Movement disorders in cerebrovascular disease

Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA.
The Lancet Neurology (Impact Factor: 21.9). 04/2013; 12(6). DOI: 10.1016/S1474-4422(13)70057-7
Source: PubMed

ABSTRACT Movement disorders can occur as primary (idiopathic) or genetic disease, as a manifestation of an underlying neurodegenerative disorder, or secondary to a wide range of neurological or systemic diseases. Cerebrovascular diseases represent up to 22% of secondary movement disorders, and involuntary movements develop after 1-4% of strokes. Post-stroke movement disorders can manifest in parkinsonism or a wide range of hyperkinetic movement disorders including chorea, ballism, athetosis, dystonia, tremor, myoclonus, stereotypies, and akathisia. Some of these disorders occur immediately after acute stroke, whereas others can develop later, and yet others represent delayed-onset progressive movement disorders. These movement disorders have been encountered in patients with ischaemic and haemorrhagic strokes, subarachnoid haemorrhage, cerebrovascular malformations, and dural arteriovenous fistula affecting the basal ganglia, their connections, or both.

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    • "Movement disorders (MD) can be classified as “primary,” which are a manifestation of an underlying neurodegenerative disorder, or “secondary” to a wide range of neurological or systemic diseases. Various etiological factors have been described causing secondary MDs (SMDs) such as cerebrovascular disease,[1] space occupying lesions, trauma and infections. Netravathi et al.[2] in their study had reported infectious causes representing up to 20.4% of all SMDs.[2] MDs secondary to infectious causes are diverse ranging from hypokinetic disorders such as parkinsonism (PAR)[34] to hyperkinetic disorders such as chorea,[56] dystonia,[7] tics,[5] tremor and myoclonus (MYO). "
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    ABSTRACT: Background:Movement disorders (MDs) associated with infections remains an important debilitating disorder in the Asian countries.Objectives:The objective of the following study is to report the clinical and imaging profile of a large cohort of patients with MDs probably associated with infection.Materials and Methods:This was a chart review of 35 patients (F:M-15:20) presenting with MD in the Neurology services of National Institute of Mental Health and Neurosciences, India. The demographic profile, type of infection, time from infection to MD, phenomenology of MD and magnetic resonance imaging (MRI) findings were reviewed.Results:The mean age at presentation was 22.6 ± 13.3 years, (5-60), age of onset of MD was 15.7 ± 15 years, and duration of symptoms was 6.9 ± 8.1 years (42 days to 32 years). The mean latency of onset of MD after the infection was 5.9 ± 4.2 weeks. The phenomenology of MD were: (1) Pure dystonia-28.6%, (2) dystonia with choreoathetosis-22.9%, (3) Parkinsonism-14.6%, (4) pure tremor, hemiballismus, myoclonus and chorea-2.9% each, and (5) mixed MD-22.9%. Most often the MD was generalized (60%), followed by right upper limb (31.4%) and left upper limb (8.6%). A viral encephalitic type of neuroinfection was the most common infection (85.7%), which was associated with MD. Abnormalities of brain MRI, seen in 79.2%, included signal changes in (1) thalamus-52.0%, (2) putamen and subcortical white matter-16% each, (3) pons-12%, (4) striatopallidum, striatum and grey matter-8% each, and (5) caudate, cerebellum, lentiform nucleus, midbrain and subthalamic nucleus-4.0% each.Conclusions:MDs associated with infection were the most often post-encephalitic. Dystonia was the most common MD, and thalamus was the most common anatomical site involved.
    Annals of Indian Academy of Neurology 07/2014; 17(3):292-7. DOI:10.4103/0972-2327.138503 · 0.60 Impact Factor
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    • "Dystonia: Evidence for striatal dysfunction A combination of clinical, neuroimaging, and basic scientific observations support a central role for striatal dysfunction in the pathophysiology of primary dystonia. Damage to the striatum and associated structures (e.g., pallidum , thalamus) are a common cause of secondary dystonia (Marsden, Obeso, Zarranz, & Lang, 1985; Mehanna & Jankovic, 2013). Metabolic diseases that disrupt striatal function (e.g., Wilson's disease, pantothenate kinase-associated neurodegeneration) also cause secondary dystonia (Gordon, 2002; Lorincz, 2012). "
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    ABSTRACT: This chapter focuses on neurodevelopmental diseases that are tightly linked to abnormal function of the striatum and connected structures. We begin with an overview of three representative diseases in which striatal dysfunction plays a key role-Tourette syndrome and obsessive-compulsive disorder, Rett's syndrome, and primary dystonia. These diseases highlight distinct etiologies that disrupt striatal integrity and function during development, and showcase the varied clinical manifestations of striatal dysfunction. We then review striatal organization and function, including evidence for striatal roles in online motor control/action selection, reinforcement learning, habit formation, and action sequencing. A key barrier to progress has been the relative lack of animal models of these diseases, though recently there has been considerable progress. We review these efforts, including their relative merits providing insight into disease pathogenesis, disease symptomatology, and basal ganglia function.
    Current Topics in Developmental Biology 06/2014; 109:97-169. DOI:10.1016/B978-0-12-397920-9.00001-9 · 4.68 Impact Factor
    • "Modulated by the substantia nigra pars compacta, the indirect pathway exerts surround inhibition and thus facilitates an excitatory drive to muscles responsible for a given movement and suppresses unwanted motor activity not relevant to the primary movement. Thus, PD is thought to result from over-activation of the indirect pathway leading to an increased output from the GPi and a decrease in spontaneous movement [12]. This model of the basal ganglia and its connections is, of course, an oversimplification of a complex network that, when disrupted, can result in a range of motor abnormalities [13]. "
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    ABSTRACT: For the last 50 years, levodopa has been the cornerstone of Parkinson's disease management. However, a majority of patients develop motor complications a few years after therapy onset. Deep brain stimulation has been approved by the FDA as an adjunctive treatment in Parkinson disease, especially aimed at controlling these complications. However, the exact mechanism of action of deep brain stimulation, the best nucleus to target as well as the best timing for surgery are still debatable. We here provide an in-depth and critical review of the current literature on this topic.
    Translational Neurodegeneration 11/2013; 2(1):22. DOI:10.1186/2047-9158-2-22
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