Artykuły w czasopismach: „Basal ganglia”

1

Redgrave, Peter. "Basal ganglia". Scholarpedia 2, nr 6 (2007): 1825. http://dx.doi.org/10.4249/scholarpedia.1825.

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Brüggemann, Norbert, Susanne A. Schneider, Thurid Sander, Christine Klein i Johann Hagenah. "Distinct basal ganglia hyperechogenicity in idiopathic basal ganglia calcification". Movement Disorders 25, nr 15 (27.08.2010): 2661–64. http://dx.doi.org/10.1002/mds.23264.

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Tso, Winnie Wan-Yee, Ada Wing-Yan Yung, Hin-Yue Lau i Godfrey Chi-Fung Chan. "Basal Ganglia Germinoma". Journal of Pediatric Hematology/Oncology 36, nr 7 (październik 2014): e443-e447. http://dx.doi.org/10.1097/mph.0000000000000014.

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Patell, R. D., R. V. Dosi, H. K. Joshi i P. C. Shah. "Basal ganglia calcification". Case Reports 2013, aug13 1 (13.08.2013): bcr2013200399. http://dx.doi.org/10.1136/bcr-2013-200399.

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Albin, Roger L. "BASAL GANGLIA NEUROTOXINS". Neurologic Clinics 18, nr 3 (sierpień 2000): 665–80. http://dx.doi.org/10.1016/s0733-8619(05)70217-6.

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Graybiel, Ann M. "The basal ganglia". Current Biology 10, nr 14 (lipiec 2000): R509—R511. http://dx.doi.org/10.1016/s0960-9822(00)00593-5.

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Graybiel, Ann M. "The basal ganglia". Trends in Neurosciences 18, nr 2 (luty 1995): 60–62. http://dx.doi.org/10.1016/0166-2236(95)80019-x.

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KONSTANTINOU, GERASIMOS, ANASTASIA STAVRINOU, SAVVINA MYLONA, GEORGE PASCHALAKIS i POLYXENI VASILOPOULOU. "Basal Ganglia Calcification". Journal of Psychiatric Practice 25, nr 5 (wrzesień 2019): 391–94. http://dx.doi.org/10.1097/pra.0000000000000410.

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9

Braunlich, Kurt, i Carol Seger. "The basal ganglia". Wiley Interdisciplinary Reviews: Cognitive Science 4, nr 2 (21.12.2012): 135–48. http://dx.doi.org/10.1002/wcs.1217.

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Vaštík Kateřina Menšíková Sandra Kurčová, Miroslav, i Michaela Kaiserová Zuzana Matejčíková Petr Kaňovský. "Functional basal ganglia interconnection". Neurologie pro praxi 18, nr 4 (1.10.2017): 266–70. http://dx.doi.org/10.36290/neu.2017.097.

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Farries, Michael A. "How Basal' Are the Basal Ganglia?" Brain, Behavior and Evolution 82, nr 4 (2013): 211–14. http://dx.doi.org/10.1159/000356101.

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Dale, Russell C., i Fabienne Brilot. "Autoimmune Basal Ganglia Disorders". Journal of Child Neurology 27, nr 11 (25.07.2012): 1470–81. http://dx.doi.org/10.1177/0883073812451327.

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The basal ganglia are deep nuclei in the brain that include the caudate, putamen, globus pallidus, and substantia nigra. Pathological processes involving the basal ganglia often result in disorders of movement and behavior. A number of different autoimmune disorders predominantly involve the basal ganglia and can result in movement and psychiatric disorders. The classic basal ganglia autoimmune disorder is Sydenham chorea, a poststreptococcal neuropsychiatric disorder. Resurgence in the interest in Sydenham chorea is the result of the descriptions of other poststreptococcal neuropsychiatric disorders including tics and obsessive-compulsive disorder, broadly termed pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection. Encephalitic processes affecting the basal ganglia are also described including the syndromes basal ganglia encephalitis, encephalitis lethargica, and bilateral striatal necrosis. Last, systemic autoimmune disorders such as systemic lupus erythematosus and antiphospholipid syndrome can result in chorea or parkinsonism. Using paradigms learned from other autoantibody associated disorders, the authors discuss the autoantibody hypothesis and the role of systemic inflammation in autoimmune basal ganglia disorders. Identification of these entities is important as the clinician has an increasing therapeutic repertoire to modulate or suppress the aberrant immune system.

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Hikosaka, Okihide. "Dopamine and Basal Ganglia". Psychiatry and Clinical Neurosciences 45, nr 2 (czerwiec 1991): 511. http://dx.doi.org/10.1111/j.1440-1819.1991.tb02535.x.

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Jellinger, K. "Traumatic basal ganglia hemorrhage". Neurology 40, nr 5 (1.05.1990): 862. http://dx.doi.org/10.1212/wnl.40.5.862-a.

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Katz, D. I., i M. P. Alexander. "Traumatic basal ganglia hemorrhage". Neurology 40, nr 5 (1.05.1990): 862. http://dx.doi.org/10.1212/wnl.40.5.862-b.

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BROOKS, DAVID J. "Imaging basal ganglia function". Journal of Anatomy 196, nr 4 (maj 2000): 543–54. http://dx.doi.org/10.1046/j.1469-7580.2000.19640543.x.

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Jellinger, K. A. "The Basal Ganglia IX". European Journal of Neurology 17, nr 2 (7.12.2009): e11-e11. http://dx.doi.org/10.1111/j.1468-1331.2009.02881.x.

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18

Alexander, Garrett E. "Basal Ganglia-Thalamocortical Circuits". Journal of Clinical Neurophysiology 11, nr 4 (lipiec 1994): 420–31. http://dx.doi.org/10.1097/00004691-199407000-00004.

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Alexander B. Norinsky, D. O., i Vidhi J. Parikh. "Bilateral basal ganglia lesions". Visual Journal of Emergency Medicine 6 (styczeń 2017): 29–30. http://dx.doi.org/10.1016/j.visj.2016.07.006.

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Chaudhuri, Abhijit, i Peter O. Behan. "Fatigue and basal ganglia". Journal of the Neurological Sciences 179, nr 1-2 (październik 2000): 34–42. http://dx.doi.org/10.1016/s0022-510x(00)00411-1.

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21

Houk, Jim. "Models of basal ganglia". Scholarpedia 2, nr 10 (2007): 1633. http://dx.doi.org/10.4249/scholarpedia.1633.

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Alloway, Kevin. "Vibrissal basal ganglia circuits". Scholarpedia 8, nr 9 (2013): 7279. http://dx.doi.org/10.4249/scholarpedia.7279.

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23

Malwitz, Kari, Judith H. Crossett i Susan K. Schultz. "Idiopathic Basal Ganglia Calcification". American Journal of Geriatric Psychiatry 25, nr 3 (marzec 2017): S83—S84. http://dx.doi.org/10.1016/j.jagp.2017.01.095.

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Miocinovic, Svjetlana. "Beyond the Basal Ganglia". JAMA Neurology 71, nr 1 (1.01.2014): 8. http://dx.doi.org/10.1001/jamaneurol.2013.4643.

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Siderowf, A. "The Basal Ganglia V". Archives of Neurology 55, nr 2 (1.02.1998): 255. http://dx.doi.org/10.1001/archneur.55.2.255.

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Tuan, Ho Xuan, Nguyen-Thi Huyen, Nguyen Duc Son, Nguyen Viet Trung, Nguyen-Thi Hai Anh, Nguyen Duy Hung i Nguyen Minh Duc. "Germinoma of basal ganglia". Radiology Case Reports 19, nr 5 (maj 2024): 2072–80. http://dx.doi.org/10.1016/j.radcr.2024.02.047.

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27

Rudroff, Thorsten. "Decoding Post-Viral Fatigue: The Basal Ganglia’s Complex Role in Long-COVID". Neurology International 16, nr 2 (28.03.2024): 380–93. http://dx.doi.org/10.3390/neurolint16020028.

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Long-COVID afflicts millions with relentless fatigue, disrupting daily life. The objective of this narrative review is to synthesize current evidence on the role of the basal ganglia in long-COVID fatigue, discuss potential mechanisms, and highlight promising therapeutic interventions. A comprehensive literature search was conducted using PubMed, Scopus, and Web of Science databases. Mounting evidence from PET, MRI, and functional connectivity data reveals basal ganglia disturbances in long-COVID exhaustion, including inflammation, metabolic disruption, volume changes, and network alterations focused on striatal dopamine circuitry regulating motivation. Theories suggest inflammation-induced signaling disturbances could impede effort/reward valuation, disrupt cortical–subcortical motivational pathways, or diminish excitatory input to arousal centers, attenuating drive initiation. Recent therapeutic pilots targeting basal ganglia abnormalities show provisional efficacy. However, heterogeneous outcomes, inconsistent metrics, and perceived versus objective fatigue discrepancies temper insights. Despite the growing research, gaps remain in understanding the precise pathways linking basal ganglia dysfunction to fatigue and validating treatment efficacy. Further research is needed to advance understanding of the basal ganglia’s contribution to long-COVID neurological sequelae and offer hope for improving function across the expanding affected population.

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28

Da Cunha, Claudio, Suelen L. Boschen, Alexander Gómez-A, Erika K. Ross, William S. J. Gibson, Hoon-Ki Min, Kendall H. Lee i Charles D. Blaha. "Toward sophisticated basal ganglia neuromodulation: Review on basal ganglia deep brain stimulation". Neuroscience & Biobehavioral Reviews 58 (listopad 2015): 186–210. http://dx.doi.org/10.1016/j.neubiorev.2015.02.003.

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Groenewegen, Henk J. "The Basal Ganglia and Motor Control". Neural Plasticity 10, nr 1-2 (2003): 107–20. http://dx.doi.org/10.1155/np.2003.107.

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This paper briefly reviews the functional anatomy of the basal ganglia and their relationships with the thalamocortical system. The basal ganglia, including the striatum, pallidum, subthalamic nucleus, and substantia nigra, are involved in a number of parallel, functionally segregated cortical-subcortical circuits. These circuits support a wide range of sensorimotor, cognitive and emotional-motivational brain functions. A main role of the basal ganglia is the learning and selection of the most appropriate motor or behavioral programs. The internal functional organization of the basal ganglia is very well suited for such selection mechanisms, both in development and in adulthood. The question of whether clumsiness may be, at least in part, attributed to dysfunction of the basal ganglia is discussed in the context of the differential, complementary, or interactive roles of the basal ganglia and the cerebellum in the development of motor control.

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30

Visser, Jasper E., i Bastiaan R. Bloem. "Role of the Basal Ganglia in Balance Control". Neural Plasticity 12, nr 2-3 (2005): 161–74. http://dx.doi.org/10.1155/np.2005.161.

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In this review paper, we summarize the important contributions of the basal ganglia to the regulation of postural control. After a brief overview of basal ganglia circuitries, the emphasis is on clinical observations in patients with focal lesions in parts of the basal ganglia, as the impairments seen here can serve to highlight the normal functions of the basal ganglia nuclei in postural control. Two particularly relevant functions are discussed in detail: first, the contribution of the basal ganglia to flexibility and to gaining control of balancecorrecting responses, including the ability to lend priority to the elements of a postural task; and second, processing afferent information by the basal ganglia, which is increasingly recognized as being highly relevant for postural control.

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31

Lou, Jau-Shin. "Pathophysiology of Basal Ganglia Disorders". CNS Spectrums 3, nr 2 (luty 1998): 36–40. http://dx.doi.org/10.1017/s1092852900005514.

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AbstractParkinson's disease is the most common basal ganglia disorder that is caused by the degeneration of dopaminergic neurons in the substantia nigra. This article reviews the normal physiology of the basal ganglia in the normal state, as well as the pathophysiology of Parkinson's disease (PD) and other movement disorders associated with the basal ganglia. Also discussed is the pathophysiological basis for the surgical treatment of PD.

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32

Paprocka, Justyna, Magdalena Machnikowska-Sokołowska, Katarzyna Gruszczyńska i Ewa Emich-Widera. "Neuroimaging of Basal Ganglia in Neurometabolic Diseases in Children". Brain Sciences 10, nr 11 (12.11.2020): 849. http://dx.doi.org/10.3390/brainsci10110849.

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Diseases primarily affecting the basal ganglia in children result in characteristic disturbances of movement and muscle tone. Both experimental and clinical evidence indicates that the basal ganglia also play a role in higher mental states. The basal ganglia can be affected by neurometabolic, degenerative diseases or other conditions from which they must be differentiated. Neuroradiological findings in basal ganglia diseases are also known. However, they may be similar in different diseases. Their assessment in children may require repeated MRI examinations depending on the stage of brain development (mainly the level of myelination). A large spectrum of pathological changes in the basal ganglia in many diseases is caused by their vulnerability to metabolic abnormalities and chemical or ischemic trauma. The diagnosis is usually established by correlation of clinical and radiological findings. Neuroimaging of basal ganglia in neurometabolic diseases is helpful in early diagnosis and monitoring of changes for optimal therapy. This review focuses on neuroimaging of basal ganglia and its role in the differential diagnosis of inborn errors of metabolism.

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33

Lopez-Rodriguez, Faustino, Ibrahim Gunay i Nancy Glaser. "Obsessive Compulsive Disorder in a Woman with Left Basal Ganglia Infarct: A Case Report". Behavioural Neurology 10, nr 2-3 (1997): 101–3. http://dx.doi.org/10.1155/1997/309471.

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This report presents a syndrome resembling obsessive convulsive disorder (OCD) secondary to a stroke in the left basal ganglia. The patient's syndrome is virtually identical to those that have been described in bilateral damage of the basal ganglia. However, the stroke described in this case report is located unilaterally in the left basal ganglia. In addition, experience in treating a patient with OCD induced by structural damage of basal ganglia is presented.

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Wright, Christopher I., Bradley S. Peterson i Scott L. Rauch. "Neuroimaging Studies in Tourette Syndrome". CNS Spectrums 4, nr 3 (marzec 1999): 54–61. http://dx.doi.org/10.1017/s1092852900000821.

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ABSTRACTTourette syndrome (TS) is a complex neurobehavioral disorder principally characterized by motor and vocal tics. However, features of obsessive-compulsive and attention-deficit/hyperactivity disorders are often present. The basal ganglia and associated brain structures have been implicated in the pathophysiology of TS, as well as in these related conditions. Specifically, it is believed that the neuroanatomically and functionally defined basal ganglia thalamocortical loops are involved in TS. These loops are composed of a sequence of connections originating in the cortex and passing in series through the striatum (caudate and putamen), globus pallidus, and thalamus before returning to the cortical areas of origin. This review concentrates on the neuroimaging findings in Ts, particularly as they relate to alterations in components of the basal ganglia thalamocortical circuits. These neuroimaging data suggest that the major abnormalities in TS involve striatal or cortical dysfunction, as well as dysfunction of dopaminergic systems that regulate basas ganglia neurotransmission.

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Persad, A., i V. Mehta. "P.112 Permanent isolated micrographia from traumatic basal ganglia injury". Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 46, s1 (czerwiec 2019): S43. http://dx.doi.org/10.1017/cjn.2019.205.

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Background: Micrographia is a rare neurological finding in isolation. Most cases of isolated micrographia have been found in association with focal ischemia of the left basal ganglia. Methods: We present a case of post-traumatic micrographia stemming from contusion to the left basal ganglia. We performed a detailed analysis of the patient’s writing at three-year follow-up. Results: A halthy 15 year old male was admitted following a BM accident. CT showed contusion to the left basall ganglia/external capsule. MRI was negative for underlying lesion. He had a short stay in the ICU and then was discharged. Two years later, he expressed concern regarding difficulty with sma, cramped writing at school. Writing analysis revealed micrographia with spontaneous printing as well as printing to dictation, but not with copied English nor Japanese writing. Conclusions: Isolated micrographia is a rare neurological finding. We present the incidence of this symptom folllowing gliding contusion to the et basal ganglia and external capsule.

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36

Azizi, Heela, Alexander Kilpatrick, Olaniyi Olayinka, Olusegun Poopola, Maleeha Ahmad, Alexa Kahn, Tasmia Khan i in. "On Neuropsychiatric Manifestations of Basal Ganglia Injury: A Report of Three Cases and Literature Review". Case Reports in Neurological Medicine 2019 (4.04.2019): 1–11. http://dx.doi.org/10.1155/2019/3298791.

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The basal ganglia have been considered to primarily play a role in motor processing. A growing body of theoretical and clinical evidence shows that in addition to the motor functions the basal ganglia play a key role in perceptual and visual disturbances. This role may be evident in patients with basal ganglia pathology and subsequent manifestation of symptoms that include cognitive, perceptual, and affective disturbances. We present three cases with basal ganglia pathology that demonstrate affective and psychotic symptoms. Two of the cases presented with late onset psychotic disturbances suggesting likely neurological etiologies. The third case presented with treatment refractory psychosis and symptoms that are rare for a diagnosis of schizophrenia. The role of incidental bilateral basal ganglia calcifications in all the cases is discussed. A review of current literature highlighting various neuropsychiatric manifestations of basal ganglia pathologies in various patients with psychiatric symptoms is presented.

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37

Avetisyan, Tamara, Nune Kuyumjyan, Biayna Sukhudyan, Eugen Boltshauser, Annette Hackenberg i Sandra Toelle. "Infantile Basal Ganglia Stroke after Mild Head Trauma Associated with Mineralizing Angiopathy of Lenticulostriate Arteries: An Under Recognized Entity". Neuropediatrics 49, nr 04 (23.05.2018): 262–68. http://dx.doi.org/10.1055/s-0038-1649501.

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AbstractBasal ganglia infarction in young children, mostly after mild head trauma, has been repeatedly reported. The pathogenesis and the risk factors are not fully understood. Lenticulostriate vasculopathy, usually referred to as basal ganglia calcification, is discussed as one of them. We describe five young (7–13 months old on presentation) male children who suffered from hemiparesis due to ischemic stroke of the basal ganglia, four of them after minor head trauma. All of them had calcification in the basal ganglia visible on computed tomography or cranial ultrasound but not on magnetic resonance imaging. Follow-up care was remarkable for recurrent infarction in three patients. One patient had a second symptomatic stroke on the contralateral side, and two patients showed new asymptomatic infarctions in the contralateral basal ganglia on imaging. In view of the scant literature, this clinic-radiologic entity seems under recognized. We review the published cases and hypothesize that male sex and iron deficiency anemia are risk factors for basal ganglia stroke after minor trauma in the context of basal ganglia calcification in infants. We suggest to perform appropriate targeted neuroimaging in case of infantile basal ganglia stroke, and to consider prophylactic medical treatment, although its value in this context is not proven.

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38

Finke, C., J. Schlichting, S. Papazoglou, M. Scheel, A. Freing, C. Soemmer, LM Pech i in. "Altered basal ganglia functional connectivity in multiple sclerosis patients with fatigue". Multiple Sclerosis Journal 21, nr 7 (12.11.2014): 925–34. http://dx.doi.org/10.1177/1352458514555784.

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Background: Fatigue is one of the most frequent and disabling symptoms in multiple sclerosis, but its pathophysiological mechanisms are poorly understood. It is in particular unclear whether and how fatigue relates to structural and functional brain changes. Objective: We aimed to analyse the association of fatigue severity with basal ganglia functional connectivity, basal ganglia volumes, white matter integrity and grey matter density. Methods: In 44 patients with relapsing–remitting multiple sclerosis and 20 age- and gender-matched healthy controls, resting-state fMRI, diffusion tensor imaging and voxel-based morphometry was performed. Results: In comparison with healthy controls, patients showed alteration of grey matter density, white matter integrity, basal ganglia volumes and basal ganglia functional connectivity. No association of fatigue severity with grey matter density, white matter integrity and basal ganglia volumes was observed within patients. In contrast, fatigue severity was negatively correlated with functional connectivity of basal ganglia nuclei with medial prefrontal cortex, precuneus and posterior cingulate cortex in patients. Furthermore, fatigue severity was positively correlated with functional connectivity between caudate nucleus and motor cortex. Conclusion: Fatigue is associated with distinct alterations of basal ganglia functional connectivity independent of overall disability. The pattern of connectivity changes suggests that disruption of motor and non-motor basal ganglia functions, including motivation and reward processing, contributes to fatigue pathophysiology in multiple sclerosis.

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Dubey, Roopak, Kamal Kumar Sen, Mayank Goyal, D. Sindhu Reddy i Suma MK. "Is Fahr’s disease a saviour for intracranial hypertensive bleeds? - A review". Panacea Journal of Medical Sciences 11, nr 2 (15.08.2021): 360–63. http://dx.doi.org/10.18231/j.pjms.2021.072.

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Fahr’s disease (FD) is a rare disorder characterised by abnormal deposition of calcium in different parts of brain especially in basal ganglia, thalamus and dentate nucleus. Association of FD with ischemic stroke has been described in past but very less literature available showing association of FD with haemorrhagic stroke. We present here a case of 70 years old hypertensive male patient suffering from FD with left thalamic acute haemorrhage. Although basal ganglia is a common site for hypertensive bleed, but in this hypertensive patient, basal ganglia was spared. We assume that this could be due to presence of calcification within vessel walls of basal ganglia that strengthen the walls and hence act as a saviour for basal ganglia bleed in this case.

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Maia, Alex S. S. Freire, Egberto Reis Barbosa, Paulo Rossi Menezes i Eurípedes C. Miguel Filho. "Relationship between obsessive-compulsive disorders and diseases affecting primarily the basal ganglia". Revista do Hospital das Clínicas 54, nr 6 (grudzień 1999): 213–21. http://dx.doi.org/10.1590/s0041-87811999000600008.

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Obsessive-compulsive disorder (OCD) has been reported in association with some neurological diseases that affect the basal ganglia such as Tourette's syndrome, Sydenham's chorea, Parkinson's disease, and Huntington's disease. Furthermore, studies such as neuroimaging, suggest a role of the basal ganglia in the pathophysiology of OCD. The aim of this paper is to describe the association of OCD and several neurologic disorders affecting the basal ganglia, report the existing evidences of the role of the basal ganglia in the pathophysiology of OCD, and analyze the mechanisms probably involved in this pathophysiology.

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De Mori, Roberta, Mariasavina Severino, Maria Margherita Mancardi, Danila Anello, Silvia Tardivo, Tommaso Biagini, Valeria Capra i in. "Agenesis of the putamen and globus pallidus caused by recessive mutations in the homeobox gene GSX2". Brain 142, nr 10 (14.08.2019): 2965–78. http://dx.doi.org/10.1093/brain/awz247.

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Congenital malformations of the basal ganglia are rare. De Mori et al. describe a novel syndrome of severe dystonic tetraparesis and intellectual impairment, with hypo/agenesis of the basal ganglia. The syndrome is caused by recessive mutations in GSX2, a homeobox gene expressed in ganglionic eminences and essential for basal ganglia development.

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Coleman, Melissa J., i Stephanie A. White. "Basal ganglia: Bursting with song". Current Biology 31, nr 12 (czerwiec 2021): R791—R793. http://dx.doi.org/10.1016/j.cub.2021.04.064.

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Ugawa, Yoshikazu. "Sensory input and basal ganglia". Rinsho Shinkeigaku 52, nr 11 (2012): 862–65. http://dx.doi.org/10.5692/clinicalneurol.52.862.

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Millichap, J. Gordon. "Basal Ganglia and Thalamic Infarction". Pediatric Neurology Briefs 11, nr 1 (1.01.1997): 1. http://dx.doi.org/10.15844/pedneurbriefs-11-1-1.

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Maleki, Nasim, Lino Becerra, Lauren Nutile, Gautam Pendse, Jennifer Brawn, Marcelo Bigal, Rami Burstein i David Borsook. "Migraine Attacks the Basal Ganglia". Molecular Pain 7 (styczeń 2011): 1744–8069. http://dx.doi.org/10.1186/1744-8069-7-71.

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Brown, P. "Oscillations in the Basal Ganglia". Neuromodulation: Technology at the Neural Interface 6, nr 3 (26.06.2003): 191. http://dx.doi.org/10.1046/j.1525-1403.2003.03027_2.x.

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Madu, Ezemonye, i Hamid Alam. "Chorea, Hyperglycemia, Basal Ganglia Syndrome". Journal of the American Osteopathic Association 115, nr 7 (1.07.2015): 465. http://dx.doi.org/10.7556/jaoa.2015.099.

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Barker, Roger A. "The Basal Ganglia and Pain". International Journal of Neuroscience 41, nr 1-2 (styczeń 1988): 29–34. http://dx.doi.org/10.3109/00207458808985739.

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Wichmann, Thomas, i Mahlon R. DeLong. "Oscillations in the basal ganglia". Nature 400, nr 6745 (sierpień 1999): 621–22. http://dx.doi.org/10.1038/23148.

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Fernández-Ruiz, J., I. Lastres-Becker, A. Cabranes, S. González i J. A. Ramos. "Endocannabinoids and basal ganglia functionality". Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA) 66, nr 2-3 (luty 2002): 257–67. http://dx.doi.org/10.1054/plef.2001.0350.

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