fir_q31 c

compiling arm_fir_sparse_f32 c

compiling

arm_fir_sparse_init_f32 c

compiling

arm_fir_sparse_init_q7 c

compiling

arm_fir_sparse_init_q15 c

compiling

arm_fir_sparse_init_q31 c

compiling arm_fir_sparse_q7 c

compiling arm_fir_sparse_q15 c

compiling arm_fir_sparse_q31 c

compiling arm_iir_lattice_f32

c compiling

arm_iir_lattice_init_f32 c

compiling

arm_iir_lattice_init_q15 c

compiling

arm_iir_lattice_init_q31 c

compiling arm_iir_lattice_q15

c compiling

arm_iir_lattice_q31 c

compiling arm_lms_f32 c

compiling arm_lms_init_f32 c

compiling arm_lms_init_q15 c

compiling arm_lms_init_q31 c

compiling arm_lms_norm_f32 c

compiling

arm_lms_norm_init_f32 c

compiling

arm_lms_norm_init_q15 c

compiling

arm_lms_norm_init_q31 c

compiling arm_lms_norm_q15 c

compiling arm_lms_norm_q31 c

compiling arm_lms_q15 c

compiling arm_lms_q31 c

compiling arm_mat_add_f32 c

compiling arm_mat_add_q15 c

compiling arm_mat_add_q31 c

compiling arm_mat_init_f32 c

compiling arm_mat_init_q15 c

compiling arm_mat_init_q31 c

compiling arm_mat_inverse_f32

c compiling arm_mat_mult_f32 c

compiling

arm_mat_mult_fast_q15 c

compiling

arm_mat_mult_fast_q31 c

compiling arm_mat_mult_q15 c

compiling arm_mat_mult_q31 c

compiling arm_mat_scale_f32 c

compiling arm_mat_scale_q15 c

compiling arm_mat_scale_q31 c

compiling arm_mat_sub_f32 c

compiling arm_mat_sub_q15 c

compiling arm_mat_sub_q31 c

compiling arm_mat_trans_f32 c

compiling arm_mat_trans_q15 c

compiling arm_mat_trans_q31 c

compiling arm_bitreversal c

compiling arm_cfft_radix2_f32

c compiling

arm_cfft_radix2_init_f32 c

compiling

arm_cfft_radix2_init_q15 c

compiling

arm_cfft_radix2_init_q31 c

compiling arm_cfft_radix2_q15

c compiling

arm_cfft_radix2_q31 c

compiling arm_cfft_radix4_f32

c compiling

arm_cfft_radix4_init_f32 c

compiling

arm_cfft_radix4_init_q15 c

compiling

arm_cfft_radix4_init_q31 c

compiling arm_cfft_radix4_q15

c compiling

arm_cfft_radix4_q31 c

compiling arm_dct4_f32 c

compiling arm_dct4_init_f32 c

compiling arm_dct4_init_q15 c

compiling arm_dct4_init_q31 c

compiling arm_dct4_q15 c

compiling arm_dct4_q31 c

compiling arm_rfft_f32 c

compiling arm_rfft_init_f32 c

compiling arm_rfft_init_q15 c

compiling arm_rfft_init_q31 c

compiling arm_rfft_q15 c

compiling arm_rfft_q31 c

compiling arm_pid_init_f32 c

compiling arm_pid_init_q15 c

compiling arm_pid_init_q31 c

compiling arm_pid_reset_f32 c

compiling arm_pid_reset_q15 c

compiling arm_pid_reset_q31 c

compiling arm_sin_cos_f32 c

compiling arm_sin_cos_q31 c

compiling arm_max_f32 c

compiling arm_max_q7 c

compiling arm_max_q15 c

compiling arm_max_q31 c

compiling arm_mean_f32 c

compiling arm_mean_q7 c

compiling arm_mean_q15 c

compiling arm_mean_q31 c

compiling arm_min_f32 c

compiling arm_min_q7 c

compiling arm_min_q15 c

compiling arm_min_q31 c

compiling arm_power_f32 c

compiling arm_power_q7 c

compiling arm_power_q15 c

compiling arm_power_q31 c

compiling arm_rms_f32 c

compiling arm_rms_q15 c

compiling arm_rms_q31 c

compiling arm_std_f32 c

compiling arm_std_q15 c

compiling arm_std_q31 c

compiling arm_var_f32 c

compiling arm_var_q15 c

compiling arm_var_q31 c

compiling arm_copy_f32 c

compiling arm_copy_q7 c

compiling arm_copy_q15 c

compiling arm_copy_q31 c

compiling arm_fill_f32 c

compiling arm_fill_q7 c

compiling arm_fill_q15 c

compiling arm_fill_q31 c

compiling arm_float_to_q7 c

compiling arm_float_to_q15 c

compiling arm_float_to_q31 c

compiling arm_q7_to_float c

compiling arm_q7_to_q15 c

compiling arm_q7_to_q31 c

compiling arm_q15_to_float c

compiling arm_q15_to_q7 c

compiling arm_q15_to_q31 c

compiling arm_q31_to_float c

compiling arm_q31_to_q7 c

compiling arm_q31_to_q15 c

compiling arm_common_tables c

creating Library User command 	file (s) copied.".\intermediateFiles\arm_cortexM0l_math.lib"-0 Error(s)

Function Documentation

          Rebuild target DSP_Lib CM0 LE compiling arm_abs_f32 c compiling arm_abs_q7 c compiling arm_abs_q15 c compiling arm_abs_q31 c compiling arm_add_f32 c compiling arm_add_q7 c compiling arm_add_q15 c compiling arm_add_q31 c compiling arm_dot_prod_f32 c compiling arm_dot_prod_q7 c compiling arm_dot_prod_q15 c compiling arm_dot_prod_q31 c compiling arm_mult_f32 c compiling arm_mult_q7 c compiling arm_mult_q15 c compiling arm_mult_q31 c compiling arm_negate_f32 c compiling arm_negate_q7 c compiling arm_negate_q15 c compiling arm_negate_q31 c compiling arm_offset_f32 c compiling arm_offset_q7 c compiling arm_offset_q15 c compiling arm_offset_q31 c compiling arm_scale_f32 c compiling arm_scale_q7 c compiling arm_scale_q15 c compiling arm_scale_q31 c compiling arm_shift_q7 c compiling arm_shift_q15 c compiling arm_shift_q31 c compiling arm_sub_f32 c compiling arm_sub_q7 c compiling arm_sub_q15 c compiling arm_sub_q31 c compiling arm_cos_f32 c compiling arm_cos_q15 c compiling arm_cos_q31 c compiling arm_sin_f32 c compiling arm_sin_q15 c compiling arm_sin_q31 c compiling arm_sqrt_q15 c compiling arm_sqrt_q31 c compiling arm_cmplx_conj_f32 c compiling arm_cmplx_conj_q15 c compiling arm_cmplx_conj_q31 c compiling arm_cmplx_dot_prod_f32 c compiling arm_cmplx_dot_prod_q15 c compiling arm_cmplx_dot_prod_q31 c compiling arm_cmplx_mag_f32 c compiling arm_cmplx_mag_q15 c compiling arm_cmplx_mag_q31 c compiling arm_cmplx_mag_squared_f32 c compiling arm_cmplx_mag_squared_q15 c compiling arm_cmplx_mag_squared_q31 c compiling arm_cmplx_mult_cmplx_f32 c compiling arm_cmplx_mult_cmplx_q15 c compiling arm_cmplx_mult_cmplx_q31 c compiling arm_cmplx_mult_real_f32 c compiling arm_cmplx_mult_real_q15 c compiling arm_cmplx_mult_real_q31 c compiling arm_biquad_cascade_df1_32x64_init_q31 c compiling arm_biquad_cascade_df1_32x64_q31 c compiling arm_biquad_cascade_df1_f32 c compiling arm_biquad_cascade_df1_fast_q15 c compiling arm_biquad_cascade_df1_fast_q31 c compiling arm_biquad_cascade_df1_init_f32 c compiling arm_biquad_cascade_df1_init_q15 c compiling arm_biquad_cascade_df1_init_q31 c compiling arm_biquad_cascade_df1_q15 c compiling arm_biquad_cascade_df1_q31 c compiling arm_biquad_cascade_df2T_f32 c compiling arm_biquad_cascade_df2T_init_f32 c compiling arm_conv_f32 c compiling arm_conv_fast_q15 c compiling arm_conv_fast_opt_q15 c compiling arm_conv_fast_q31 c compiling arm_conv_partial_f32 c compiling arm_conv_partial_fast_q15 c compiling arm_conv_partial_fast_opt_q15 c compiling arm_conv_partial_fast_q31 c compiling arm_conv_partial_q7 c compiling arm_conv_partial_opt_q7 c compiling arm_conv_partial_q15 c compiling arm_conv_partial_opt_q15 c compiling arm_conv_partial_q31 c compiling arm_conv_q7 c compiling arm_conv_opt_q7 c compiling arm_conv_q15 c compiling arm_conv_opt_q15 c compiling arm_conv_q31 c compiling arm_correlate_f32 c compiling arm_correlate_fast_q15 c compiling arm_correlate_fast_opt_q15 c compiling arm_correlate_fast_q31 c compiling arm_correlate_q7 c compiling arm_correlate_opt_q7 c compiling arm_correlate_q15 c compiling arm_correlate_opt_q15 c compiling arm_correlate_q31 c compiling arm_fir_decimate_f32 c compiling arm_fir_decimate_fast_q15 c compiling arm_fir_decimate_fast_q31 c compiling arm_fir_decimate_init_f32 c compiling arm_fir_decimate_init_q15 c compiling arm_fir_decimate_init_q31 c compiling arm_fir_decimate_q15 c compiling arm_fir_decimate_q31 c compiling arm_fir_f32 c compiling arm_fir_fast_q15 c compiling arm_fir_fast_q31 c compiling arm_fir_init_f32 c compiling arm_fir_init_q7 c compiling arm_fir_init_q15 c compiling arm_fir_init_q31 c compiling arm_fir_interpolate_f32 c compiling arm_fir_interpolate_init_f32 c compiling arm_fir_interpolate_init_q15 c compiling arm_fir_interpolate_init_q31 c compiling arm_fir_interpolate_q15 c compiling arm_fir_interpolate_q31 c compiling arm_fir_lattice_f32 c compiling arm_fir_lattice_init_f32 c compiling arm_fir_lattice_init_q15 c compiling arm_fir_lattice_init_q31 c compiling arm_fir_lattice_q15 c compiling arm_fir_lattice_q31 c compiling arm_fir_q7 c compiling arm_fir_q15 c compiling arm_fir_q31 c compiling arm_fir_sparse_f32 c compiling arm_fir_sparse_init_f32 c compiling arm_fir_sparse_init_q7 c compiling arm_fir_sparse_init_q15 c compiling arm_fir_sparse_init_q31 c compiling arm_fir_sparse_q7 c compiling arm_fir_sparse_q15 c compiling arm_fir_sparse_q31 c compiling arm_iir_lattice_f32 c compiling arm_iir_lattice_init_f32 c compiling arm_iir_lattice_init_q15 c compiling arm_iir_lattice_init_q31 c compiling arm_iir_lattice_q15 c compiling arm_iir_lattice_q31 c compiling arm_lms_f32 c compiling arm_lms_init_f32 c compiling arm_lms_init_q15 c compiling arm_lms_init_q31 c compiling arm_lms_norm_f32 c compiling arm_lms_norm_init_f32 c compiling arm_lms_norm_init_q15 c compiling arm_lms_norm_init_q31 c compiling arm_lms_norm_q15 c compiling arm_lms_norm_q31 c compiling arm_lms_q15 c compiling arm_lms_q31 c compiling arm_mat_add_f32 c compiling arm_mat_add_q15 c compiling arm_mat_add_q31 c compiling arm_mat_init_f32 c compiling arm_mat_init_q15 c compiling arm_mat_init_q31 c compiling arm_mat_inverse_f32 c compiling arm_mat_mult_f32 c compiling arm_mat_mult_fast_q15 c compiling arm_mat_mult_fast_q31 c compiling arm_mat_mult_q15 c compiling arm_mat_mult_q31 c compiling arm_mat_scale_f32 c compiling arm_mat_scale_q15 c compiling arm_mat_scale_q31 c compiling arm_mat_sub_f32 c compiling arm_mat_sub_q15 c compiling arm_mat_sub_q31 c compiling arm_mat_trans_f32 c compiling arm_mat_trans_q15 c compiling arm_mat_trans_q31 c compiling arm_bitreversal c compiling arm_cfft_radix2_f32 c compiling arm_cfft_radix2_init_f32 c compiling arm_cfft_radix2_init_q15 c compiling arm_cfft_radix2_init_q31 c compiling arm_cfft_radix2_q15 c compiling arm_cfft_radix2_q31 c compiling arm_cfft_radix4_f32 c compiling arm_cfft_radix4_init_f32 c compiling arm_cfft_radix4_init_q15 c compiling arm_cfft_radix4_init_q31 c compiling arm_cfft_radix4_q15 c compiling arm_cfft_radix4_q31 c compiling arm_dct4_f32 c compiling arm_dct4_init_f32 c compiling arm_dct4_init_q15 c compiling arm_dct4_init_q31 c compiling arm_dct4_q15 c compiling arm_dct4_q31 c compiling arm_rfft_f32 c compiling arm_rfft_init_f32 c compiling arm_rfft_init_q15 c compiling arm_rfft_init_q31 c compiling arm_rfft_q15 c compiling arm_rfft_q31 c compiling arm_pid_init_f32 c compiling arm_pid_init_q15 c compiling arm_pid_init_q31 c compiling arm_pid_reset_f32 c compiling arm_pid_reset_q15 c compiling arm_pid_reset_q31 c compiling arm_sin_cos_f32 c compiling arm_sin_cos_q31 c compiling arm_max_f32 c compiling arm_max_q7 c compiling arm_max_q15 c compiling arm_max_q31 c compiling arm_mean_f32 c compiling arm_mean_q7 c compiling arm_mean_q15 c compiling arm_mean_q31 c compiling arm_min_f32 c compiling arm_min_q7 c compiling arm_min_q15 c compiling arm_min_q31 c compiling arm_power_f32 c compiling arm_power_q7 c compiling arm_power_q15 c compiling arm_power_q31 c compiling arm_rms_f32 c compiling arm_rms_q15 c compiling arm_rms_q31 c compiling arm_std_f32 c compiling arm_std_q15 c compiling arm_std_q31 c compiling arm_var_f32 c compiling arm_var_q15 c compiling arm_var_q31 c compiling arm_copy_f32 c compiling arm_copy_q7 c compiling arm_copy_q15 c compiling arm_copy_q31 c compiling arm_fill_f32 c compiling arm_fill_q7 c compiling arm_fill_q15 c compiling arm_fill_q31 c compiling arm_float_to_q7 c compiling arm_float_to_q15 c compiling arm_float_to_q31 c compiling arm_q7_to_float c compiling arm_q7_to_q15 c compiling arm_q7_to_q31 c compiling arm_q15_to_float c compiling arm_q15_to_q7 c compiling arm_q15_to_q31 c compiling arm_q31_to_float c compiling arm_q31_to_q7 c compiling arm_q31_to_q15 c compiling arm_common_tables c creating Library User command file
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DSP_Lib CM0 LE.txt

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Generated on Wed Mar 28 2012 15:38:08 for CMSIS-DSP by ARM Ltd. All rights reserved.


Keys to Vehicle Leasing

On July 21, 2011, rulewriting authority for consumer protection laws related to mortgages, credit cards, bank accounts and other consumer financial products transferred from the Federal Reserve Board to the Consumer Financial Protection Bureau (CFPB). For information on recent regulatory changes, as well as additional information about shopping for and using consumer financial products, please visit the CFPB's website.

Quick Consumer Guide

Under the federal Consumer Leasing Act, you, the consumer, have a right to information about the costs and terms of a vehicle lease. This information will help you compare lease offers and negotiate a lease that best fits your needs, budget, and driving patterns.

This quick consumer guide is for a closed-end lease, the most common type of vehicle lease. With a closed-end lease, you may return the vehicle at the end of the lease term, pay any end-of-lease costs, and walk away. The sample leasing form shows the types of information the dealer or leasing company must give you before you sign a lease. The glossary gives definitions of terms associated with vehicle leasing.

Leasing is different from buying. Here's how . . .

Leasing: You do not own the vehicle. You get to use it but must return it at the end of the lease unless you choose to buy it.

Buying: You own the vehicle and get to keep it at the end of the financing term.

Up-front costs

Leasing: Up-front costs may include the first month's payment, a refundable security deposit, a capitalized cost reduction (like a down payment), taxes, registration and other fees, and other charges.

Buying: Up-front costs include the cash price or a down payment, taxes, registration and other fees, and other charges.

Monthly payments

Leasing: Monthly lease payments are usually lower than monthly loan payments because you are paying only for the vehicle's depreciation during the lease term, plus rent charges (like interest), taxes, and fees.

Buying: Monthly loan payments are usually higher than monthly lease payments because you are paying for the entire purchase price of the vehicle, plus interest and other finance charges, taxes, and fees.

Early termination

Leasing: You are responsible for any early termination charges if you end the lease early.

Buying: You are responsible for any pay-off amount if you end the loan early.

Vehicle return

Leasing: You may return the vehicle at lease-end, pay any end-of-lease costs, and "walk away."

Buying: You may have to sell or trade the vehicle when you decide you want a different vehicle.

Future value

Leasing: The lessor has the risk of the future market value of the vehicle.

Buying: You have the risk of the vehicle's market value when you trade or sell it.

Mileage

Leasing: Most leases limit the number of miles you may drive (often 12,000-15,000 per year). You can negotiate a higher mileage limit and pay a higher monthly payment. You will likely have to pay charges for exceeding those limits if you return the vehicle.

Buying: You may drive as many miles as you want, but higher mileage will lower the vehicle's trade-in or resale value.

Excessive wear

Leasing: Most leases limit wear to the vehicle during the lease term. You will likely have to pay extra charges for exceeding those limits if you return the vehicle.

Buying: There are no limits or charges for excessive wear to the vehicle, but excessive wear will lower the vehicle's trade-in or resale value.

End of term

Leasing: At the end of the lease (typically 2-4 years), you may have a new payment either to finance the purchase of the existing vehicle or to lease another vehicle.

Buying: At the end of the loan term (typically 4-6 years), you have no further loan payments.

Consider beginning, middle, and end-of-lease costs

At the beginning of the lease, you may have to pay your first monthly payment; a refundable security deposit or your last monthly payment; other fees for licenses, registration, and title; a capitalized cost reduction (like a down payment); an acquisition fee (also called a processing or assignment fee); freight or destination charges; and state or local taxes.

During the lease, you will have to pay your monthly payment; any additional taxes not included in the payment such as sales, use, and personal property taxes; insurance premiums; ongoing maintenance costs; and any fees for late payment. You'll also have to pay for safety and emissions inspections and any traffic tickets. If you end your lease early, you may have to pay substantial early termination charges.

At the end of the lease, if you don't buy the vehicle, you may have to pay a disposition fee and charges for excess miles and excessive wear.

You can compare different lease offers and negotiate some terms. Consider . . .

The agreed-upon value of the vehicle--a lower value can reduce your monthly payment

Up-front payments, including the capitalized cost reduction

The length of the lease

The monthly lease payment

Any end-of-lease fees and charges

The mileage allowed and per-mile charges for excess miles

The option to purchase either at lease-end or earlier

Whether your lease includes "gap" coverage, which protects you if the vehicle is stolen or totaled in an accident.

Ask for alternatives to advertised specials and other lease offerings.

Know your rights and responsibilities

When you lease a vehicle, you have the right to

Use it for an agreed-upon number of months and miles

Turn it in at lease-end, pay any end-of-lease fees and charges, and "walk away"

Buy the vehicle if you have a purchase option

Take advantage of any warranties, recalls, or other services that apply to the vehicle.

You may be responsible for

Excess mileage charges when you return the vehicle. Your lease agreement will tell you how many miles you can drive before you must pay for extra miles and how much the per-mile charge will be.

Excessive wear charges when you return the vehicle. The standards for excessive wear, such as for body damage or worn tires, are in your lease agreement.

Substantial payments if you end the lease early. The earlier you end the lease, the greater these charges are likely to be.

For more information . . .

The federal Consumer Leasing Act and some state laws may provide you with additional consumer rights not covered in your lease agreement. For information on these laws, contact your state's consumer protection agency or attorney general's office. You also can contact


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