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Anterior cord syndrome due to anterior spinal cord infarction is commonly described in the medical literature, however, in clinical practice, this entity is rarely encountered. We present a 58-year-old man with sudden onset of bilateral lower limb weakness, followed by bilateral upper limbs involvement. Magnetic resonance imaging (MRI) of the whole spine was performed and he was diagnosed to have anterior spinal cord infarct. The characteristic imaging findings were highlighted.

Introduction. Guillain-Barre syndrome (GBS) is the commonest cause of acute flaccid paralysis. However, clinicians should not miss the other causes of acute flaccid paralysis which may mimic GBS. Results. We present 3 cases of flaccid areflexic paralysis which presented acute/subacutely resembling GBS. Case 1: A 29-year-old lady presented with 2-week history of bilateral lower limb weakness with left hip pain for 3 years. Investigations revealed hypercalcaemia, hypophosphataemia, elevated ALP, vitamin D deficiency, hyperparathyroidism with right parathyroid adenoma from parathyroid ultrasonography and scintigraphy. She had plasma exchange for presumed GBS, but her lower limb weakness worsened and progressed to involve upper limbs and facial muscles. Her weakness improved after parathyroidectomy and the diagnosis was revised to hyperparathyroidism-related polyneuropathy. Case 2: A 28-year- old lady with underlying epilepsy and intellectual disability presented with progressive weakness of extremities over 3 weeks after prolonged fasting. Her weakness did not improve after treatment with immunoglobulin for GBS. Investigations showed positive urine porphobilinogen and raised urine delta-aminolaevulinic acid. A diagnosis of acute intermittent porphyria was considered most likely and her weakness improved after continuous glucose loading. Case 3: A 52-year-old lady who had bariatric surgery presented with bilateral lower limb weakness over 4 weeks after recurrent bouts of vomiting and excessive weight loss. Investigations revealed vitamin D deficiency, hypoalbuminaemia, hyperhomocysteinemia, low folate and low normal serum thiamine. As her weakness continued to progress, a diagnosis of acute nutritional neuropathy was considered more likely. Her weakness improved following multivitamins replacement. All 3 patients had normal CSF analysis except Case 1 who showed cyto-albuminologic dissociation. Sensorimotor axonal polyneuropathy was the electrodiagnosis demonstrated in all the cases. Conclusion. Clinicians should have high index of suspicion when treating acute flaccid paralysis with progressive disease and null response to immunotherapy as the neurology is reversible with treatment of the underlying cause.

Cerebral venous thrombosis (CVT) is a neurological condition occurring because of thrombosis involving the cerebral venous sinuses. This case report is an unusual clinical manifestation of cerebral venous thrombosis in a 76-year-old Chinese man who presented with restricted eye movement and double vision. Despite extensive investigation, there was no better explanation for his clinical symptom and sign apart from cerebral venous thrombosis which was confirmed by magnetic resonance venography (MRV) of the brain. Once cerebral venous thrombosis was diagnosed, he was initiated on anticoagulation and discharged with oral warfarin. This case emphasizes the need to consider cerebral venous thrombosis as one of the rare causes of complex ophthalmoplegia especially when typical cardiovascular risk factors are lacking in an individual.