Pilot study of a robotic protocol to treat shoulder subluxation in patients with chronic stroke.

BACKGROUND: Shoulder subluxation is a frequent complication of motor impairment after stroke, leading to soft tissue damage, stretching of the joint capsule, rotator cuff injury, and in some cases pain, thus limiting use of the affected extremity beyond weakness. In this pilot study, we determined whether robotic treatment of chronic shoulder subluxation can lead to functional improvement and whether any improvement was robust. METHODS: 18 patients with chronic stroke (3.9 ± 2.9 years from acute stroke), completed 6 weeks of robotic training using the linear shoulder robot. Training was performed 3 times per week on alternate days. Each session consisted of 3 sets of 320 repetitions of the affected arm, and the robotic protocol alternated between training vertical arm movements, shoulder flexion and extension, in an anti-gravity plane, and training horizontal arm movements, scapular protraction and retraction, in a gravity eliminated plane. RESULTS: Training with the linear robot improved shoulder stability, motor power, and resulted in improved functional outcomes that were robust 3 months after training. CONCLUSION: In this uncontrolled pilot study, the robotic protocol effectively treated shoulder subluxation in chronic stroke patients. Treatment of subluxation can lead to improved functional use of the affected arm, likely by increasing motor power in the trained muscles.

Management of medical complications.

Medical comorbidities and complications are expected following stroke, traumatic brain injury, and spinal cord injury. The neurorehabilitation physician's role is to manage these comorbidities, prevent complications, and serve as a medical and neurologic resource for the patient, family, and neurorehabilitation team. The most common comorbidities are similar to those found in the general population, namely hypertension, dyslipidemia, diabetes mellitus, and ischemic heart disease. Frequent complications encountered in the neurorehabilitation unit relate to medication side effects, medical comorbidities, and the direct effect of the neurologic injury. They include orthostatic hypotension; syncope or presyncope; cardiac arrhythmia; bowel and bladder dysfunction; seizures; pressure sores; dysphagia-related pneumonia, dehydration, and malnutrition; venous thromboembolism; falls; and sexual dysfunction. This article discusses strategies for managing comorbidities and avoiding complications.

Spatial distribution of long-term potentiation in the surround of visual cortex lesions in vitro.

Focal visual cortex lesions lead to functional changes in the surrounding cortical network, possibly mediated through synaptic long-term potentiation (LTP). Although a post-lesional facilitation of LTP has been observed, nothing is known about the spatial profile of LTP in the normal and focally lesioned visual cortex of rats. We used a 64-multielectrode array to characterise the spread of LTP induced by theta-burst stimulation in layer IV. Measurements were made at comparable distances from the midline in the visual cortex of controls, sham-operated and lesioned animals. In control rats, LTP was elicited in projections to all visual cortex layers. However, we completely failed to observe LTP in sham-operated animals 1-4 days after surgery. At comparable survival times, no LTP could be elicited in the lesion-treated rats in direct vicinity of the border of the injury, while LTP was successfully induced at larger distances from the lesion. The maximal reach of this restored post-lesion LTP was spatially more limited than in controls and equal in all directions, accordingly absolute distance and not maximal length or density of connections seems to rule local lesion-induced functional remodelling.

Leukoencephalopathy in adults: is it adrenoleukodystrophy? A case report and molecular analysis.

Adult onset cerebral X-ALD (AOCALD) is a rare disease, but should be considered an important differential diagnosis in adults presenting with leukencephalopathy. We here report the case of a 40-year-old man with a history of progressive cognitive decline who presented with a first-time seizure. Initial workup included magnetic resonance imaging (MRI) of the brain which showed extensive frontotemporal leukoencephalopathy. A subsequent brain biopsy showed demyelination and perivascular macrophages. Further workup included serum very long chain fatty acid concentration (VLCFA), which was found to be elevated. An MRI of the total spine showed diffuse atrophy, but no intrinsic cord signal changes, and the diagnosis of AOCALD was established. Genomic sequencing revealed a nonsense mutation in exon 8 (2188G-->A, W601X), to our knowledge not reported in context with AOCALD. A family pedigree was obtained, and other family members at risk were identified and underwent genetic counseling. In conclusion, AOCALD is an important differential diagnosis in adults presenting with cognitive decline. While treatment for affected patients is often supportive only, molecular diagnosis serves as a basis for genetic counseling, identification of relatives at risk and timely referral to a treatment program.

Midbrain serotonergic neurons are central pH chemoreceptors.

Serotonergic neurons in the medulla are central respiratory chemoreceptors. Here we show that serotonergic neurons in the midbrain of rats are also highly chemosensitive to small changes in CO2/pH and are closely associated with large penetrating arteries. We propose that midbrain raphé neurons are sensors of blood CO2 that maintain pH homeostasis by inducing arousal, anxiety and changes in cerebrovascular tone in response to respiratory acidosis.