We report a case of Guillain-Barré syndrome (GBS) occurring soon after the first dose of Vaxzevria (previously known as COVID-19 vaccine AstraZeneca). Thus far, there has been no evidence of an increased risk of GBS resulting from either COVID-19 infection nor from COVID-19 vaccines; however, individual cases and population cohorts should be scrutinised, in order to ensure the constant evaluation of such risks. It is as yet not possible to draw conclusions about any significant association between COVID-19 vaccination and GBS. A temporal correlation does not imply, and should not be deemed to signify, causality. However, it is important to remain vigilant, so that any potential increased risk is properly evaluated. The specific presentation of bifacial weakness as the initial symptom may be a characteristic feature of GBS in the context of recent COVID-19 vaccination.
We present an unusual case of Eagle’s syndrome with bilateral internal carotid artery dissection in a 45-year-old man. Initial symptomatology included ipsilateral headaches and facial sensory symptoms. A right horner’s syndrome was present on clinical examination. Radiological imaging revealed an old infarct, with bilateral carotid dissections and bilateral elongated styloid processes consistent with Eagle’s syndrome. Despite initiation of secondary prevention with antiplatelet therapy, he had two further ischaemic events. The case highlights the symptomatology and complications of Eagle’s syndrome, with its management discussed through a review of similar case reports.
An MRI-guided and MRI-verified approach to DBS was successfully implemented through cross border collaboration with achievement of expected clinical results. This healthcare collaboration developed out of necessity and opportunity, taking advantage of a UK-based neurosurgeon from Malta. The UK healthcare system benefits from numerous immigrants at Consultant level. Such a mutually beneficial arrangement could enable such individuals to offer their expertise to citizens in the UK as well as their country of origin.
The late-onset variant of radiation-induced brachial plexopathy is most often seen after treatment for breast or lung cancers. It has an insidious onset, with symptoms noted years after receiving radiotherapy, and the condition gradually continues to deteriorate with time. We present the case of an elderly man who we saw in view of worsening paraesthesias and weakness of his left arm with associated prominent muscle wasting along the left shoulder girdle. Fifteen years prior to this, he had received radiotherapy for the treatment of nasopharyngeal carcinoma.
SummaryA 25-year-old man presented with blurred vision, headache and dizziness. On questioning, there was also a history of a preceding diarrhoeal illness. Initial investigations were normal. However, after a week, he represented with a Parinaud's syndrome. In view of the preceding diarrhoea, the transient unsteadiness and the areflexia on examination, anti-GQ1b antibodies were requested. The resulting titre was positive confirming the suspected diagnosis of Miller Fisher syndrome. He responded to intravenous immunoglobulins with full resolution of his symptoms and signs. Although various unusual neuro-ophthalmological signs have been reported localising to the brainstem, to our knowledge, this is the first case report of Parinaud's syndrome being the presenting symptom of Miller Fisher syndrome.
BACKGROUND
A 66-year-old man presented with chest pain and a 1-year history of generalised weakness, accompanied with generalised aches and pains. Symptoms worsened when he was initiated on statins. Investigations yielded high creatine kinase, high HMG-coenzymeA reductase (HMGCR) antibody titre, myopathic features on electromyography and muscle biopsy, and muscle atrophy on MRI. These results were in keeping with anti-HMGCR antibody myopathy. The patient responded well to immunosuppressive therapy.
A young woman presented to neurology with a 1 month history of progressive diplopia on lateral gaze and a 1 week history of headaches. On examination she was found to have complex ophthalmoparesis with binocular horizontal diplopia, failure of abduction bilaterally and limited upgaze with convergence-retraction nystagmus. The rest of the neurological examination was normal. She was admitted for investigations: blood, CT brain, MR brain and lumbar puncture results were normal. Anti-GD1a antibodies were strongly positive; anti-GM1, anti-GM2 and anti-GD1b were also positive. On follow-up 3 weeks later, the complex ophthalmoplegia persisted. It was decided to treat with intravenous immunoglobulins (IVIgs) with good response but recurrence at 2 weeks post infusion. She was treated with 4 weekly IVIg courses and remains responsive and controlled over 1 year since presentation but becomes symptomatic in the week running up to each dose; thus, disease modifying treatment is currently being considered.
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