Journal of the neurological sciences
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We investigated the combination of robot-assisted rehabilitation (RT) using a single-joint hybrid assistive limb (HAL-SJ) and botulinum toxin A (BTX-A) as therapy for paretic arm with spasticity in post-stroke patients. Participants were seven patients (4 females, 3 males; mean (±SD) age: 60.6±8.4years) who had spastic hemiplegia following chronic stroke. On the day following BTX-A injection, we started RT, which was performed for 20 sessions of 60min each over a two-week period. ⋯ FMA, MAL, and DAS scores significantly improved at two weeks and four months (p<0.05), except DAS scores at four months (p=0.068). The fNIRS study showed that cortical activation increased in the ipsilesional primary sensorimotor area at two weeks and at the four months follow-up. Our pilot study showed that the combination of RT and BTX-A therapy was an effective approach for treating spastic hemiplegia due to stroke, and functional imaging study showed neuroplasticity induced by the treatment.
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Central pontine myelinolysis (CPM) is a potentially-devastating complication of rapid osmolar shifts, classically attributed to overlyaggressive correction of chronic hyponatremia. Magnetic resonance imaging (MRI) allowed earlier diagnosis of CPM, but most importantly, it has revealed that the odds of good functional recovery are surprisingly high. ⋯ Due to the rarity of CPM, very little has been published on the evolution of these MRI findings. We present a case of CPM in an alcoholic young man, and describe the temporal evolution of both the trident and piglet signs on MRI in CPM.
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Letter Historical Article
"Puttin' on the Ritz": Young Frankenstein and neurology.
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Hemorrhagic transformation and cerebral edema are feared complications of acute ischemic stroke but mechanisms are poorly understood and reliable early markers are lacking. Early assessment of cerebrovascular hemodynamics may advance our knowledge in both areas. We examined the relationship between dynamic cerebral autoregulation (CA) in the early hours post ischemia, and the risk of developing hemorrhagic transformation and cerebral edema at 24h post stroke METHODS: We prospectively enrolled 46 patients from our center with acute ischemic stroke in the middle cerebral artery territory. Cerebrovascular resistance index was calculated. Dynamic CA was assessed by transfer function analysis (coherence, phase and gain) of the spontaneous blood flow velocity and blood pressure oscillations. Infarct volume, hemorrhagic transformation, cerebral edema, and white matter changes were collected from computed tomography performed at presentation and 24h. ⋯ At admission, phase was lower (worse CA) in patients with hemorrhagic transformation [6.6±30 versus 45±38°; adjusted odds ratio 0.95 (95% confidence internal 0.94-0.98), p=0.023] and with cerebral edema [6.6±30 versus 45±38°, adjusted odds ratio 0.96 (0.92-0.999), p=0.044]. Progression to edema was associated with lower cerebrovascular resistance (1.4±0.2 versus 2.3±1.5mmHg/cm/s, p=0.033) and increased cerebral blood flow velocity (51±25 versus 42±17cm/s, p=0.033) at presentation. All hemodynamic differences resolved at 3months CONCLUSIONS: Less effective CA in the early hour post ischemic stroke is associated with increased risk of hemorrhagic transformation and cerebral edema, possibly reflecting breakthrough hyperperfusion and microvascular injury. Early assessment of dynamic CA could be useful in identifying individuals at risk for these complications.
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Canine degenerative myelopathy (DM) is a fatal neurodegenerative disorder. Dogs with typical clinical signs carry homozygous mutations in the superoxide dismutase 1 (SOD1) gene; therefore, DM is regarded as a naturally-occurring model of amyotrophic lateral sclerosis (ALS). Despite the presence of a toxic mutant protein, E40K-SOD1 heterozygotes rarely develop clinical signs. ⋯ In contrast, all symptomatic E40K-homozygotes contained 16G9-reactive SOD1 in their spinal neurons and reactive astrocytes. These results suggest that mutant SOD1 proteins accumulate in reactive astrocytes during the early phase of DM pathology, which may contribute to subclinical neurodegeneration. The early involvement of reactive astrocytes in the pathogenesis of DM is strongly suspected and warrants further investigations in the context of non-cell autonomous neuronal death, as proposed for ALS.