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Background: Neurological symptoms are common manifestation in acute COVID-19. This includes hyper- and hypokinetic movement disorders. Data on their outcome, however, is limited., Methods: Cases with new-onset COVID-19-associated movement disorders were identified by searching the literature. Authors were contacted for outcome data which were reviewed and analyzed., Results: Movement disorders began 12.6 days on average after the initial onset of COVID-19. 92% of patients required hospital admission (mean duration 23 days). In a fraction of patients (6 of 27; 22%; 4 males/2 females, mean age 66.8 years) the movement disorder (ataxia, myoclonus, tremor, parkinsonism) was still present after a follow-up period of 7.5 ± 3 weeks. Severe COVID-19 in general and development of encephalopathy were risk factors, albeit not strong predictors, for the persistence., Conclusions: The prognosis of new-onset COVID-19-associated movement disorder appears to be generally good. The majority recovered without residual symptoms within several weeks or months. Permanent cases may be due to unmasking of a previous subclinical movement disorder or due to vascular/demyelinating damage. Given the relatively low response rate of one third only and the heterogeneity of mechanisms firm conclusions on the (long-term) outome cannot, however, be drawn., (© 2023. The Author(s).)

Background: SPG4 is a subtype of hereditary spastic paraplegia (HSP), an upper motor neuron disorder characterized by axonal degeneration of the corticospinal tracts and the fasciculus gracilis. The few neuroimaging studies that have focused on the spinal cord in HSP are based mainly on the analysis of structural characteristics., Methods: We assessed diffusion-related characteristics of the spinal cord using diffusion tensor imaging (DTI), as well as structural and shape-related properties in 12 SPG4 patients and 14 controls. We used linear mixed effects models up to T3 in order to analyze the global effects of 'group' and 'clinical data' on structural and diffusion data. For DTI, we carried out a region of interest (ROI) analysis in native space for the whole spinal cord, the anterior and lateral funiculi, and the dorsal columns. We also performed a voxelwise analysis of the spinal cord to study local diffusion-related changes., Results: A reduced cross-sectional area was observed in the cervical region of SPG4 patients, with significant anteroposterior flattening. DTI analyses revealed significantly decreased fractional anisotropy (FA) and increased radial diffusivity at all the cervical and thoracic levels, particularly in the lateral funiculi and dorsal columns. The FA changes in SPG4 patients were significantly related to disease severity, measured as the Spastic Paraplegia Rating Scale score., Conclusions: Our results in SPG4 indicate tract-specific axonal damage at the level of the cervical and thoracic spinal cord. This finding is correlated with the degree of motor disability., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.)

SPG4 is an autosomal dominant pure form of hereditary spastic paraplegia (HSP) caused by mutations in the SPAST gene. HSP is considered an upper motor neuron disorder characterized by progressive spasticity and weakness of the lower limbs caused by degeneration of the corticospinal tract. In other neurodegenerative motor disorders, the thalamus and basal ganglia are affected, with a considerable impact on disease progression. However, only a few works have studied these brain structures in HSP, mainly in complex forms of this disease. Our research aims to detect potential alterations in the volume and shape of the thalamus and various basal ganglia structures by comparing 12 patients with pure HSP and 18 healthy controls. We used two neuroimaging procedures: automated segmentation of the subcortical structures (thalamus, hippocampus, caudate nucleus, globus pallidus, and putamen) in native space and shape analysis of the structures. We found a significant reduction in thalamic volume bilaterally, as well as an inward deformation, mainly in the sensory-motor thalamic regions in patients with pure HSP and a mutation in SPG4. We also observed a significant negative correlation between the shape of the thalamus and clinical scores (the Spastic Paraplegia Rating Scale score and disease duration). Moreover, we found a 'Group × Age' interaction that was closely related to the severity of the disease. No differences in volume or in shape were found in the remaining subcortical structures studied. Our results suggest that changes in structure of the thalamus could be an imaging biomarker of disease progression in pHSP.

Introduction: Traumatic brain injury (TBI) in the elderly is becoming an increasingly frequent phenomenon. Studies have mainly analyzed the influence of age as a continuous variable and have not specifically looked at geriatric patients as a group. The aim of this study is to map the magnitude and characteristics of geriatric TBI and to identify factors contributing to their poorer outcome., Material and Methods: Based on the ICD-9 register of the University Hospitals Leuven demographic and clinical variables of TBI were analyzed (2002-2008). The influence of older age on physiological variables was assessed using the Brain-IT database., Results: The elderly (aged ≥65 years) accounted for 38.2% of non-concussion TBI and 32.6% of ICU admissions, representing the largest age group. The elderly had a significantly lower ICP (median 10.06 mmHg versus median 14.52 mmHg; p = 0.048), but no difference in their measure of autoregulation (daily mABP/ICP correlation coefficient) compared with 20-35 year-olds. TBI was caused by a fall in 78.9% of elderly patients and 42.3% suffered a mass lesion. 72.1% had cardiovascular comorbidity. Complications did not differ from their younger counterparts., Discussion: Geriatric TBI is a significant phenomenon. Poorer outcomes are not yet sufficiently explained by physiological monitoring data, but reduced vascular versatility is likely to contribute. More research is needed in order to develop specific management protocols.

Unlabelled: A literature review was conducted to assess risk of cardiac valve regurgitation (CVR) associated with use of ergot-derived and non-ergot dopamine agonists (DAs) in patients with Parkinson's disease (PD)., Inclusion Criteria: case-control/observational studies of >10 patients with PD treated with DAs, including a control group and assessment of incidence/risk of CVR. Of the 166 publications identified, 14 met all inclusion criteria and included 1,750 patients. In 11 of the studies, a significant increase in CVR frequency of any severity (at the aortic, mitral or tricuspid valve) in the ergot group vs. the non-ergot or control group was described. No study reported increased risk of CVR for non-ergot DAs, compared with controls. In the studies identified in the literature, the use of ergot-derived DAs (pergolide and cabergoline) in patients with PD was associated with increased risk of CVR. Increased risk of CVR was not associated with the use of non-ergot DAs.

To identify putative risk factors for levodopa-induced dyskinesias we studied the effect of several clinical variables on the occurrence of dyskinesias in a series of 168 consecutive patients with Parkinson's disease treated for at least 6 months with levodopa. Of these, 108 (64%) developed dyskinesias after a mean duration of levodopa treatment of 51.4 +/- 43.3 months. Patients tended to suffer dyskinesias on the side of the body first affected by Parkinson's disease. The overall probability of developing dyskinesias increased with levodopa treatment duration, about 10% per year during the first 7 years. Univariate and multivariate logistic regression analysis identified the age at onset of Parkinson's disease (OR 0.923; 95% CI 0.883-0.964) and the initial levodopa dose (mean dose of the first 6 months of treatment; OR 1.004; 95% CI 1.002-1.006) as the main independent predictors. Survival curves showed that onset of Parkinson's disease at age 50 years or before (logrank, P < 0.05) and initial levodopa treatment with more than 600 mg/day (logrank, P < 0.05) were associated with a higher risk for the appearance of dyskinesias.

Eyelid motor abnormalities found in progressive supranuclear palsy are reviewed. Electrophysiological correlates of blepharospasm, levator inhibition (blepharokolysis) and supranuclear paralysis of lid closure are presented. Disorders of eyelid motility are not uncommon in progressive supranuclear palsy (PSP). They may be found in about one third of patients with this syndrome (Jackson et al., 1983; Golbe et al., 1989). This is not surprising since ocular and eyelid movements are highly coordinated, mainly in the vertical plane (Gordon, 1951; Kennard and Smith, 1963; Kennard and Glaser, 1964), and a supranuclear ophthalmoplegia with down gaze impairment is a cardinal feature of PSP (Steele et al., 1964). The spectrum of eyelid motor disorders described in PSP includes blinking abnormalities, lid retraction, blepharospasm, levator inhibition and supranuclear palsy of eye closure.

To assess the extent of overlap between clinically diagnosed patients with progressive supranuclear palsy (PSP) and corticobasal ganglionic degeneration (CBGD) we compared clinical scores for rigidity, bradykinesia, supranuclear gaze abnormalities, hemineglect and limb apraxia, postural instability, neck rigidity, and limb dystonia in 15 patients with a degenerative rigid-akinetic syndrome at presentation and at follow-up 3 to 120 months later. Only the presence of hemineglect, usually in combination with limb apraxia, was a reliable and early clinical factor for discriminating between these two conditions. These symptoms were present at admission in all 4 CBGD patients but not in any of the 11 PSP patients either at presentation or later during serial examinations. Though supranuclear ophthalmoplegia, neck rigidity, and postural instability were already observed in most CBGD patients at presentation, their scores remained low compared to those for PSP patients over the longterm. CT-scans and MRI were helpful in supporting clinically-based diagnoses made at presentation in that the vast majority of the PSP patients exhibited various degrees of midbrain atrophy and 50 percent of the CBGD patients exhibited asymmetric pericentral cortical atrophy.