The mechanisms contributing to the pathogenesis of tremor and/or dysmetria in multiple sclerosis (MS) are poorly understood. Abnormal oscillations within the olivo-cerebello-thalamo-cortical networks are believed to play an important part in tremor aetiology, but could also contribute to intention dysmetria due to disruptions in motor timing. Conversely, delayed central motor conduction times are a common feature of ataxias, but could also contribute to the expression of dysmetria in MS. This study examined the roles of central conduction delays in the manifestation of tremor and/or dysmetria in MS.Twenty-three individuals with MS participated: 8 with no movement disorder, 6 with tremor, 4 with pure dysmetria and 5 with both tremor and dysmetria. Median nerve somatosensory evoked potentials (SEPs), transcranial magnetic stimulation (TMS) over the motor cortex and cervical spine, stretch reflexes were used assess sensory and motor conduction times.Central, but not peripheral, sensory conductions time were significantly delayed in participants with dysmetria, regardless of the presence of tremor. Similarly, the TMS evoked muscles responses and the long-latency component of stretch reflexes were significantly delayed in those with dysmetria, but not pure tremor.Dysmetria in MS is associated with delays in central conduction of sensory or motor pathways, or both, likely leading to disruption of muscle activation timing and terminal oscillations that contribute to dysmetria.The presence of dysmetria in MS is associated with decreased conduction velocities in central sensory and/or motor pathways likely reflects greater demyelination of these axons compared to those with no movement disorder or pure tremor.
Latero-posterior thalamic strokes are reported to result in delayed onset action tremor, dystonia, pseudoathetosis, chorea and myoclonus. This complex disorder is usually associated with proprioceptive sensory loss and limb ataxia. The tremor has a large amplitude postural component whichworsens on targeted movements; this with the associated sensory loss renders it incapacitating. Thalamic VIM ablation has been reported to improve this tremor. However, deep brain stimulation (DBS) has not. We report 3 cases with post-thalamic stroke tremor, 2 of which have been successfully treated with thalamic DBS; the third is being considered. The first was a 41 year old female who presented with a left sided tremor resulting from a right thalamic stroke after a vertebral artery dissection. The second was a 69 year old male with a right sided tremor resulting from an ischaemic stroke of the left thalamus and the third had bilateral arm tremor resulting from bilateral latero posterior thalamic strokes following a syringomyelia decompression surgery. The tremor in all was of the cerebellar type with joint position sense loss up to the wrist; pseudoathetosis and dystonic posturing. Thalamic DBS ameliorated the large amplitude component of the tremor improving arm function.
A man in his 20s presented following a generalised tonic-clonic seizure on a background of a recent diagnosis of hepatitis B (HBV). During admission, he was severely hypertensive and imaging findings confirmed a diagnosis of posterior reversible leukoencephalopathy syndrome (PRES). The patient subsequently developed multiorgan involvement with an axonal sensorimotor neuropathy, vascular cutaneous lesions and multiple bilateral renal and splenic infarcts. Based on the 2012 Revised International Chapel Hill Consensus Criteria, a diagnosis of polyarteritis nodosa (PAN) with secondary PRES was made. The patient was given intravenous methylprednisolone, followed by a prolonged course of oral prednisolone, and tenofovir antiviral therapy to target HBV seroconversion. He made a good neurological recovery with resolution of imaging changes. This case highlights the importance of a low threshold for systemic screening for young patients presenting with PRES secondary to uncontrolled hypertension and the importance of viral screening, particularly for HBV.
Achieving the best outcome from STN stimulation for the treatment of Parkinson’s disease depends on ideal electrode placement and optimum stimulation settings. Motor symptoms are known to respond well to stimulation of the dorsolateral nucleus of the subthalamus and avoidance of tissue activation of the surrounding structures that may give rise to unwanted side effects including slurred speech, gait problems and neuropsychiatric symptoms. The recent development of multidirectional stimulation systems has enabled electrical current steering to activate the desired tissue areas in order to achieve effective neuromodulation. In this audit of 16 patients who underwent STN-DBS, we looked at the short-term neuropsychiatric outcomes in patients in whom current steering was deployed to achieve the best motor control to those in whom control was achieved by conventional ring mode stimulation. The patients’ symptoms were assessed at baseline and at 12 months using validated scales for anxiety, depression, apathy, and impulsivity. There was no statistical difference in the neuro-psychiatric outcomes between the two groups. However, the number of patients in this study was small and larger studies for longer periods are required to evaluate the potential benefit of this new development in minimising the neuropsychiatric complications of this treatment.
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