Editing Caudate nucleus (section)

===Caudate stroke===
Strokes can occur in the caudate nucleus and studies of patients with these kinds of strokes followed the introduction and widespread availability of [[computed tomography]] (CT) scanning in the 1970s and early 1980s.<ref name="ChungCaplan2012" /><ref name="Caplan2002" /> Major studies of caudate strokes have included Stein et al. (1984),<ref name="pmid6504325">{{cite journal | vauthors = Stein RW, Kase CS, Hier DB, Caplan LR, Mohr JP, Hemmati M, Henderson K | title = Caudate hemorrhage | journal = Neurology | volume = 34 | issue = 12 | pages = 1549–54 | date = December 1984 | pmid = 6504325 | doi = 10.1212/wnl.34.12.1549 | url = }}</ref> Weisberg et al. (1984),<ref name="pmid6477232">{{cite journal | vauthors = Weisberg LA | title = Caudate hemorrhage | journal = Arch Neurol | volume = 41 | issue = 9 | pages = 971–4 | date = September 1984 | pmid = 6477232 | doi = 10.1001/archneur.1984.04050200077021 | url = }}</ref> Mendez et al. (1989),<ref name="pmid2927642">{{cite journal | vauthors = Mendez MF, Adams NL, Lewandowski KS | title = Neurobehavioral changes associated with caudate lesions | journal = Neurology | volume = 39 | issue = 3 | pages = 349–54 | date = March 1989 | pmid = 2927642 | doi = 10.1212/wnl.39.3.349 | url = }}</ref> Caplan et al. (1990),<ref name="pmid2405818">{{cite journal | vauthors = Caplan LR, Schmahmann JD, Kase CS, Feldmann E, Baquis G, Greenberg JP, Gorelick PB, Helgason C, Hier DB | title = Caudate infarcts | journal = Arch Neurol | volume = 47 | issue = 2 | pages = 133–43 | date = February 1990 | pmid = 2405818 | doi = 10.1001/archneur.1990.00530020029011 | url = }}</ref> Caplan & Helgason (1995),<ref name="CaplanHelgason1995" /> Bokura & Robinson (1997),<ref name="pmid9158635">{{cite journal | vauthors = Bokura H, Robinson RG | title = Long-term cognitive impairment associated with caudate stroke | journal = Stroke | volume = 28 | issue = 5 | pages = 970–5 | date = May 1997 | pmid = 9158635 | doi = 10.1161/01.str.28.5.970 | url = }}</ref> Kumral et al. (1999),<ref name="pmid9880396">{{cite journal | vauthors = Kumral E, Evyapan D, Balkir K | title = Acute caudate vascular lesions | journal = Stroke | volume = 30 | issue = 1 | pages = 100–8 | date = January 1999 | pmid = 9880396 | doi = 10.1161/01.str.30.1.100 | url = | doi-access = free }}</ref> Gnanashanmugam (2011),<ref name="Gnanashanmugam2011" /> and Kumral et al. (2023).<ref name="pmid35872616">{{cite journal | vauthors = Kumral E, Çetin FE, Özdemir HN | title = A Neuropsychiatric and Neuroimaging Study of Unilateral and Bilateral Striatal Ischemic Lesions | journal = J Neuropsychiatry Clin Neurosci | volume = 35 | issue = 1 | pages = 48–58 | date = 2023 | pmid = 35872616 | doi = 10.1176/appi.neuropsych.21030083 | url = }}</ref><ref name="ChungCaplan2012" /><ref name="Caplan2002" /> A number of [[literature review]]s on caudate nucleus strokes have been published,<ref name="ChungCaplan2012" /><ref name="Caplan2002" /><ref name="CaplanHelgason1995" /><ref name="PellizzaroVentiPaciaroniCaso2012" /><ref name="Gnanashanmugam2011" /> as well as a 1994 [[meta-analysis]] of [[basal ganglia]] lesions that included analysis of caudate lesions (Bhatia & Marsden, 1994).<ref name="pmid7922471" /> Caudate strokes are rare, representing only 1% of all strokes in one population of about 3,000 stroke patients.<ref name="pmid26268364">{{cite journal | vauthors = Grönholm EO, Roll MC, Horne MA, Sundgren PC, Lindgren AG | title = Predominance of caudate nucleus lesions in acute ischaemic stroke patients with impairment in language and speech | journal = Eur J Neurol | volume = 23 | issue = 1 | pages = 148–53 | date = January 2016 | pmid = 26268364 | pmc = 5042068 | doi = 10.1111/ene.12822 | url = | quote = The occurrence of stroke involving only the caudate nucleus seems overall rather uncommon. In one register study 23, it was reported that patients with caudate stroke constituted only 1% of a total number of 3050 stroke patients (2450 ischaemic stroke and 600 haemorrhagic stroke). In the present study, at least nine of the 925 patients initially included in the investigation had lesions involving an area in the superior part of the body of the left caudate nucleus and the adjacent corona radiata.}}</ref><ref name="pmid9880396" /> Caudate hemorrhages account for about 7% of all [[intracerebral hemorrhage]]s.<ref name="ChungCaplan2012" /> Research on caudate strokes has consisted of small clinical series of patients and [[case reports]].<ref name="Caplan2002" /><ref name="ChungCaplan2012" /> A 2002 review described 108 patients with 119 caudate infarcts that had been characterized, with three of the largest series having a total of 64 patients.<ref name="Caplan2002" /> In the 1994 meta-analysis, there were 43 patients with lesions confined to the caudate nucleus and 129 patients with lesions involving both the caudate and other structures, with 172 patients in total.<ref name="pmid7922471" />

Caudate nucleus strokes can be diagnosed with CT or [[magnetic resonance imaging]] (MRI) scanning.<ref name="Caplan2002" /><ref name="CaplanHelgason1995" /> They are a type of [[subcortical]] stroke and are classified as [[ischemic stroke|ischemic]] ([[infarct]]s) or [[hemorrhagic stroke|hemorrhagic]].<ref name="ChungCaplan2012" /><ref name="PellizzaroVentiPaciaroniCaso2012">{{cite book | last1=Pellizzaro Venti | first1=Michele | last2=Paciaroni | first2=Maurizio | last3=Caso | first3=Valeria | title=Frontiers of Neurology and Neuroscience | editor1-last = Paciaroni | editor1-first = M. | editor2-last = Agnelli | editor2-first = G. | editor3-last = Caso | editor3-first = V. | editor4-last = Bogousslavsky | editor4-first = J. | chapter=Caudate Infarcts and Hemorrhages | publisher=S. Karger AG | volume=30 | date=2012 | isbn=978-3-8055-9910-8 | doi=10.1159/000333616 | pages=137–140}}</ref> In one series of patients, 80% of strokes were ischemic and 20% were hemorrhagic.<ref name="Gnanashanmugam2011" /><ref name="pmid9880396" /> Caudate infarcts can be [[lacunar infarct]]s, which are small and are due to a single perforating artery occlusion, or can be striatocapsular (caudate–putamen–internal capsule) infarcts, which are larger and are due to multiple perforating artery occlusion.<ref name="pmid19810969">{{cite journal | vauthors = Gerraty RP | title = Clinical diagnosis of subcortical cerebral infarction | journal = Expert Rev Neurother | volume = 3 | issue = 5 | pages = 703–11 | date = September 2003 | pmid = 19810969 | doi = 10.1586/14737175.3.5.703 | url = | quote = Clinical diagnosis of subcortical infarction, chiefly lacunar stroke, [...] Subcortical infarction is unfortunately often considered synonymous with lacunar stroke, [...] Not all subcortical strokes are lacunes. The large striatocapsular infarct, even though confined to subcortical structures, usually does give cortical signs [3,4]. The smaller restricted striatocapsular infarct, also due to embolism as is the larger variety, usually does not give cortical signs and is an underacknowledged entity [5,6]. There are other subcortical strokes, including internal borderzone (watershed) infarction, considered most likely due to hypoperfusion and others with even less certain patho-etiologies (TABLE 1) [5,7].}}</ref><ref name="Weiller2002">{{cite book | last=Weiller | first=C. | chapter = Striatocapsular infarcts | editor-last=Donnan | editor-first=G. | title=Subcortical Stroke | publisher=Oxford University Press | series=Oxford medical publications | year=2002 | isbn=978-0-19-263157-2 | chapter-url=https://books.google.com/books?id=ZdF2DwAAQBAJ&pg=PA195 | access-date=9 December 2023 | pages=195–208}}</ref> Caudate nucleus strokes infrequently affect only the caudate, but usually also involve neighboring areas like the anterior portion of the [[putamen]], adjacent [[Internal capsule#Anterior limb|anterior limb]] of the [[internal capsule]], adjacent [[corona radiata]] [[white matter]], and [[globus pallidus]].<ref name="ChungCaplan2012" /><ref name="pmid7922471" /> About 25 to 30% of lesions are confined exclusively to the caudate.<ref name="pmid7922471" /><ref name="Caplan2002" /><ref name="ChungCaplan2012" /><ref name="CaplanHelgason1995">{{ cite book | last1 = Caplan | first1 = L. R. | last2 = Helgason | first2 = C. M. | chapter = Caudate infarcts | editor1-last = Donnan | editor1-first = G. A. | editor2-last = Norrving | editor2-first = B. | editor3-last = Bamford | editor3-first = J. M. | editor4-last = Bogousslavsky | editor4-first = J. | title = Lacunar and Other Subcortical Infarctions | pages = 117–130 | year = 1995 | publisher = Oxford University Press | location = Oxford | chapter-url = https://archive.org/details/lacunarothersubc0000unse/page/117/mode/1up}}</ref> Caudate strokes are usually unilateral, but can also be bilateral, affecting both the left and right caudate nuclei.<ref name="Caplan2002" /><ref name="ChungCaplan2012" /> In the 1994 meta-analysis, 90% of isolated caudate infarcts were unilateral and 10% were bilateral.<ref name="pmid7922471" /> [[Small vessel disease]] or penetrating-branch disease is a major mechanism of caudate strokes.<ref name="ChungCaplan2012" /><ref name="PellizzaroVentiPaciaroniCaso2012" /> Major [[risk factor]]s and causes of caudate infarcts include [[hypertension]], [[hypercholesterolemia]], [[diabetes mellitus]], previous [[myocardial infarct]], [[cigarette smoking]], large artery lesions, rupture of [[internal carotid artery]] [[aneurysm]]s, rupture of [[arteriovenous malformation]]s, [[embolism|cardiac embolism]], and [[carotid artery stenosis|carotid artery stenosis and occlusion]].<ref name="ChungCaplan2012" /><ref name="PellizzaroVentiPaciaroniCaso2012" /> Less common risk factors may include [[non-valvular atrial fibrillation]], myocardial dyskinesia, [[cardiac aneurysm]] with a [[mural thrombus]], [[syphilis]], [[Hodgkin's lymphoma]], and [[Moyamoya disease]].<ref name="ChungCaplan2012" /><ref name="PellizzaroVentiPaciaroniCaso2012" /> Additionally, a case report of lacunar infarction of the caudate and adjacent structures due to high-dose oral [[methylphenidate]] use has been published.<ref name="pmid18515459">{{cite journal | vauthors = Godfrey J | title = Safety of therapeutic methylphenidate in adults: a systematic review of the evidence | journal = J Psychopharmacol | volume = 23 | issue = 2 | pages = 194–205 | date = March 2009 | pmid = 18515459 | doi = 10.1177/0269881108089809 | url = }}</ref><ref name="pmid15038480">{{cite journal | vauthors = Sadeghian H | title = Lacunar stroke associated with methylphenidate abuse | journal = Can J Neurol Sci | volume = 31 | issue = 1 | pages = 109–11 | date = February 2004 | pmid = 15038480 | doi = 10.1017/s0317167100002924 | url = | doi-access = free }}</ref>

Caudate nucleus strokes have been associated with a variety of clinical symptoms.<ref name="pmid20407491">{{cite journal | vauthors = Villablanca JR | title = Why do we have a caudate nucleus? | journal = Acta Neurobiol Exp (Wars) | volume = 70 | issue = 1 | pages = 95–105 | date = 2010 | pmid = 20407491 | doi = | url = }}</ref><ref name="Caplan2002">{{cite book | last=Caplan | first=L R | title=Subcortical Stroke | chapter=Caudate infarcts | publisher=Oxford University PressNew York, NY | date=2002-04-11 | isbn=978-0-19-263157-2 | doi=10.1093/oso/9780192631572.003.0018 | pages=209–224}}</ref><ref name="ChungCaplan2012">{{cite book | last1=Chung | first1=Chin-Sang | last2=Caplan | first2=Louis R. | editor1-last = Caplan | editor1-first = Louis R. | editor2-last = van Gijn | editor2-first = Jan | title=Stroke syndromes | edition=3 | chapter=Caudate nucleus infarcts and hemorrhages | publisher=Cambridge University Press | location=Cambridge | date=2012-07-12 | isbn=978-1-139-09328-6 | doi=10.1017/cbo9781139093286.034 | pages=397–404}}</ref> In studies of patients with caudate infarcts, frequently occurring symptoms have included [[dysarthria]] or [[dysphonia]] (61–86%), [[weakness|motor weakness]] (40–100%), and cognitive/behavioral abnormalities (39–78%), including [[abulia]] (26–48%), [[psychomotor agitation|agitation]] (29%), [[Wikt:restlessness|restlessness]], [[hyperactivity]], [[disinhibition]] (9–11%), [[executive dysfunction]] or frontal system abnormalities (26%), [[memory impairment]], minor speech or linguistic deficits (23–50% of left-sided lesions), [[attention]] difficulties, and [[mood disorder|mood changes]] or [[depression (mood)|depression]] (14–33%).<ref name="ChungCaplan2012" /><ref name="CaplanHelgason1995" /><ref name="pmid7922471">{{cite journal | vauthors = Bhatia KP, Marsden CD | title = The behavioural and motor consequences of focal lesions of the basal ganglia in man | journal = Brain | volume = 117 ( Pt 4) | issue = 4| pages = 859–76 | date = August 1994 | pmid = 7922471 | doi = 10.1093/brain/117.4.859 | url = }}</ref><ref name="Gnanashanmugam2011" /> Motor weakness is often absent, minor/slight, or transient, and reportedly does not occur with lesions confined exclusively to the caudate nucleus.<ref name="ChungCaplan2012" /><ref name="Caplan2002" /> Abulia is defined as decreased spontaneous verbal and motor activity and slowness, with symptoms including [[apathy]], disinterest, [[flattened affect]], [[lethargy]], and lack of initiative for usual daily activities.<ref name="CaplanHelgason1995" /> Cognitive and memory impairment includes poor [[free recall]] of [[episodic memory|episodic]] and [[semantic memory|semantic]] items, verbal amnesia (33% of left-sided lesions), and visual amnesia (right-sided lesions), among other deficits.<ref name="ChungCaplan2012" /><ref name="PellizzaroVentiPaciaroniCaso2012" /><ref name="pmid35872616">{{cite journal | vauthors = Kumral E, Çetin FE, Özdemir HN | title = A Neuropsychiatric and Neuroimaging Study of Unilateral and Bilateral Striatal Ischemic Lesions | journal = J Neuropsychiatry Clin Neurosci | volume = 35 | issue = 1 | pages = 48–58 | date = 2023 | pmid = 35872616 | doi = 10.1176/appi.neuropsych.21030083 | url = }}</ref> Less commonly, there are [[motor disorder]]s (20–23%), like [[chorea]] (6–7%), [[ballism]], [[tremor]], [[parkinsonism]] (2–3%), and [[dystonia]] (9–16%), as well as more severe cognitive and behavioral problems, like [[psychic akinesia]] (loss of psychic self-activation) (12%), [[hemispatial neglect|neglect]] (10% with right-sided lesions), [[aphasia]] (2–5%), and [[dementia|global dementia]] (9%, or 1 of 11 and with bilateral lesions).<ref name="ChungCaplan2012" /><ref name="CaplanHelgason1995" /><ref name="PellizzaroVentiPaciaroniCaso2012" /><ref name="Gnanashanmugam2011" /> Among strokes in general, and/or among [[basal ganglia]] strokes specifically, certain sequelae, including apathy, abulia, [[fatigue (medical)|fatigue]], and depression, have been particularly associated with caudate strokes relative to strokes occurring in other regions.<ref name="pmid7922471" /><ref name="Gnanashanmugam2011" /><ref name="TangLiangChenChu2013">{{cite journal | last1=Tang | first1=W.K. | last2=Liang | first2=H.J. | last3=Chen | first3=Y.K. | last4=Chu | first4=Winnie C.W. | last5=Abrigo | first5=Jill | last6=Mok | first6=V.C.T. | last7=Ungvari | first7=Gabor S. | last8=Wong | first8=K.S. | title=Poststroke fatigue is associated with caudate infarcts | journal=Journal of the Neurological Sciences | volume=324 | issue=1–2 | date=2013 | doi=10.1016/j.jns.2012.10.022 | pages=131–135}}</ref><ref name="Riahi2016">Riahi, A., Derbali, H., Bedoui, I., Messelmani, M., Mansour, M., Zaouali, J., & Mrissa, R. (2016, June). Implication of Caudate nucleus lacunar infarcts in post-stroke depression. European Journal of Neurology, 23(Suppl 2), 756–756 (abstract no. P32016). https://doi.org/10.1111/ene.13094</ref><ref name="RiggiHommelJaillard2018">Riggi, F. F., Hommel, M., & Jaillard, A. (2018). Lesions in the dorsolateral caudate nucleus predict post stroke depression – a voxel-based lesion-symptom mapping study. Cerebrovascular Diseases, 45(Suppl 1), 33–33 (abstract no. OP 025). https://doi.org/10.1159/000520354</ref> Strokes in the caudate nucleus have also been strongly associated with post-stroke [[restless legs syndrome]] (RLS).<ref name="pmid35219214">{{cite journal | vauthors = Wang XX, Feng Y, Tan EK, Ondo WG, Wu YC | title = Stroke-related restless legs syndrome: epidemiology, clinical characteristics, and pathophysiology | journal = Sleep Med | volume = 90 | issue = | pages = 238–248 | date = February 2022 | pmid = 35219214 | doi = 10.1016/j.sleep.2022.02.001 | url = }}</ref><ref name="pmid32229419">{{cite journal | vauthors = Wu X, Xu J, Lu B | title = Acute post-stroke restless legs syndrome: the body of caudate nucleus considerations | journal = Sleep Med | volume = 70 | issue = | pages = 66–70 | date = June 2020 | pmid = 32229419 | doi = 10.1016/j.sleep.2019.11.1253 | url = }}</ref><ref name="pmid34889000">{{cite journal | vauthors = Ruppert E, Hacquard A, Tatu L, Namer IJ, Wolff V, Kremer S, Lagha-Boukbiza O, Bataillard M, Bourgin P | title = Stroke-related restless legs syndrome: Clinical and anatomo-functional characterization of an emerging entity | journal = Eur J Neurol | volume = 29 | issue = 4 | pages = 1011–1016 | date = April 2022 | pmid = 34889000 | doi = 10.1111/ene.15207 | url = }}</ref> Other behavioral conditions, like [[obsessive–compulsive disorder]], [[perseveration]]s, and [[mania]], have been reported rarely in individuals with caudate strokes as well.<ref name="pmid20407491" /><ref name="Caplan2002" /><ref name="ChungCaplan2012" /><ref name="pmid30638936">{{cite journal | vauthors = Akaho R, Deguchi I, Kigawa H, Nishimura K | title = Obsessive-Compulsive Disorder Following Cerebrovascular Accident: A Case Report and Literature Review | journal = J Stroke Cerebrovasc Dis | volume = 28 | issue = 4 | pages = e17–e21 | date = April 2019 | pmid = 30638936 | doi = 10.1016/j.jstrokecerebrovasdis.2018.12.034 | url = }}</ref><ref name="pmid27112231">{{cite journal | vauthors = Satzer D, Bond DJ | title = Mania secondary to focal brain lesions: implications for understanding the functional neuroanatomy of bipolar disorder | journal = Bipolar Disord | volume = 18 | issue = 3 | pages = 205–20 | date = May 2016 | pmid = 27112231 | doi = 10.1111/bdi.12387 | url = }}</ref> In one case report of bilateral caudate head damage, severe [[prospective memory]] impairment was measured, along with other deficits.<ref name="pmid20407491" /><ref name="pmid9669482">{{cite journal | vauthors = Canavero S, Fontanella M | title = Behavioral-attentional syndrome following bilateral caudate head ischaemia | journal = J Neurol | volume = 245 | issue = 6–7 | pages = 322–4 | date = 1998 | pmid = 9669482 | doi = 10.1007/s004150050226 | url = }}</ref>

The sizes, locations, and involvements of neighboring structures define the symptoms of caudate lesions.<ref name="PellizzaroVentiPaciaroniCaso2012" /> Damage to the caudate nucleus usually presents with cognitive and behavioral symptoms rather than with neurological signs.<ref name="pmid20407491" /><ref name="ChungCaplan2012" /> Cognitive and behavioral symptoms are more common than motor problems (e.g., respective rates of 39% vs. 20% in the 1994 meta-analysis).<ref name="pmid7922471" /><ref name="pmid20407491" /><ref name="ChungCaplan2012" /><ref name="Gnanashanmugam2011">Gnanashanmugam, G. (2011). A Study on Evaluation of Motor, Cognitive and Behavioral Manifestations of Basal Ganglia Infarcts (Doctoral dissertation, Madras Medical College, Chennai). http://repository-tnmgrmu.ac.in/id/eprint/580</ref> Due to the predominance of cognitive and behavioral symptoms over neurological symptoms, and frequent absence of classical stroke signs, people with caudate strokes can be misdiagnosed as having primarily [[psychological disorder|psychogenic illness]].<ref name="pmid2927642" /> This can result in enduring cognitive and behavioral deficits, which can result in significant functional limitations, being overlooked.<ref name="pmid2927642" /> The symptoms of caudate strokes are usually more severe and persistent when they are bilateral rather than unilateral.<ref name="Caplan2002" /><ref name="ChungCaplan2012" /> In addition, they are more severe when other adjacent structures are also involved.<ref name="Caplan2002" /><ref name="ChungCaplan2012" /> Mendez et al. (1989) categorized caudate stroke patients into three groups based on stroke location and patterns of clinical symptoms: (1) apathetic or abulic, with difficulties perseverating in tasks (dorsolateral caudate); (2) restless, agitated, hyperactive, disinhibited, inappropriate, impulsive, distractible, and/or inattentive (ventromedial caudate); and (3) affective disturbances ([[anxiety]], depression, [[bipolar disorder]]) with [[psychosis|psychotic]] features ([[hallucination]]s, [[delusion]]s) (dorsolateral caudate, with larger lesions and more often extending into adjacent areas).<ref name="Caplan2002" /><ref name="ChungCaplan2012" /><ref name="pmid2927642" /> Sometimes, abulia can alternate with periods of disinhibition and agitation in people with caudate strokes.<ref name="pmid7922471" /><ref name="ChungCaplan2012" /><ref name="Caplan2002" /> The symptoms of caudate infarcts are assumed to be due to interruption of [[neural circuit]]s such as cortico–striatal–thalamic–cortical loops.<ref name="Caplan2002" /><ref name="ChungCaplan2012" /><ref name="CaplanHelgason1995" />

Caudate nucleus hemorrhages can mimic the symptoms of [[subarachnoid hemorrhage]] and can include [[headache]], [[nausea]], [[vomiting]], [[neck stiffness]], [[unconsciousness|decreased level of consciousness]], [[hemiparesis]], [[aphasia]], neuropsychological disturbances, [[disorientation]], [[aphasia]], [[mental confusion]], and gaze abnormalities, among others.<ref name="ChungCaplan2012" /><ref name="PellizzaroVentiPaciaroniCaso2012" /><ref name="pmid7922471" /> Caudate hemorrhages are due to rupture of penetrating arteries.<ref name="ChungCaplan2012" /> Aside from additional acute subarachnoid hemorrhage-like symptoms, symptoms of caudate hemorrhages are similar to those of caudate infarcts, including features like behavioral abnormalities, dysarthria, movement disorders, language disorders, and memory problems.<ref name="PellizzaroVentiPaciaroniCaso2012" />

The prognosis of caudate strokes has been considered good and benign, with majorities of individuals recovering and becoming independent.<ref name="PellizzaroVentiPaciaroniCaso2012" /><ref name="ChungCaplan2012" /> However, patients with caudate strokes can have residual deficits and dependency needs, can worsen clinically with time, or can require institutionalization.<ref name="ChungCaplan2012" /> Bokura & Robinson (1997) found that some individuals with caudate strokes deteriorated on the [[mini-mental state examination]] (MMSE), a short clinical test of basic cognitive function and impairment, during follow-up over 1 to 2{{nbsp}}years, whereas patients with other subcortical lesions tended to improve over 2{{nbsp}}years.<ref name="Caplan2002" /><ref name="pmid9158635" /> People with caudate strokes only rarely die, and generally because of underlying heart disease or other problems rather than the stroke itself.<ref name="ChungCaplan2012" /> However, although having favorable prognosis in the short-term, and having previously thought to be relatively benign, lacunar strokes in general are associated with greatly increased risk of stroke recurrence, cognitive impairment and dementia, and early death in the mid- to long-term.<ref name="pmid19210194">{{cite journal | vauthors = Arboix A, Martí-Vilalta JL | title = Lacunar stroke | journal = Expert Rev Neurother | volume = 9 | issue = 2 | pages = 179–96 | date = February 2009 | pmid = 19210194 | doi = 10.1586/14737175.9.2.179 | url = | quote = Lacunar infarcts show a paradoxical clinical course with a favorable prognosis in the short term, characterized by a low early mortality and reduced functional disability on hospital discharge, but with an increased risk of death, stroke recurrence and dementia in the mid- and long term. Asymptomatic progression of small-vessel disease is a typical feature of the lacunar infarcts. For this reason, lacunar infarction should be regarded as a potentially severe condition rather than a relatively benign disorder and, therefore, lacunar stroke patients require adequate and rigorous management and follow-up.}}</ref><ref name="pmid33085363">{{cite web | vauthors = Gore M, Bansal K, Khan Suheb MZ, Asuncion RM | title = Lacunar Stroke | journal = | volume = | issue = | pages = | date = 2024| pmid = 33085363 | doi = | url = https://www.ncbi.nlm.nih.gov/books/NBK563216/ | quote = In a follow-up study, patients with lacunar infarcts are diagnosed with dementia 4 to 12 times more frequently than the average population.[15] Post-stroke dementia in accumulated lacunar infarct is common despite their small size and association with small vessel disease.[16] [...] Lacunar strokes are a common cause of vascular dementia and mild cognitive impairment, often overlooked in clinical practice. Multiple silent lacunar strokes are documented on brain MRI, with patients presenting with mild cognitive impairment and early dementia.[32]}}</ref><ref name="pmid18644908">{{cite journal | vauthors = Norrving B | title = Lacunar infarcts: no black holes in the brain are benign | journal = Pract Neurol | volume = 8 | issue = 4 | pages = 222–8 | date = August 2008 | pmid = 18644908 | doi = 10.1136/jnnp.2008.153601 | url = | quote = Recent studies have shown that the prognosis after lacunar infarcts is not benign; the risk of recurrent stroke is no lower than for other ischaemic stroke subtypes, and there is an increased risk for cognitive decline, dementia and death in the long term.}}</ref><ref name="pmid12849212">{{cite journal | vauthors = Norrving B | title = Long-term prognosis after lacunar infarction | journal = Lancet Neurol | volume = 2 | issue = 4 | pages = 238–45 | date = April 2003 | pmid = 12849212 | doi = 10.1016/s1474-4422(03)00352-1 | url = | quote = [Lacunar] infarcts have commonly been regarded as benign vascular lesions with a favourable long-term prognosis. However, recent studies have shown that this is only the case early in the disease course. A few years after infarct, there is an increased risk of death, mainly from cardiovascular causes. The risk of recurrent stroke after lacunar infarct is similar to that for most other types of stroke, and patients have an increased risk of developing cognitive decline and dementia.}}</ref><ref name="pmid19673608">{{cite journal | vauthors = Grau-Olivares M, Arboix A | title = Mild cognitive impairment in stroke patients with ischemic cerebral small-vessel disease: a forerunner of vascular dementia? | journal = Expert Rev Neurother | volume = 9 | issue = 8 | pages = 1201–17 | date = August 2009 | pmid = 19673608 | doi = 10.1586/ern.09.73 | url = }}</ref> Treatment of caudate strokes may consist of [[antiplatelet drug|antiplatelet]] or [[anticoagulant]] agents and management of stroke [[risk factor]]s like hypertension and diabetes mellitus to reduce the risk of additional strokes.<ref name="ChungCaplan2012" /> On the basis of case reports and small case series, [[disorders of diminished motivation]], like apathy, abulia, and [[akinetic mutism]], secondary to stroke and other causes, may be treated with [[dopaminergic]] agents and other [[pro-motivational agent|pro-motivational]] medications, including [[psychostimulant]]s, [[bupropion]], [[atomoxetine]], [[modafinil]], [[dopamine agonist]]s, [[levodopa]], [[selegiline]], and [[acetylcholinesterase inhibitor]]s.<ref name="pmid16030444">{{cite journal | vauthors = Marin RS, Wilkosz PA | title = Disorders of diminished motivation | journal = J Head Trauma Rehabil | volume = 20 | issue = 4 | pages = 377–88 | date = 2005 | pmid = 16030444 | doi = 10.1097/00001199-200507000-00009 | url = }}</ref><ref name="SpiegelWarren2018">{{cite journal | vauthors = Spiegel DR, Warren A, Takakura W, Servidio L, Leu N | title = Disorders of diminished motivation: What they are, and how to treat them | journal = Current Psychiatry | date = January 2018 | volume = 17 | issue = 1 | pages = 10–18,20 | url = https://cdn.mdedge.com/files/s3fs-public/Document/December-2017/CP01701010.PDF}}</ref><ref name="pmid32044373">{{cite journal | vauthors = Arnts H, van Erp WS, Lavrijsen JC, van Gaal S, Groenewegen HJ, van den Munckhof P | title = On the pathophysiology and treatment of akinetic mutism | journal = Neurosci Biobehav Rev | volume = 112 | issue = | pages = 270–278 | date = May 2020 | pmid = 32044373 | doi = 10.1016/j.neubiorev.2020.02.006 | url = | doi-access = free | hdl = 2066/225901 | hdl-access = free }}</ref>