Abstract

Early neurological deterioration is a well-established complication of an acute ischaemic stroke, however late deterioration is an uncommon finding and could be very challenging to diagnose and treat in timely manner. I report a case of an 82-year-old male who had suffered a stroke 28 years earlier and was functionally performing very well afterwards and living independently. This patient was presented to Worcestershire Hospital with signs and symptoms consistent with Urinary Tract Infection diagnosis. He was treated with Trimethoprim and his clinical condition improved significantly. While awaiting for his social rehab he suddenly developed dysphonia and dysphagia, along with mixed upper and lower motor neuron lesion signs consistent with a posterior circulation stroke. He was investigated extensively and MRI spine ruled out any spinal cord compression however MRI head revealed old infarcts in left parietal lobe, cerebellar region and thalamic area (no acute changes). Surprisingly MRI head also shown global atrophic change with significant atrophy of midbrain in comparison to the pons (Hummingbird sign) which rose suspicion of progressive supranuclear palsy. Initially patient was treated for acute stroke as per stroke team advice however patient was later reviewed by neurologist who explained that symptoms were attributed due to neurological decompensation of chronic infarcts (left parietal, thalamic, cerebellar) exacerbated by acute infection. Progressive Supranuclear Palsy was also excluded based on sudden onset of symptoms as compared to gradual onset of actual disease. His neurological symptoms improved slowly, but the dysphagia and dysphonia persisted. The risk of aspiration pre-empted the insertion of a percutaneous endoscopic gastrostomy (PEG) for feeding before he was discharged for rehabilitation.

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