A case of subacute parkinsonism presenting as bilateral basal ganglia legions by MRI in diabetic uremic syndrome

Nishimura, Yoshiko; Shibata, Koichi; Funaki, Takenori; Ito, Hiroyuki; Ito, Eiichi; Otsuka, Kuniaki

doi:10.5692/clinicalneurol.53.217

Cited by 11 publications

(14 citation statements)

References 24 publications

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“…To our knowledge, this is the largest cohort which followed patients with uremia without or with BG lesions and its related movement disorders for 2 years to determine their clinical and neuroimaging outcomes. In the literature, there are approximately 40 case reports of extrapyramidal movement disorders due to BG lesions with uremia [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] . Among them, only Wang and Cheng 5 prospectively studied six patients with uremia who had BG-related movement disorders.…”

Section: Discussionmentioning

confidence: 99%

Movement Disorders Due to Selective Basal Ganglia Lesions with Uremia

Hamed

Mohamed

Elhameed

et al. 2020

Can. J. Neurol. Sci.

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ABSTRACT:Background:Basal ganglia (BG) lesions are rarely reported in patients with uremia and may manifest by movement disorders. However, their exact incidence and pathogenesis have not been extensively studied. This study aimed to determine the frequency, types, risk variables (clinical, laboratory, and imaging), and manifestations of BG lesions with uremia and patients’ neurologic outcomes.Methods:This observational study included 70 adults (mean age: 45.87 ± 3.36 years; duration of uremia: 5.5 ± 1.5 years). They underwent extensive evaluations (clinical, laboratory, and neuroimaging) and had prospectively evaluated clinically every 3 months for 2 years. Repeated magnetic resonance imaging (MRI) brains were done to patients with movement disorders and correlated with their neurologic outcomes.Results:BG lesions were found in 15 patients (21.4%) and 6 (8.6%) had movement disorders [Parkinsonism (n = 4), choreo-dystonia (n = 1) and dystonia (n = 1)] after the onset of uremia (mean = 10 months). There were no characteristic risk variables that distinguished patients with movement disorders from those without. Five developed movement disorders prior to the period of the study and one was de novo. The majority was females and had diabetes and higher frequencies of abnormal renal dysfunction, metabolic derangements, and white matter hyperintensities in MRIs. Movement disorders persisted in all patients despite the resolution of neuroimaging in three patients.Conclusions:There is no clear threshold for renal failure to result in movement disorders due to BG lesions. The clinical outcome is variables depending on each patient’s comorbidities and complications. Persistent neuronal damage (due to uremic toxins/metabolic/nutritional and ischemic/microvascular factors) has been suggested as the cause of poor neurologic outcomes.

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Section: Discussionmentioning

confidence: 99%

Movement Disorders Due to Selective Basal Ganglia Lesions with Uremia

Hamed

Mohamed

Elhameed

et al. 2020

Can. J. Neurol. Sci.

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“…Other symptoms of the syndrome include disturbances in consciousness, dysarthria, dysphagia, and chorea. [1][2][3][4] Neurologic symptoms improve in some patients, and lesions usually regress (as assessed by conventional MRI); however, the overall prognosis is poor in the majority of cases. 1 The diffusion abnormalities observed in the present case were consistent with those reported previously.…”

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confidence: 99%

“…8 In addition, a human study demonstrated that cerebral vasodilatory capacity is decreased in patients with anemia secondary to chronic renal failure, 9 indicating that anemia deserves more attention, although hematologic findings have rarely been described in this syndrome. 3 Considering the frequent occurrence of peridialytic blood pressure changes, 10 it is tempting to speculate that blood pressure changes contribute to failed autoregulation of perforating arteries, resulting in edematous lentiform nucleus lesions in cases of long-term kidney failure, particularly in those with diabetes and anemia. The present case highlights the clinical and radiologic characteristics of diabetic uremic syndrome, or, more precisely, uremic lenticulostriate syndrome.…”

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Mystery Case: Parkinsonism in a diabetic uremic patient

et al. 2016

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A 71-year-old man noticed a sudden feeling of weakness in the limbs after a routine hemodialysis session, and was admitted to the hospital. He had a history of hypertension and diabetes mellitus for approximately 20 years and diabetic nephropathy requiring hemodialysis for over 1 year. He was taking metformin, which was changed from sulfonylurea 2 months before. His consciousness level deteriorated 1 day after symptom onset, and laboratory examination revealed a blood glucose level of 42 mg/dL. His level of consciousness improved after glycemic treatment, but the weakness did not. MRI of the brain revealed abnormalities in the bilateral basal ganglia (figure e-1 on the Neurology ® Web site at Neurology.org).The patient was referred to our hospital 8 days after symptom onset. Neurologic examination revealed normal consciousness, symmetric rigid-akinetic parkinsonism (rigidity of the neck and limbs, akinesia, severe postural instability, Myerson sign, and absence of tremor), proximal muscle weakness, bilateral hyperreflexia, and bilateral Babinski signs. Blood tests were as follows: hemoglobin 9.8 g/dL, hematocrit 32.9%, mean corpuscular volume 83.1 fL, blood urea nitrogen 44 mg/dL, creatinine 9.2 mg/dL, sodium 134 mEq/L, potassium 4.0 mEq/L, calcium 8.8 mg/dL, inorganic phosphorus 4.7 mg/dL (reference range 2.5-4.5 mg/dL), magnesium 3.0 mg/dL (reference range 1.9-2.5 mg/dL), iron 26 mg/dL (reference range 60-210 mg/dL), glucose 158 mg/dL, and HbA1c 6.1%. Brain MRI (3.0T) acquired 10 days after symptom onset demonstrated edematous changes in the basal ganglia bilaterally, particularly in the putamen and globus pallidus ( figure 1A). Abnormalities in the bilateral globus pallidus on diffusion-weighted imaging and apparent diffusion coefficient (ADC) map were less evident than they were on the initial MRI ( figure 1, B and C). Of note, pseudocontinuous arterial spin labeling (pCASL), which is a perfusion imaging technique without contrast media use, revealed marked hyperperfusion in the bilateral basal ganglia ( figure 1D), accompanied by dilated perforating branches, or lenticulostriate arteries (figure 1, E and F).

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“…The most prominent MRI findings were T1‐hyperintense lesions involving the basal ganglia in C‐NKH patients and T2‐hyperintense lesions involving the basal ganglia in C‐URE patients. These distinctive MRI features provide indications of the different pathogenic mechanisms that occur in the basal ganglia, although the precise mechanisms remain unclear …”

Section: Discussionmentioning

confidence: 99%

Chorea due to diabetic hyperglycemia and uremia: Distinct clinical and imaging features

Kim

et al. 2015

Movement Disorders

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This study was undertaken to describe the clinical and imaging characteristics of patients with chorea associated with nonketotic hyperglycemia (C-NKH) in comparison with patients with chorea associated with uremia (C-URE). We retrospectively analyzed the clinical data of consecutive 10 C-NKH and five C-URE patients who were treated between January 1, 2001 and January 31, 2013. Women were more frequently affected by C-NKH (70% vs. 30%) and C-URE (80% vs. 20%) compared with men. The C-NKH patients demonstrated T1-hyperintense and inhomogeneous lesions in the basal ganglia, whereas C-URE patients demonstrated T2-hyperintense and homogeneous lesions in the basal ganglia. The mean time for chorea resolution after treatment was significantly shorter in C-NKH patients than in C-URE patients (4.4 ± 2.6 d vs. 73.8 ± 14.2 d, respectively; P = 0.005). The clinical and imaging features are remarkably different between C-NKH and C-URE patients, suggesting distinct pathogenic mechanisms.

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A case of subacute parkinsonism presenting as bilateral basal ganglia legions by MRI in diabetic uremic syndrome

Cited by 11 publications

References 24 publications

Movement Disorders Due to Selective Basal Ganglia Lesions with Uremia

Movement Disorders Due to Selective Basal Ganglia Lesions with Uremia

Mystery Case: Parkinsonism in a diabetic uremic patient

Chorea due to diabetic hyperglycemia and uremia: Distinct clinical and imaging features

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