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PubMed2005

Emerging therapies in narcolepsy-cataplexy.

In the past, narcolepsy was primarily treated using amphetamine-like stimulants and tricyclic antidepressants. Newer and novel agents, such as the wake-promoting compound modafinil and more selective reuptake inhibitors targeting the adrenergic, dopaminergic, and/or serotoninergic reuptake sites (ie, venlafaxine, atomoxetine) are better-tolerated available alternatives. The development of these agents, together with sodium oxybate (a slow-wave sleep-enhancing agent that consolidates nocturnal sleep, reduces cataplexy, and improves sleepiness), has led to improved functioning and quality of life for many patients with the disorder. However, these treatments are all symptomatically based and do not target hypocretin, a major neurotransmitter involved in the pathophysiology of narcolepsy. In this review, we discuss emerging therapies in the area of narcolepsy. These include novel antidepressant or anticataplectic, wake-promoting, and hypnotic compounds. We also report on novel strategies designed to compensate for hypocretin deficiency and on the use of immunosupression at the time of narcolepsy onset.

Genetic Therapy↗

PubMed2006

ADHD: new pharmacological treatments on the horizon.

Attention-deficit/hyperactivity disorder (ADHD) is the most common neurobehavioral disorder affecting school-age children. In many cases, symptoms persist into adolescence and adulthood, causing significant lifelong impairments in academic, career, and social functioning. The stimulants methylphenidate and amphetamines have been used for decades as first-line therapy for the treatment of ADHD. Short-acting stimulant formulations control symptoms only for a few hours, creating the need for multiple daily doses of the medication. For school-age children, this necessitates administering medication during school hours, creating the potential for embarrassment and noncompliance. To offset these problems, longer acting stimulant formulations have been developed. Long-acting medications often control symptoms for up to 8 hours with only one daily dose of the medication, eliminating the need for in-school administration. Some long-acting stimulants are designed to control symptoms for up to 10 to 12 hours. Although stimulants are effective in most cases, some children are unable to tolerate these medications. Nonstimulant options are available for the treatment of ADHD and include atomoxetine, alpha-adrenergic agents, and antidepressants. Of these, atomoxetine is the only medication approved to treat ADHD. In spite of the number of medications available for the management of ADHD, treatment options with greater flexibility and reduced side effects are still desirable. A transdermal methylphenidate patch has recently been approved, and advances to existing stimulants currently under development include an amphetamine prodrug and a longer acting formulation of amphetamine. In addition, a number of nonstimulant entities, including guanfacine and modafinil, are under development for the treatment of ADHD.

Adrenergic Uptake Inhibitors↗

PubMed2006

Drugs for sleep disorders: mechanisms and therapeutic prospects.

The past decade has witnessed an explosion of knowledge about the neural mechanisms that control sleep and arousal, triggered by two discoveries relating to the sleep disorder narcolepsy. Narcolepsy is caused by the loss of orexin-containing neurons in the hypothalamus, and a novel nonstimulant wakefulness-promoting drug, modafinil, alleviates excessive day-time sleepiness associated with the disorder. The level of arousal is controlled by an intricate interplay between distinct wakefulness- and sleep-promoting nuclei situated in the hypothalamus and brainstem and the interconnections between the nuclei and the neurotransmitters involved have been mapped. Wakefulness-promoting nuclei include the orexinergic lateral hypothalamic/perifornical area, the histaminergic tuberomammillary nucleus, the cholinergic pedunculopontine tegmental nucleus, the noradrenergic locus coeruleus, the 5-hydroxytryptaminergic raphe nuclei and possibly the dopaminergic ventral tegmental area. The major sleep-promoting nucleus is the GABAergic ventrolateral preoptic nucleus of the hypothalamus. Currently available and future drugs exert their therapeutic effects in the three major classes of sleep disorder (insomnia, hypersomnia, parasomnia) by modifying neurotransmission at distinct sites within the arousal-controlling neuronal network. This enables classification of therapeutic drugs for sleep disorders on the basis of their modes of action: drugs that interact with the GABAergic sleep-promoting system, drugs that interact with different wakefulness-promoting systems and drugs that modulate the level of arousal by mechanisms that do not initially involve the basic network (e.g. melatonin, adenosine). The development of novel therapeutic drugs for sleep disorders is based on the synthesis of molecular/cellular mechanisms and the sites of action within the arousal-controlling neuronal network.

Adenosine↗

PubMed2006

Abusive prescription of psychostimulants: a study of two cases.

Because psychostimulants have serious possible side effects and particular potential for abuse, their therapeutic indications are today exclusively limited to disorders such as obesity, narcolepsy, or attention deficit/hyperactivity disorder. We report two cases of abusive prescription of these drugs. The first concerns a woman who was treated for a 3 kg weight gain with fenproporex for 5 years and presented a withdrawal syndrome when this drug was no longer marketed in France. In the second case, a woman who complained of atypical sleep problems was prescribed modafinil, methylphenidate, clobazam, lormetazepam, meprobamate, and aceprometazine, and was found dead in her home a few weeks later in unexplained circumstances. For these two patients, neither the indications, nor the contraindications, nor the prescribing rules for these restricted drugs had been complied with. This case report highlights the extreme danger of these substances and stresses the importance of adhering to the rules of prescription.

Adult↗

PubMed2003

Fatigue associated with multiple sclerosis: diagnosis, impact and management.

In patients with multiple sclerosis (MS) fatigue is the most common symptom and one of the most disabling features. As many as 40% have described it as the single most disabling symptom--a higher percentage than weakness, spasticity, motor problems, or bowel or bladder problems. The etiology and pathophysiology of MS-related fatigue remain unknown. Studies have failed to demonstrate an association between MS-related fatigue and the level of disability, clinical disease subtype, or gender, although recent data show an association between MS-related fatigue and depression and quality of life. Imaging studies using positron emission tomography suggest that fatigue in MS is related to hypometabolism of specific brain areas, including the frontal and subcortical circuits. The impact of fatigue on patient functioning and quality of life clearly warrants intervention. In addition to nonpharmacologic measures, such as exercise and energy conservation strategies, several pharmacologic agents have been evaluated for their ability to reduce MS-related fatigue, including amantadine, central nervous system stimulants (pemoline), and the novel wake-promoting agent modafinil.

Amantadine↗

PubMed2004

Fluctuations in cognition and alertness in Parkinson's disease and dementia.

Fluctuations in cognition and alertness (FC/FA) are key manifestations of dementia with Lewy bodies (DLB) and also have been recognized recently in patients with Parkinson's disease (PD) with dementia, a condition that shares important clinical, genetic, and neuropathologic characteristics with DLB. A comprehensive assessment of potential episodes of FC/FA is required for adequate clinical management, and several interesting clinical instruments are being developed for that purpose. FC/FA should be differentiated from episodes of excessive daytime sleepiness (EDS). Such diagnostic differentiation appears to be necessary, particularly in the light of the different therapeutic approaches to FA and EDS. Based on the deficit in cholinergic transmission observed in DLB patients, cholinesterase inhibitors, such as rivastigmine, may have a beneficial effect on FC/FA. Other therapies, such as melatonin or modafinil, require further investigation.

Awareness↗

PubMed2005

Neurostimulant medication usage during stroke rehabilitation: the Post-Stroke Rehabilitation Outcomes Project (PSROP).

Motor recovery after a stroke depends upon many upon different modalities. Intensive therapy using compensatory and facilitatory techniques is the primary method to improve movement and function in affected extremities. However, medications used to modulate neurotransmitters may be useful in augmenting therapy approaches. The Post-Stroke Rehabilitation Outcomes Project (PSROP) database was used to describe the frequency of prescribing neurostimulant medications; the types of neurostimulant medications used; and how the use of neurostimulant medications affected rehabilitation length of stay, motor recovery, cognitive recovery, and discharge destination. Of the 1,161 patients in the PSROP database, 929 (80.0%) patients did not receive any treatment with methylphenidate, modafinil, levodopa, amantadine, or bromocriptine. Patients who received neurostimulant medications did not have any more significant changes in length of stay, motor recovery, cognitive recovery, or discharge destination than patients who did not receive neurostimulant medications. Much research needs to be completed before clinicians know precisely whether and how rehabilitation therapies and medications interact to assist in functional recovery.

Aged↗

PubMed2006

Pharmacological management of sleep apnoea.

Obstructive sleep apnoea poses a significant health hazard that is associated with leading causes of mortality and morbidity. Nasal continuous positive airway pressure is the primary treatment modality, with surgical treatments as alternatives. Oral appliances and pharmacological therapy remain adjunctive modalities. Non-specific treatments include weight loss, postural therapy and behavioural measures. Pharmacotherapy goals include the reduction of risk factors for sleep apnoea; correction of underlying predisposing metabolic diseases, such as hypothyroidism or acromegaly; treatment of associated symptoms, including excessive daytime sleepiness; and prevention of apnoeas/hypopnoeas. This paper reviews data supporting the treatment of sleep apnoea with various pharmacological agents, including intranasal corticosteroids, decongestant sprays, nicotine therapy, opiate antagonists, methylxanthine derivatives, oestrogen and progesterone, testosterone, thyroid hormone, growth hormone therapy for acromegaly, beta-blockers, alpha-adrenergic agonists, angiotensin-converting enzyme inhibitors, glutamate antagonists, acetazolamide, selective serotonin re-uptake inhibitors, tricyclic antidepressants, physostigmine, modafinil and TNF-alpha antagonists, in addition to supplemental oxygen, and carbon dioxide inhalation. Some of these drugs have received very little testing and are the subject of few research articles.

Disease Management↗

PubMed2006

Neuroprotective agents in schizophrenia and affective disorders.

With the exception of dementia, the use of neuroprotective agents in psychiatric disorders is not yet well established. However, recent data from brain imaging studies and clinical trials support the view that neurodegenerative mechanisms may play a role in the pathophysiology of schizophrenia and affective disorders. Further evidence for the use of neuroprotective agents can be drawn from the findings that second-generation antipsychotics, mood stabilizers and antidepressants have been shown to have neuroprotective effects in vitro and in vivo. Neuroprotective agents as add-on therapies (e.g., modafinil, erythropoietin, glycine, D-serine, memantine and celecoxib) are currently being evaluated in schizophrenia and related disorders. This paper reviews the current options for neuroprotective treatment approaches focusing on schizophrenia and affective disorders.

Animals↗

PubMed2001

Medications for the treatment of narcolepsy.

Narcolepsy is a syndrome of unknown aetiology characterised by excessive daytime sleepiness (often severe) usually in association with cataplexy (brief episodes of partial or complete muscle paralysis) and often with other uncommon symptoms. Due to limited disease-specific knowledge, medication treatment for this condition has focussed on specific symptom amelioration rather than improving or eliminating underlying disease mechanisms. Such treatment generally consists of stimulants for daytime sleepiness and anticataplectic medication for cataplexy; hence, both types of agents are reviewed in this article. Recent discoveries, including the finding that canine familial narcolepsy is caused by a single gene defect in the hypocretin receptor, coupled with the findings in human narcoleptics of undetectable hypocretin levels in the CSF and of severe hypocretin-containing neuronal atrophy in brains of deceased narcoleptics, have shifted the focus of narcolepsy treatment research to the hypocretin system. The hope is that a single agent can be developed to provide effective treatment for all symptoms of narcolepsy. While the mechanism of action in narcolepsy is unknown, gamma-hydroxybutyrate (GHB) is proving to be such an agent. Interestingly, GHB is not known to impact hypocretin pathways in the brain, yet specific research exploring this possible interaction has not been performed. The market for medications limited to use by narcoleptics is small because of the relatively low prevalence of narcolepsy; however, the prevalence of clinically important daytime sleepiness and/or fatigue is surprisingly high. New agents that effectively manage the sleepiness of narcolepsy thus have a much larger potential for appropriate use in treating sleepiness and fatigue in the general population. This fact has recently been demonstrated by the tremendous success of modafinil, a drug introduced to the market a little over 2 years ago, which was developed to treat sleepiness in narcolepsy but now is used in a much larger patient population.

Journal Article↗

PubMed2004

New drugs for the treatment of attention-deficit/hyperactivity disorder.

Attention-deficit/hyperactivity disorder (ADHD) is the most common neuropsychiatric disorder of childhood. Recent research indicates that ADHD most often persists into adolescence and adulthood, and is associated with impairments in academic, social and occupational functioning. The ADHD diagnosis is based on history and clinical examination. There are no objective laboratory measures for diagnosis. ADHD is largely heritable. Its underlying pathophysiology has been theorised to include dysregulation of inhibitory noradrenergic frontocortical activity on dopaminergic striatal structures. Evidence shows that ADHD is highly responsive to pharmacological treatments resulting in global functional improvements. Although pharmacotherapy is recognised as the most effective treatment, additional components to optimise ADHD management include proper educational placement, parent management training and social skills development. Central nervous system stimulants, specifically methylphenidate and amphetamine, remain first-line pharmacological treatments. Atomoxetine, a selective noradrenergic re-uptake inhibitor, is the first non-stimulant compound to receive FDA approval for paediatric and adult ADHD. Other medication classes, including alpha-agonist antihypertensives, tricyclic antidepressants, other antidepressants such as buproprion, and the wake-promoting agent modafinil, are prescribed in off-label therapy. Ongoing development of new ADHD medications is expected to emphasise alternative and extended-release delivery systems and non-stimulant compounds.

Amphetamines↗

PubMed2003

Pharmacogenomics in the treatment of narcolepsy.

Narcolepsy is a neurological disorder characterized by excessive daytime sleepiness and cataplexy. Available treatments of narcolepsy include stimulants and antidepressants but the recent discovery of orexin/hypocretin deficiency in narcolepsy opens up new perspectives. Narcolepsy is a complex disorder involving genetic, immune and environmental factors. Although only a strong association is found with the HLA DQB1*0602 gene, other genetic susceptibility factors might be involved. Among these, the functional polymorphism of the catechol-O-methyltransferase (COMT) gene is critically involved in the severity of narcolepsy and in the response to the stimulant modafinil. Other pharmacogenetic targets include the orexinergic, noradrenergic and possibly the serotonergic pathways.

Carrier Proteins↗

PubMed2006

Innovations and recent trends in the treatment of ADHD.

Initiatives to develop better-tolerated, more efficacious pharmacological agents with improved drug delivery systems have driven recent research in attention-deficit hyperactivity disorder (ADHD). While stimulants are the primary pharmacotherapy for ADHD, these drugs have a limited duration of action and a subset of patients will either fail to respond to these medications or have side effects that preclude their use. The development of atomoxetine, the first nonstimulant approved for ADHD, has been followed by additional innovative research, such as the methylphenidate transdermal system, modafinil, NRP-104 and cholinergic agents. This review highlights some of the recent trends in ADHD treatment and the current status of promising treatment options that may help to shape the future of ADHD treatment.

Adrenergic alpha-Agonists↗

PubMed2003

Narcolepsy in the older adult: epidemiology, diagnosis and management.

Narcolepsy is a disorder of impaired expression of wakefulness and rapid-eye-movement (REM) sleep. This manifests as excessive daytime sleepiness and expression of individual physiological correlates of REM sleep that include cataplexy and sleep paralysis (REM sleep atonia intruding into wakefulness), impaired maintenance of REM sleep atonia (e.g. REM sleep behaviour disorder [RBD]), and dream imagery intruding into wakefulness (e.g. hypnagogic and hypnopompic hallucinations). Excessive sleepiness typically begins in the second or third decade followed by expression of auxiliary symptoms. Only cataplexy exhibits a high specificity for diagnosis of narcolepsy. While the natural history is poorly defined, narcolepsy appears to be lifelong but not progressive. Mild disease severity, misdiagnoses or long delays in cataplexy expression often cause long intervals between symptom onset, presentation and diagnosis. Only 15-30% of narcoleptic individuals are ever diagnosed or treated, and nearly half first present for diagnosis after the age of 40 years. Attention to periodic leg movements (PLM), sleep apnoea and RBD is particularly important in the management of the older narcoleptic patient, in whom these conditions are more likely to occur. Diagnosis requires nocturnal polysomnography (NPSG) followed by multiple sleep latency testing (MSLT). The NPSG of a narcoleptic patient may be totally normal, or demonstrate the patient has a short nocturnal REM sleep latency, exhibits unexplained arousals or PLM. The MSLT diagnostic criteria for narcolepsy include short sleep latencies (<8 minutes) and at least two naps with sleep-onset REM sleep. Treatment includes counselling as to the chronic nature of narcolepsy, the potential for developing further symptoms reflective of REM sleep dyscontrol, and the hazards associated with driving and operating machinery. Elderly narcoleptic patients, despite age-related decrements in sleep quality, are generally less sleepy and less likely to evidence REM sleep dyscontrol. Nonpharmacological management also includes maintenance of a strict wake-sleep schedule, good sleep hygiene, the benefits of afternoon naps and a programme of regular exercise. Thereafter, treatment is highly individualised, depending on the severity of daytime sleepiness, cataplexy and sleep disruption. Wake-promoting agents include the traditional psychostimulants. More recently, treatment with the 'activating' antidepressants and the novel wake-promoting agent modafinil has been advocated. Cataplexy is especially responsive to antidepressants which enhance synaptic levels of noradrenaline (norepinephrine) and/or serotonin. Obstructive sleep apnoea and PLMs are more common in narcolepsy and should be suspected when previously well controlled older narcolepsy patients exhibit a worsening of symptoms. The discovery that narcolepsy/cataplexy results from the absence of neuroexcitatory properties of the hypothalamic hypocretin-peptidergic system will significantly advance understanding and treatment of the symptom complex in the future.

Adult↗

PubMed2003

Excessive daytime sleepiness and sleep disturbances in patients with neurological diseases: epidemiology and management.

Up to 12% of the general population experience excessive daytime sleepiness (EDS), with increasing prevalence in the elderly. EDS may lead to cognitive impairment, resulting in inattentiveness, poor memory, mood disorders and an increased risk of accidents. As a result, quality of life is reduced in most patients with EDS as well as in their caregiving spouses. There are a variety of causes leading to EDS, including CNS pathology, neurological dysfunction, associated sleep disorders with insufficient or fragmented sleep, and drug therapy. Since EDS accompanies many neurological disorders, such as neurodegenerative and neuromuscular diseases, neurologists should be familiar with the diagnosis, its major causes and with treatment options. The main focus of this article is on movement disorders, neuromuscular diseases, multiple sclerosis, dementia, cerebrovascular diseases, head and brain trauma, pain and epilepsy. General management strategies for EDS in all these neurological diseases include sleep hygiene aspects such as extensions of noctural time in bed and frequent naps during the day. Pharmacological treatment is generally achieved with stimulants such as amphetamine, methylphenidate and pemoline, or newer compounds such as modafinil.

Aged↗

PubMed2003

Fatigue in multiple sclerosis: definition, pathophysiology and treatment.

Fatigue is a common disabling symptom of multiple sclerosis (MS). It is often considered a state of exhaustion distinct from depressed mood or physical weakness. Fatigue can be assessed by either self-report scales or performance-based measures; however, neither method captures all features of fatigue. Fatigue in MS frequently leads to unemployment. It is associated with a sense of loss of control over one's environment, low positive affect, psychological distress and neurological impairment. To date there is no reproducible neuroimaging marker or biological correlate that has been identified. Proposed pathological mechanisms of fatigue in MS include neuronal factors such as dysfunction of premotor, limbic, basal ganglia or hypothalamic areas; disruption of the neuroendrocrine axis leading to low arousal; alteration in serotoninergic pathways; changes in neurotransmitter levels; and altered CNS functioning caused by a disruption of the immune response. Treatment of fatigue is best approached in a multidisciplinary fashion that incorporates nonpharmacological interventions as well as medication. Amantadine and modafinil are among the most commonly used medications for fatigue associated with MS. Both medications have been studied with positive results in controlled clinical trials. Additional research towards measurement and pathogenesis of fatigue will hopefully lead to improved therapies.

Disability Evaluation↗

PubMed2005

Neuropsychiatric adverse effects of interferon-alpha: recognition and management.

Recombinant preparations of the cytokine interferon (IFN)-alpha are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFN alpha induces a variety of neuropsychiatric adverse effects, including an acute confusional state that develops rapidly after initiation of high-dose IFN alpha, a depressive syndrome that develops more slowly over weeks to months of treatment, and manic conditions most often characterised by extreme irritability and agitation, but also occasionally by euphoria. Acute IFN alpha-induced confusional states are typically characterised by disorientation, lethargy, somnolence, psychomotor retardation, difficulties with speaking and writing, parkinsonism and psychotic symptoms. Strategies for managing delirium should be employed, including treatment of contributing medical conditions, use of either typical or atypical antipsychotic agents and avoidance of medications likely to worsen mental status. Significant depressive symptoms occur in 21-58% of patients receiving IFN alpha, with symptoms typically manifesting over the first several months of treatment. The most replicated risk factor for developing depression is the presence of mood and anxiety symptoms prior to treatment. Other potential, but less frequently replicated, risk factors include a past history of major depression, being female and increasing IFN alpha dosage and treatment duration. The available data support two approaches to the pharmacological management of IFN alpha-induced depression: antidepressant pretreatment or symptomatic treatment once IFN alpha has been initiated. Pretreatment might be best reserved for patients already receiving antidepressants or for patients who endorse depression or anxiety symptoms of mild or greater severity prior to therapy. Several recent studies demonstrate that antidepressants effectively treat IFN alpha-induced depression once it has developed, allowing the vast majority of subjects to complete treatment successfully. Recent data suggest that IFN alpha-induced depression may be composed of two overlapping syndromes: a depression-specific syndrome characterised by mood, anxiety and cognitive complaints, and a neurovegetative syndrome characterised by fatigue, anorexia, pain and psychomotor slowing. Depression-specific symptoms are highly responsive to serotonergic antidepressants, whereas neurovegetative symptoms are significantly less responsive to these agents. These symptoms may be more effectively treated by agents that modulate catecholaminergic functioning, such as combined serotonin-noradrenaline (norepinephrine) antidepressants, bupropion, psychostimulants or modafinil. Additional factors to consider in selecting an antidepressant include potential drug-drug interactions and adverse effect profile. Finally, IFN alpha appears capable of inducing manic symptoms. Mania, especially when severe, is a clinical emergency. When this occurs, IFN alpha and antidepressants should be stopped, an emergency psychiatric consultation should be obtained, and treatment with a mood stabilizer should be initiated.

Antiviral Agents↗

PubMed2006

Cognitive deficits and psychosis in Parkinson's disease: a review of pathophysiology and therapeutic options.

Parkinson's disease is a neurodegenerative disorder causing not only motor dysfunction but also cognitive, psychiatric, autonomic and sensory disturbances. Symptoms of dementia and psychosis are common: longitudinal studies suggest that up to 75% of patients with Parkinson's disease may eventually develop dementia, and the prevalence of hallucinations ranges from 16-17% in population-based surveys to 30-40% in hospital-based series. These cognitive and behavioural features are important in terms of prognosis, nursing home placement and mortality. The pattern of cognitive deficits in Parkinson's disease is variable, but often includes executive impairment similar to that seen in patients with frontal lesions, as well as episodic memory impairment, visuospatial dysfunction and impaired verbal fluency. The most common manifestation of psychosis in Parkinson's disease is visual hallucinations, but delusions, paranoid beliefs, agitation and florid psychosis can also occur. An understanding of the pathophysiology underlying these symptoms is essential to the development of targeted therapeutic strategies. Post-mortem studies suggest an association between Lewy body deposition and dementia in Parkinson's disease, and indeed Parkinson's disease and dementia with Lewy bodies may form part of the same disease spectrum. Whether Lewy bodies actually play a causative role in cognitive dysfunction, however, is unknown. Deficits in neurotransmitter systems provide more obvious therapeutic targets and dysfunction of dopaminergic, cholinergic, noradrenergic and serotonergic systems have all been implicated; these may each underlie different features of Parkinson's disease dementia, perhaps explaining some of the heterogeneity of the syndrome. Psychosis has traditionally been considered as a dopaminergic drug-induced phenomenon, but factors intrinsic to the disease process itself also cause hallucinations and delusions. These factors may include Lewy body deposition in the limbic system, cholinergic deficits and impairments of primary visual processing. Therapeutic intervention for cognitive and behavioural symptoms in Parkinson's disease currently focuses on two main groups of drugs: cholinesterase inhibitors and atypical antipsychotics. A recent large, randomised, controlled trial suggests that cholinesterase inhibitors can produce a modest improvement in cognitive function, as well as psychotic symptoms, generally without an adverse effect on motor function. Certain atypical antipsychotics allow hallucinations, delusions and behavioural problems to be brought under control with minimal deleterious effects on motor function and cognition, but their safety in elderly patients has recently been called into question. Deep brain stimulation does not appear to be a useful treatment for cognitive and psychiatric dysfunction in patients with Parkinson's disease. Modafinil improves alertness in Parkinson's disease and warrants further investigation to establish its effects on cognitive performance.

Cognition Disorders↗