Axial motor disturbances after hypoxic lesions of the globus pallidus

Fève, A; Fénelon, Gilles; Wallays, C.; Rémy, Philippe; Guillard, A

doi:10.1002/mds.870080311

Cited by 77 publications

(52 citation statements)

References 30 publications

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“…The symptoms of our patient were attributable to the damage of the motor system, including putamen and globus pallidus, as an adverse effect of the hypoxia. However, the sensory system of our patient was intact, which is consistent with previous reports that show that the predominant clinical residues after hypoxic injury of the brain are motor disorders [7][8][9][10].…”

Section: Discussionsupporting

confidence: 92%

“…Feve AP and Fenelon G have also suggested that the globus pallidus plays an important role in controlling axial motion. In their study, four patients were examined due to axial motor impairment after hypoxic injury, and MRI scans found lesions of the globus pallidus in all four cases [8]. It is also generally accepted that parkinsonism or axial motor problems are commonly related to the pallidal lesions, and dystonia is related to lesions in the putamen [3].…”

Section: Discussionmentioning

confidence: 99%

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Extrapyramidal Dysfunction as a Consequence of Hypoxic Brain Injury

Tserensodnom,

Baatar,

Jambaldorj

et al. 2017

Cent. Asian j. Med. Sci.

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Objective: A case of parkinsonism after hypoxic ischemic encephalopathy is reported. Methods and Results:A 34-year-old woman presented parkinsonism due to hypoxicanoxic encephalopathy. The manifestation of parkinsonian syndrome was more present axially, than in the limb. She has also experienced cognitive deficits. The brain Magnetic Resonance Imaging (MRI) studies have shown abnormalities in putamen, caudate nucleus, globus pallidus and cerebral cortex. Conclusions: Diversity of clinical features may be depend on different neuropathological damage and neurotransmitter disbalance within the basal ganglia after a hypoxic-ischemic arrest, as seen in our patient. Therefore, understanding of all factors that contribute hypoxic brain injury is important to determine the clinical outcome and further management of patients.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Extrapyramidal Dysfunction as a Consequence of Hypoxic Brain Injury

Tserensodnom,

Baatar,

Jambaldorj

et al. 2017

Cent. Asian j. Med. Sci.

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show abstract

“…Feve et al 44 described 4 patients with pure pallidal lesions due to hypoxia who experienced freezing gait, postural impairment, speech disorder, micrographia, and mild appendicular bradykinesia. Similar cases with hypoxia caused by carbon monoxide poisoning have also been reported.…”

Section: Commentmentioning

confidence: 98%

The Natural History of the Syndrome of Primary Progressive Freezing Gait

Factor¹,

Jennings²,

Molho³

et al. 2002

Arch Neurol

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Primary progressive freezing gait appears to be a clinically distinct progressive neurological disorder that primarily affects gait, initially resulting in freezing and later in postural instability. A wheelchair-bound state often develops within 5 years. It is accompanied by other parkinsonian features, particularly bradykinesia, but is unresponsive to dopaminergic medications. It progresses in a fairly stereotyped manner. Primary progressive freezing gait disorder should be a unifying term for this disorder that has gone by many names in the literature and should be classified as a Parkinson-plus disorder.

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“…Published case reports have included nigropallidal degeneration, 59 pallidonigroluyisian degeneration (PNLD), 60 -62 primary CNS lymphoma, 63 HallervordenSpatz disease 64 and hypoxic ischemic lesions. 65 In addition, PD, diagnosed pathologically, has been shown to have the phenotype of PA with the notable exception of levodopa responsiveness. 66 …”

Section: Pure Akinesiamentioning

confidence: 99%

The clinical spectrum of freezing of gait in atypical parkinsonism

Factor

2008

Mov. Disord.

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Freezing of gait (FOG), commonly seen in advanced Parkinson's disease (PD), has been classified as its fifth cardinal feature. However, its presence frequently leads to a misdiagnosis of PD. FOG is actually more common in atypical parkinsonism (AP): including vascular Parkinsonism (VP), progressive supranuclear palsy (PSP), multiple system atrophy (MSA), corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), and higher level gait disorders (HLGDs). VP is the result of multiple small vessel infarcts (lacunar state or Binswanger's disease), particularly involving the frontal, parietal, and basal ganglia regions. Approximately 50% have FOG (often referred to as lower body parkinsonism). FOG is also common in neurodegenerative forms of AP, present in 45-57%. Of these, FOG is present in 53% of PSP, 54% MSA, 54% DLB, 25% CBD, and 40% HLGD. It is generally seen in the late stages. There are two syndromes closely associated with AP that are dominated by FOG; pure akinesia (PA) and primary progressive freezing gait (PPFG). PA is characterized by akinesia of gait (including FOG), writing, and speech. Tremor, rigidity, dementia, and response to levodopa are notably absent. PPFG is defined by early FOG (often the initial feature) that progresses to include postural instability. It is accompanied by bradykinesia, rigidity, postural tremor, dementia, and levodopa unresponsiveness. Both syndromes are heterogeneous but PSP seems to be the most common cause. CBD and DLB can also present as PPFG. FOG is a common feature of AP and although typically occurring late in disease may also be an early symptom.

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Axial motor disturbances after hypoxic lesions of the globus pallidus

Cited by 77 publications

References 30 publications

Extrapyramidal Dysfunction as a Consequence of Hypoxic Brain Injury

Extrapyramidal Dysfunction as a Consequence of Hypoxic Brain Injury

The Natural History of the Syndrome of Primary Progressive Freezing Gait

The clinical spectrum of freezing of gait in atypical parkinsonism

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