Poststroke aphasia : epidemiology, pathophysiology and treatment

Aphasia, the loss or impairment of language caused by brain damage, is one of the most devastating cognitive impairments of stroke. Aphasia is present in 21-38% of acute stroke patients and is associated with high short- and long-term morbidity, mortality and expenditure. Recovery from aphasia is possible even in severe cases. While speech-language therapy remains the mainstay treatment of aphasia, the effectiveness of conventional therapies has not been conclusively proved. This has motivated attempts to integrate knowledge from several domains in an effort to plan more rational therapies and to introduce other therapeutic strategies, including the use of intensive language therapy and pharmacological agents.Several placebo-controlled trials suggest that piracetam is effective in recovery from aphasia when started soon after the stroke, but its efficacy vanishes in patients with chronic aphasia. Drugs acting on catecholamine systems (bromocriptine, dexamfetamine) have shown varying degrees of efficacy in case series, open-label studies and placebo-controlled trials. Bromocriptine is useful in acute and chronic aphasias, but its beneficial action appears restricted to nonfluent aphasias with reduced initiation of spontaneous verbal messages. Dexamfetamine improves language function in subacute aphasia and the beneficial effect is maintained in the long term, but its use is restricted to highly selected samples.Pharmacological agents operating on the cholinergic system (e.g. donepezil) have shown promise. Data from single-case studies, case series and an open-label study suggest that donepezil may have beneficial effects on chronic poststroke aphasia. Preliminary evidence suggests that donepezil is well tolerated and its efficacy is maintained in the long term. Randomised controlled trials of donepezil and other cholinergic agents in poststroke aphasia are warranted.     

Juvenile myoclonic epilepsy: epidemiology, pathophysiology, and management

Juvenile myoclonic epilepsy (JME) is a common epilepsy syndrome that begins most frequently in the early teenage years. It is officially classified as a type of idiopathic generalized epilepsy and is often under-recognized or misdiagnosed. This syndrome has a strong genetic component with multiple gene mutations being associated with the clinical presentation. Based upon genetic associations, there may be multiple pathophysiologic mechanisms for the disorder; the pathophysiology has not been clearly defined. A diagnosis of JME is made using the clinical history and EEG findings. Valproic acid is the primary antiepileptic drug (AED) used for JME, but some newer AEDs may be effective alternatives. Selection of an appropriate AED is essential to the proper management of JME, because of the possibility of exacerbation of seizures by some AEDs and the adverse effect profiles of effective drugs. It is important for clinicians to understand JME to correctly diagnose and manage patients with this syndrome.     

HIV-associated neuropathic pain: epidemiology, pathophysiology and management

Peripheral neuropathy is associated with numerous systemic illnesses including HIV infection. Neuropathic pain constitutes approximately 25-50% of all pain clinic visits. Distal symmetrical polyneuropathy (DSP) is the most common form of peripheral neuropathy in individuals with HIV infection. DSP is distinguished from other forms of neuropathy on the basis of history and neurological examination. The pain associated with DSP can be debilitating. Therefore, it is important to diagnose HIV-associated DSP properly and treat the neuropathic pain in order to improve quality of life. We review the clinical manifestations, epidemiology, pathophysiology and management strategies for HIV-associated DSP.     

Antipsychotic-induced rabbit syndrome: epidemiology, management and pathophysiology

Rabbit syndrome is an antipsychotic-induced rhythmic motion of the mouth/lips, resembling the chewing movements of a rabbit. The movement consists of a vertical-only motion, at about 5Hz, with no involvement of the tongue. Usually, the involuntary movements associated with rabbit syndrome appear after a long period (in most cases months or years) of antipsychotic treatment; however, a few patients with the syndrome have had treatment histories with no antipsychotic involvement. The reported prevalence of rabbit syndrome ranges from 2.3 to 4.4% of patients treated with typical antipsychotics. There have been isolated reports of rabbit syndrome in patients treated with the atypical agents risperidone and clozapine.Patients with rabbit syndrome are most often misdiagnosed as having oral tardive dyskinesia. In such cases the key for correct diagnosis is the involvement of tardive tongue movements, which does not occur in rabbit syndrome.The treatment of rabbit syndrome is empirical, reflecting poor understanding of its neuropathology. The first step is to reduce the amount of antipsychotic treatment as much as possible. However, since, in most cases, full withdrawal of antipsychotic treatment is impossible, the syndrome cannot be completely abolished without additional measures. The next stage of treatment involves specific drugs that aim to control the syndrome. Anticholinergic drugs are the best known treatment. Rabbit syndrome does not respond to treatment with levodopa or dopamine agonists.The most striking aspect of this syndrome is its specificity. Rabbit syndrome affects only the buccal region, and within this area it involves a highly stereotyped involuntary movement. This immediately focuses attention on the basal ganglia, in particular the substantia nigra pars reticulata, which is also implicated in oral dyskinesia. Continuing neurophysiological and pharmacological research of the basal ganglia holds the key to better understanding and treatment of this syndrome in the coming years.     

Cataplexy associated with narcolepsy: epidemiology, pathophysiology and management

Although narcolepsy was first described over 100 years ago, most of what is known about the pathological changes in the CNS that are responsible for this unusual disease has been learned during the past few years. It is now known that narcolepsy is caused by the loss of a relatively few neurons that are responsible for producing the neuropeptide hypocretin in the CNS. The onset of narcolepsy typically occurs in early adulthood and may consist of a variety of symptoms; however, cataplexy (an abrupt, bilateral loss of skeletal muscle tone) is most specific to narcolepsy. TCAs were found to be beneficial for the treatment of cataplexy over 40 years ago and, more recently, the SSRIs have been used to treat the condition. The recent availability of sodium oxybate (the first drug to receive regulatory approval for the treatment of cataplexy) represents a significant advance in the treatment of narcolepsy, as it is highly efficacious for the treatment of cataplexy and shows promise for the treatment of excessive sleepiness and for improving sleep quality in patients with narcolepsy.     

Seizures in alcohol-dependent patients: epidemiology, pathophysiology and management

The relationship between alcohol and seizures is complex and multifaceted. The prevalence of epilepsy in alcohol-dependent patients of western industrialised countries may be at least triple that in the general population, whereas the prevalence of alcoholism is only slightly higher in patients with epilepsy than in the general population. The seizure threshold is raised by alcohol drinking and declines on cessation of drinking. As a result, during withdrawal from alcohol, usually 6-48 hours after the cessation of drinking, seizures may occur. Alcohol acts on the brain through several mechanisms that influence seizure threshold. These include effects on calcium and chloride flux through the ion-gated glutamate NMDA and GABA receptors. During prolonged intoxication, the CNS adapts to the effects of alcohol, resulting in tolerance; however, these adaptive effects seem to be transient, disappearing after alcohol intake is stopped. Although the relationship of seizures to alcohol use is likely to be dose dependent and causal, the available clinical data do not suggest that alcohol use results in seizure genesis. However, a genetic predisposition to alcohol withdrawal seizures is possible. Other seizures in alcohol-dependent individuals may be due to concurrent metabolic, toxic, infectious, traumatic, neoplastic and cerebrovascular diseases and are frequently partial-onset seizures. Alcohol abuse is a major precipitant of status epilepticus (9-25% of cases), which may even be the first-ever seizure type. Prompt treatment of alcohol withdrawal seizures is recommended to prevent status epilepticus. During the detoxification process, primary and secondary preventative measures can be taken. A meta-analysis of controlled trials for the primary prevention of alcohol withdrawal seizures demonstrated a highly significant risk reduction for seizures with benzodiazepines and antiepileptic drugs and an increased risk with antipsychotics. A meta-analysis of randomised, placebo-controlled trials for the secondary prevention of seizures after alcohol withdrawal showed lorazepam to be effective, whereas phenytoin was ineffective. Because withdrawal seizures do not recur if the patient remains abstinent, long-term administration of antiepileptic drugs is unnecessary in abstinent patients. The first seizure not related to alcohol withdrawal should not result in permanent drug treatment in an alcohol-dependent patient, because of poor compliance and the high likelihood of remission. The treatment of alcohol dependence is more important and should be prioritised before the prevention of further seizures.     

Delirium in critically ill patients: epidemiology, pathophysiology, diagnosis and management

Delirium is commonly observed in critically ill patients and is associated with negative outcomes. The pathophysiology of delirium is not completely understood. However, alterations to neurotransmitters, especially acetylcholine and dopamine, inflammatory pathways and an aberrant stress response are proposed mechanisms leading to intensive care unit (ICU) delirium. Detection of delirium using a validated delirium assessment tool makes early treatment possible, which may improve prognosis. Patients at high risk of delirium, especially those with cognitive decline and advanced age, should be identified in the first 24 hours of admission to the ICU. Whether these high-risk patients benefit from haloperidol prophylaxis deserves further study. The effectiveness of a multicomponent, non-pharmacological approach is shown in non-ICU patients, which provides proof of concept for use in the ICU. The few studies on this approach in ICU patients suggest that the burden of ICU delirium may be reduced by early mobility, increased daylight exposure and the use of earplugs. In addition, the combined use of sedation, ventilation, delirium and physical therapy protocols can reduce the frequency and severity of adverse outcomes and should become part of routine practice in the ICU, as should avoidance of deliriogenic medication such as anticholinergic drugs and benzodiazepines. Once delirium develops, symptomatic treatment with antipsychotics is recommended, with haloperidol being the drug of first choice. However, there is limited evidence on the safety and effectiveness of antipsychotics in ICU delirium.     

Chronic non-infectious uveitis in the elderly: epidemiology, pathophysiology and management

Intraocular inflammatory diseases are collectively known as uveitis. The aetiology of this condition can be diverse, as inflammation may result from direct involvement of the uveal tract or indirect inflammation of adjacent tissues. Uveitis can present challenges to diagnosis and treatment, and is potentially a severe sight-threatening disease. In the elderly, uveitis can present de novo after the age of 60 years or may represent a process earlier in life continuing after the age of 60 years, although many cases will have become quiescent by that time. More recent studies suggest that uveitis presenting after 60 years of age is more common than previously believed. Most cases of uveitis are of unknown aetiology and are classed as idiopathic, although sarcoidosis, ocular ischaemia and birdshot chorioretinopathy are recognised non-infectious causes of uveitis in the elderly. Systemic immunosuppression, with its well known complications, may be required to preserve vision. In this age group, one should always have high suspicion of a masquerade syndrome, particularly a primary CNS non-Hodgkin's lymphoma. With the demographics of the elderly population changing and mean life expectancy increasing, it is important that clinicians are familiar with uveitis as a potential cause of visual impairment in this age group.     

Neuropsychiatric manifestations in systemic lupus erythematosus: epidemiology, pathophysiology and management

Systemic lupus erythematosus (SLE) is a relapsing-remitting autoimmune disease with CNS involvement occurring in up to 75% of patients. However, the frequency of neuropsychiatric manifestations in SLE studies varies widely, depending on the type of manifestations included and the method used for evaluation. CNS involvement may be considered primary if directly related to SLE activity in the CNS or secondary when related to treatment, infections, metabolic abnormalities or other systemic manifestations such as uraemia and hypertension. The pathogenesis of neuropsychiatric SLE is as yet unknown, though numerous autoantibodies and cytokines have been suggested as possible mediators. However, independent of the aetiology of the insult, the final common pathway in neuropsychiatric SLE is the involvement of the cerebral microvasculature. The diagnosis of primary CNS involvement by SLE is often difficult, as both focal and diffuse manifestations may occur and there is no gold standard for diagnosis. A high index of clinical suspicion, in addition to laboratory and neuroimaging findings may support the diagnosis. Treatment is mostly empirical, although one randomized controlled trial has shown that cyclophosphamide in addition to methylprednisolone is superior to methylprednisolone alone in severe neuropsychiatric SLE.     

Postanaesthetic shivering: epidemiology, pathophysiology, and approaches to prevention and management.

Along with nausea and vomiting, postanaesthetic shivering is one of the leading causes of discomfort for patients recovering from general anaesthesia. The distinguishing factor during electromyogram recordings between patients with postanaesthetic shivering and shivering in fully awake patients is the existence of clonus similar to that recorded in patients with spinal cord transection. Clonus coexists with the classic waxing and waning signals associated with cutaneous vasoconstriction (thermoregulatory shivering). The primary cause of postanaesthetic shivering is peroperative hypothermia, which sets in because of anaesthetic-induced inhibition of thermoregulation. However, shivering associated with cutaneous vasodilatation (non-thermoregulatory shivering) also occurs, one of the origins of which is postoperative pain. Apart from causing discomfort and aggravation of pain, postanaesthetic shivering increases metabolic demand proportionally to the solicited muscle mass and the cardiac capacity of the patient. No link has been demonstrated between the occurrence of shivering and an increase in cardiac morbidity, but it is preferable to avoid postanaesthetic shivering because it is oxygen draining. Prevention mainly entails preventing peroperative hypothermia by actively rewarming the patient. Postoperative skin surface rewarming is a rapid way of obtaining the threshold shivering temperature while raising the skin temperature and improving the comfort of the patient. However, it is less efficient than certain drugs such as meperidine, clonidine or tramadol, which act by reducing the shivering threshold temperature.     

Sleep apnoea in the older adult : pathophysiology,epidemiology, consequences and management

Sleep apnoea is a breathing disorder in sleep usually caused by repetitive upper airway obstruction. Its primary symptoms include snoring, daytime sleepiness and decreased cognitive functioning. Risk factors for the condition include obesity, anatomical abnormalities, aging, and family history. It has been associated with hypertension, cardiovascular and pulmonary diseases and increased mortality. The prevalence of sleep apnoea increases with age, although the severity of the disorder, as well as the morbidity and mortality associated with it, may actually decrease in the elderly. A decline in cognitive functioning in older adults with sleep apnoea may resemble dementia. Medical management of sleep apnoea rarely relies on drug treatment, as the few drugs (antidepressants and respiratory stimulants) tested for treatment have been found to be ineffective, or cause tolerance or serious adverse effects and complications. The treatment of choice for sleep apnoea is continuous positive airway pressure, a device which generates positive air pressure through a nose mask, creating a splint which keeps the airway unobstructed throughout the night. Weight loss significantly decreases or eliminates apnoeas. Oral appliances are used to enlarge the airway at night by moving the tongue and mandible forward. Positional therapy involves avoiding the supine position during sleep in patients who mostly have apnoeas while lying on their back. Surgical management may also be considered, although with great caution in the elderly, because of their increased risk of complications related to surgery. Surgical procedures include nasal reconstruction, somnoplasty, laser-assisted uvuloplasty, uvulopalatopharyngoplasty, genioglossus advancement and hyoid myotomy, and maxillomandibular advancement for severe cases when other treatments have failed. As a last option, tracheostomy may be performed.     

Erectile dysfunction following radical retropubic prostatectomy: epidemiology, pathophysiology and pharmacological management

Radical prostatectomy has been the time-honoured and standard treatment option for prostate cancer. Erectile dysfunction (ED) is one of the common quality-of-life issues following radical prostatectomy. The recovery of potency following radical prostatectomy varies from 16% to 86%. Although major modifications in surgical technique appear to be promising, the reported ED rates are still high. The time period required for the recovery of erectile function after surgery varies from 6 to 24 months. During this period of neuropraxia lack of natural erections produces cavernosal hypoxia. This cavernosal hypoxia has been implicated as one of the most important factors in the pathophysiology of ED. Cavernosal hypoxia predisposes to cavernosal fibrosis, ultimately producing venous leak and long-term ED. Interruption of this cascade of events has been the major challenge for physicians. Physicians have several options available for the treatment of ED. However, oral treatment options have quickly become established as first-line treatment options. Sildenafil has been most extensively studied in the radical prostatectomy population. In patients who do not respond to oral therapy alone, standard treatment options (intracavernosal injections, vacuum constriction devices and intraurethral alprostadil) are useful. Use of penile prostheses is one of the oldest treatment options available for the treatment of ED but is used only as a last resort. Initial attempts to promote the earlier recovery of erectile function appear to be promising. However, further confirmatory studies are essential. The roles of gene transfer and growth factors are still in experimental stages. In this review we discuss the epidemiology, pathophysiology and treatment options available for ED following radical prostatectomy.     

Severe asthma: epidemiology,pathophysiology and treatment

Severe asthma is poorly understood clinically, physiologically and pathologically. Whereas milder forms of asthma are generally easily treated, more severe forms often remain refractory to the best current medical care. Although some asthmatics have been severely affected for most of their lives, there appears to be a second group that develops severe disease in adulthood. Additionally, it is not clear which genetic and environmental elements may be most important in the development of severe disease. Physiologically, these patients often have airtrapping and may have loss of elastic recoil, as well. The pathology demonstrates a heterogeneity of findings, including continued eosinophilic inflammation, structural changes, and distal disease. Treatment is problematic and will probably remain so until a better understanding of this disease develops.     

Mood disorders in patients with epilepsy: epidemiology and management

Patients with epilepsy are at high risk for depression because of an incompletely understood combination of factors that may be both psychosocial and neurological. Interictal depression in patients with epilepsy is an undertreated condition, in part because of concern regarding drug interactions and the risk of exacerbating seizures with antidepressant treatment. Bipolar disorder is not described as occurring with a higher than expected frequency in the population with epilepsy, but high rates of depression and suicide are well recognised, highlighting the need for more emphasis on antidepressive treatment in this group of at-risk patients. Neurological factors, including site and lateralisation of seizure focus, may be important for the development of depression, with left-sided seizure foci having a higher association with depressive symptoms. Forced normalisation may be a factor in the paradoxical onset of depression in patients with epilepsy whose seizures suddenly become well controlled by anti-seizure treatment. Lowering of folic acid levels by some antiepileptic drugs (AEDs) may also influence the expression of depression in patients with epilepsy. New AEDs continue to emerge as beneficial treatments themselves for mood disorders, with lamotrigine, gabapentin and, to a lesser extent, topiramate having clinical trials data to support their use in patients with bipolar disease. Similar positive data are available for vagal nerve stimulation. Mood effects of AEDs can be complicated, however, as many of these drugs (e.g. tiagabine) have also been reported to cause depression as an adverse effect. Electroconvulsive therapy in depressed patients with epilepsy requires special consideration. The selective serotonin reuptake inhibitors (SSRIs) and antidepressants that act at multiple receptors (e.g. nefazodone, venlafaxine) are the most appropriate treatments for depressed patients with epilepsy. Among these agents, citalopram has a low risk of interactions with AEDs. Bupropion, clomipramine and maprotiline are associated with a greater risk of seizures compared with other antidepressants and consequently should be used with caution in the treatment of depression in patients with epilepsy.     

HIV-associated peripheral neuropathy: epidemiology, pathophysiology and treatment

Peripheral neuropathy is the most frequent neurological complication associated with human immunodeficiency virus type 1 (HIV) infection and advanced acquired immunodeficiency syndrome (AIDS). There are at least 6 patterns of HIV-associated peripheral neuropathy, although these diagnoses are often overlooked or misdiagnosed. Distal symmetrical polyneuropathy (DSP) is the most common form of peripheral neuropathy in HIV infection. DSP occurs mainly in patients with advanced immunosuppression and may also be secondary to the neurotoxicity of several antiretroviral agents. Treatment of painful DSP is primarily symptomatic, while pathogenesis-based therapies are under investigation. Reduction or discontinuation of neurotoxic agents should be considered if possible. Inflammatory demyelinating polyneuropathy (IDP) can present in an acute or chronic form. The acute form may occur at the time of primary HIV infection or seroconversion. Cerebrospinal fluid lymphocytic pleocytosis (10 to 50 cells/mm3) is helpful in the diagnosis of HIV-associated IDP. Treatment consists of immunomodulatory therapy. Progressive polyradiculopathy (PP) most commonly occurs in advanced immunosuppression and usually is caused by cytomegalovirus (CMV) infection. Rapidly progressive flaccid paraparesis, radiating pain and paresthesias, areflexia and sphincter dysfunction are the cardinal clinical features. Rapid diagnosis and treatment with anti-CMV therapy are necessary to prevent irreversible neurological deficits resulting from nerve root necrosis. Mononeuropathy multiplex (MM) that occurs in early HIV infection is characterised by self-limited sensory and motor deficits in the distribution of individual peripheral nerves. In advanced HIV infection, multiple nerves in two or more extremities or cranial nerves are affected. Treatment includes immunomodulation or anti-CMV therapy. Autonomic neuropathy may be caused by central or peripheral nervous system abnormalities. Treatment is supportive with correction of metabolic or toxic causes. Diffuse infiltrative lymphocytosis syndrome (DILS) presents as a Sj?gren's-like disorder with CD8 T cell infiltration of multiple organs. Antiretroviral therapy and steroids may be effective treatments.     

Pathological laughing and crying : epidemiology, pathophysiology and treatment

Pathological laughing and crying (PLC) is characterized by frequent, brief, intense paroxysms of uncontrollable crying and/or laughing due to a neurological disorder. When sufficiently frequent and severe, PLC may interfere with the performance of activities of daily living, interpersonal functioning, or both, and is a source of distress for affected patients and their families. PLC is also often misunderstood by patients and their families, and is under-recognized by the clinicians caring for patients with this disorder. However, this syndrome is easily recognized when understood properly and is highly responsive to treatment with a variety of pharmacological agents.This review aims to facilitate the diagnosis and treatment of patients with PLC, and begins by providing definitions of mood and affect that will help clinicians distinguish between mood disorders, such as major depression and mania, and disorders of affect, such as PLC. In addition, the various terms used to describe this syndrome are reviewed and a recommendation for the use of the term PLC is made. The core clinical features of PLC are also presented and the epidemiology of this syndrome is reviewed. A discussion of the pathophysiology of PLC, including the neuroanatomic and neurochemical bases, is provided. Finally, the evaluation and treatment of patients with PLC is described.Based on the pathophysiology of PLC and on a detailed review of published treatment studies, SSRIs are recommended as first-line pharmacotherapy for this disorder. When SSRIs are ineffective or poorly tolerated, other treatment options, including TCAs, noradrenergic reuptake inhibitors, novel antidepressants, dopaminergic agents and uncompetitive NMDA receptor antagonists may be useful second-line treatments.     

Neurologically presenting Wilson's disease: epidemiology, pathophysiology and treatment

Wilson's disease is a rare autosomal recessive disease of copper accumulation and copper toxicity, due to mutations in the ATP7B gene, which leads to a failure of copper excretion in the bile. It presents clinically primarily as liver disease, psychiatric disease, neurological disease, or a combination of these. The neurological disease is a movement disorder, with abnormalities of speech, tremor, incoordination and dystonia being common features. Diagnosis of neurologically presenting patients is usually straightforward, with Kayser-Fleischer rings and a urine copper over 100 microg/day almost invariably present. In the treatment of neurologically presenting patients, penicillamine should always be avoided, because of the high risk of permanent, drug-induced, additional neurological deterioration. A new drug we have developed, tetrathiomolybdate, given for 8-16 weeks, in combination with zinc, is our first choice for treating these patients. In the absence of availability of tetrathiomolybdate, zinc or trientine are the next best choices.     

Tinnitus in the older adult: epidemiology, pathophysiology and treatment options

Tinnitus is the perception of sound in the absence of an apparent acoustic stimulus. More than 35 million Americans experience tinnitus, with 2-3 million severely debilitated by this distressing symptom. The prevalence increases with age and there is a high incidence associated with both noise-induced and age-related hearing loss. Although there are several theories regarding the pathophysiology of tinnitus, the precise mechanism remains to be elucidated. The most compelling of these is the hypothesis that tinnitus occurs as a result of spontaneous and aberrant neural activity at any level along the auditory axis, even after cochlear nerve transection or labyrinthine ablation.There are numerous aetiologies associated with tinnitus. Tinnitus, in clinical practice, is characterised as either objective or subjective. The distinction is relevant in terms of both aetiology and treatment. Despite a large number of therapeutic interventions and studies claiming success in treating tinnitus, a cure remains elusive. However, there are several potential treatment options that offer patients varying degrees of symptomatic improvement and enhanced quality of life.It is imperative to formulate a rational and systematic approach in evaluating an older adult with tinnitus. An individualised treatment regimen and the creation of a strong therapeutic relationship are the hallmarks of successful management of the patient with tinnitus.     

Anthracycline-induced cardiotoxicity: course, pathophysiology, prevention and management

Although effective anti-neoplastic agents, anthracyclines are limited by their well recognized and pervasive cardiotoxic effects. The incidence of late progressive cardiovascular disease in long-term survivors of cancer is established and may contribute to heart failure and death. To maximize the benefits of these drugs, a high-risk population has been identified and new strategies have been investigated to minimize toxic effects, including limiting the cumulative dose, controlling the rate of administration and using liposomal preparations and novel anthracycline analogues. Dexrazoxane also shows promise as a cardioprotectant during treatment. This paper reviews these strategies, as well as medications used to manage anthracycline-induced cardiotoxicity, and functional and biochemical means of monitoring cardiotoxicity, including echocardiography, radionuclide scans and biomarker analysis. The treatment of adult cancer survivors who have had anthracycline-related cardiotoxicity has not been systematically studied. Empirically, anthracycline-associated cardiac dysfunction is treated very similarly to other forms of heart failure. These treatments include avoiding additional cardiotoxic regimens, controlling hypertension, lifestyle changes, medications and heart transplantation.