Post-stroke dyskinesias

Nakawah, Mohammad Obadah; Lai, Eugene C.

doi:10.2147/ndt.s118347

Cited by 20 publications

(22 citation statements)

References 68 publications

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“…This is consistent with current literature, which show persistent deficits in both animals and humans [52][53][54][55]. Consideration of the long-term consequences of stroke are important because sensorimotor and cognitive deficits can severely affect post-stroke quality of life [56][57][58]. Our longitudinal study parallels the rodent time frame for functional recovery and extends the translatability of our results to stroke patients.…”

Section: Cells and Significant Increases In Cd4+ T Cells And Cd8+ T supporting

confidence: 91%

Experimental Stroke Induces Chronic Gut Dysbiosis and Neuroinflammation in Male Mice

Brichacek¹,

Nwafor²,

Benkovic³

et al. 2020

Preprint

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Recent literature implicates gut epithelia mucosa and intestinal microbiota as important players in post-stroke morbidity and mortality. As most studies have focused on the acute effects of stroke on gut dysbiosis, our study objective was to measure chronic, longitudinal changes in the gut microbiota and intestinal pathology following ischemic stroke. We hypothesized that mice with experimental ischemic stroke would exhibit chronic gut dysbiosis and intestinal pathology up to 36 days post-stroke compared to sham controls. Male C57BL/6J mice were subjected to 60 minutes of transient middle cerebral artery occlusion (tMCAO) or sham surgery. To determine the long-term effects of tMCAO on gut dysbiosis, fecal boli were collected pre- and post-tMCAO on days 0, 3, 14, and 28. Bioinformatics analysis demonstrate significant differences in abundance among Firmicutes and Bacteroidetes taxa at the phylum, family, and species levels in tMCAO compared to sham mice that persisted up to one month post-stroke. The most persistent changes in post-stroke microbial abundance were a decrease in bacteria family S24-7 and significant increases in Ruminococcaceae. Overall, these changes resulted in a persistently increased Firmicutes:Bacteroidetes ratio in stroke animals. Intestinal histopathology showed evidence of chronic intestinal inflammation that included marked increases in immune cell infiltration with mild-moderate epithelial hyperplasia and villous blunting. Increased astrocyte and microglial activity were also detected one-month post-stroke. These results demonstrate that acute, post-stroke disruption of the gut-brain-microbiota axis progresses to chronic gut dysbiosis, intestinal inflammation, and chronic neuroinflammation.Clinical PerspectivesThe microbiota-gut-brain axis, recently implicated in several neurological disorders, remains largely unexplored at chronic time points post-tMCAO.Our results demonstrate chronic gut dysbiosis, prolonged behavioral deficits, and persistent cerebral and intestinal inflammation post-tMCAO in male C57BL/6J mice.These results suggest that manipulation of microbiota may help reduce poor outcomes after stroke and lead to improved post-stroke functional recovery.

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Section: Cells and Significant Increases In Cd4+ T Cells And Cd8+ T supporting

confidence: 91%

Experimental Stroke Induces Chronic Gut Dysbiosis and Neuroinflammation in Male Mice

Brichacek¹,

Nwafor²,

Benkovic³

et al. 2020

Preprint

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“…7 The correlating lesions are in the basal ganglia and adjacent white matter, usually in the territory of the middle cerebral artery or posterior cerebral artery. 7 Poststroke dyskinesias, of which the most commonly reported is hemichorea-hemiballism, 3 may present acutely or be delayed by months to years followed by a highly variable course that may be transient, recurrent, persistent, or progressive; however, they are usually self-limited and resolve within 6-12 months. 3 Hyperglycemic hemiballism is the second most common cause of acute hemiballism.…”

Section: Discussionmentioning

confidence: 99%

“…7 Poststroke dyskinesias, of which the most commonly reported is hemichorea-hemiballism, 3 may present acutely or be delayed by months to years followed by a highly variable course that may be transient, recurrent, persistent, or progressive; however, they are usually self-limited and resolve within 6-12 months. 3 Hyperglycemic hemiballism is the second most common cause of acute hemiballism. 2 The first case of hemichoreahemiballism associated with hyperglycemia was described by Bedwell in 1960 and was initially most frequently reported in elderly, typically East Asian, women with diabetes mellitus type 2.…”

Section: Discussionmentioning

confidence: 99%

“…The initial differential of acquired causes of hemichoreahemiballism includes vascular, autoimmune/inflammatory, metabolic, infectious, toxin/drug-induced, and neoplastic or other structural etiologies. [1][2][3] In particular, stroke, Wilson disease, thyrotoxicosis, hyperglycemia, and systemic lupus erythematosus have been known to cause this syndrome. 1 Genetic causes were less likely given age and CT abnormalities.…”

Section: Sectionmentioning

confidence: 99%

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Clinical Reasoning: A 65-year-old woman with subacute hemiballism

et al. 2019

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A 65-year-old, right-hand-dominant woman with a history of hypertension, hyperlipidemia, poorly controlled diabetes, and remote breast cancer presented with 1 week of progressive, involuntary left hemibody movements. One month prior, she was a restrained driver in a headon motor vehicle collision with possible brief loss of consciousness. The patient was evaluated at an emergency department and was noted to have musculoskeletal injuries not requiring intervention. No imaging was performed. Since the accident, she described feeling a "mental fog" with slurred speech that has progressively worsened and persistent left shoulder pain.About 1 week prior to presentation at our facility, she developed nonvoluntary movements starting in her left shoulder, described as "flopping," with gradual progression to incorporate the whole upper limb that spread to the ipsilateral leg and face. These movements became more frequent and increased in amplitude over a week. There was no change in consciousness, loss of bowel/bladder function, or tongue biting during these movements, and no postevent confusion. Due to interference with daily activities, she presented to the emergency department for further evaluation, where a CT head demonstrated a hyperdense lesion in the right basal ganglia with limited surrounding edema.The patient's vital signs were within normal limits and neurologic examination was notable for mild dysarthria with dyskinetic oromandibular facial movements, intact strength throughout (though limited by left shoulder pain), mild left dysmetria, and left dysdiadochokinesia. At rest, she had intermittent ballistic-choreic movements of her left upper and lower extremities with involvement of the face and tongue, which worsened with intentional maneuvers.

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“…As a consequence, it might increase GABAergic neurotransmission and thereby modulate movement disorders 6,12. In clinical practice, clonazepam has been proven to be effective in several poststroke movement disorders including hemichorea, hemiballism, dystonia, myoclonus, and tremor 13,14…”

Section: Discussionmentioning

confidence: 99%

Punding following posterior cerebral artery infarction: a case report and review of literature

Lin

Lien

et al. 2017

NDT

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IntroductionPunding is a complex stereotyped behavior, characterized by excessiveness, non-goal orientation, and repetitiveness. It is mostly associated with Parkinson’s disease, and very few cases in non-Parkinson’s disease have been reported. We report a case of punding associated with supratentorial ischemic stroke.Case presentationWe present a 70-year-old man with left posterior cerebral artery infarction with quetiapine-induced punding manifesting as repetitive unidirectional body turning. Remission of punding behavior ensued after cessation of quetiapine and administration of clonazepam.ConclusionThis case describes the clinical course of quetiapine-induced punding in a patient with left posterior cerebral artery infarction. It suggests clonazepam may serve as a treatment option for poststroke punding.

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Post-stroke dyskinesias

Cited by 20 publications

References 68 publications

Experimental Stroke Induces Chronic Gut Dysbiosis and Neuroinflammation in Male Mice

Experimental Stroke Induces Chronic Gut Dysbiosis and Neuroinflammation in Male Mice

Clinical Reasoning: A 65-year-old woman with subacute hemiballism

Punding following posterior cerebral artery infarction: a case report and review of literature

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