An unusual case of paroxysmal kinesigenic dyskinesia

Thomas, Reji; Behari, M; Gaikwad, Shailesh; Prasad, Kameshwar

doi:10.1054/jocn.2000.0905

Cited by 7 publications

(4 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Prolonged hypocalcemia causes irritability of these partially damaged neurons, which triggers PKD. This is further supported by the finding that the dyskinesia improves when serum calcium levels return to baseline, although with persistent basal ganglia calcification 9 . Paroxysmal dyskinesia can occur in patients with normal calcium levels with basal ganglia calcifications and in cases of PHP without basal ganglia calcification 7,10 .…”

Section: Discussionmentioning

confidence: 73%

“…This is further supported by the finding that the dyskinesia improves when serum calcium levels return to baseline, although with persistent basal ganglia calcification. 9 Paroxysmal dyskinesia can occur in patients with normal calcium levels with basal ganglia calcifications and in cases of PHP without basal ganglia calcification. 7,10 Severity of movement abnormality does not correlate with calcifications in the brain or the level of PTH.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Paroxysmal Kinesigenic Dyskinesia Secondary to Pseudohypoparathyroidism Responding to Correction of Calcium

Mudassir

Kumar

Sinha

et al. 2022

Movement Disord Clin Pract

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 73%

mentioning

confidence: 99%

Paroxysmal Kinesigenic Dyskinesia Secondary to Pseudohypoparathyroidism Responding to Correction of Calcium

Mudassir

Kumar

Sinha

et al. 2022

Movement Disord Clin Pract

View full text Add to dashboard Cite

“…Important clues that a paroxysmal dyskinesia is secondary rather than primary include the presence of significant pain [ 59 ] and an abnormal interictal examination. Secondary paroxysmal dyskinesias may occur in hypoparathyroidism [ 60 ], pseudohypoparathyroidism [ 61 , 62 ], supraspinal lesions [ 59 , 63 ], spinal cord glioma [ 64 ] and spinal cord compression [ 65 , 66 ].…”

Section: Reviewmentioning

confidence: 99%

Spinal-generated movement disorders: a clinical review

Termsarasab

Thammongkolchai

2015

J Clin Mov Disord

View full text Add to dashboard Cite

Spinal-generated movement disorders (SGMDs) include spinal segmental myoclonus, propriospinal myoclonus, orthostatic tremor, secondary paroxysmal dyskinesias, stiff person syndrome and its variants, movements in brain death, and painful legs-moving toes syndrome. In this paper, we review the relevant anatomy and physiology of SGMDs, characterize and demonstrate their clinical features, and present a practical approach to the diagnosis and management of these unusual disorders.Electronic supplementary materialThe online version of this article (doi:10.1186/s40734-015-0028-1) contains supplementary material, which is available to authorized users.

show abstract

“…[15][16][17] However, there is still a large proportion of patients with PKD with unclear genetic causes. The common etiology of secondary PKD consists of multiple sclerosis, 18 brain calcification, 19,20 and metabolic abnormalities (hyperthyroidism, 21 hypoparathyroidism, 22,23 and hyperglycemia 24 ).…”

Section: Introductionmentioning

confidence: 99%

The Pathogenesis of Paroxysmal Kinesigenic Dyskinesia: Current Concepts

Tian

Huang

et al. 2023

Movement Disorders

View full text Add to dashboard Cite

Paroxysmal kinesigenic dyskinesia (PKD) is a movement disorder characterized by recurrent and transient episodes of involuntary movements, including dystonia, chorea, ballism, or a combination of these, which are typically triggered by sudden voluntary movement. Disturbance of the basal ganglia‐thalamo‐cortical circuit has long been considered the cause of involuntary movements. Impairment of the gating function of the basal ganglia can cause an aberrant output toward the thalamus, which in turn leads to excessive activation of the cerebral cortex. Structural and functional abnormalities in the basal ganglia, thalamus, and cortex and abnormal connections between these brain regions have been found in patients with PKD. Recent studies have highlighted the role of the cerebellum in PKD. Insufficient suppression from the cerebellar cortex to the deep cerebellar nuclei could lead to overexcitation of the thalamocortical pathway. Therefore, this literature review aims to provide a comprehensive overview of the current research progress to explore the neural circuits and pathogenesis of PKD and promote further understanding and outlook on the pathophysiological mechanism of movement disorders. © 2023 International Parkinson and Movement Disorder Society.

show abstract

An unusual case of paroxysmal kinesigenic dyskinesia

Cited by 7 publications

References 22 publications

Paroxysmal Kinesigenic Dyskinesia Secondary to Pseudohypoparathyroidism Responding to Correction of Calcium

Paroxysmal Kinesigenic Dyskinesia Secondary to Pseudohypoparathyroidism Responding to Correction of Calcium

Spinal-generated movement disorders: a clinical review

The Pathogenesis of Paroxysmal Kinesigenic Dyskinesia: Current Concepts

Contact Info

Product

Resources

About