Guillain-Barre syndrome of acute motor axonal neuropathy (AMAN) type associated with herpes zoster: a case report.

Guillain Barre syndrome (GBS) following Varicella zoster is a rare presentation and has only been reported in a few cases around the world. Of the reported cases, the type of GBS is not specified in the majority, and where specified is of the acute inflammatory demyelinating polyradiculoneuropathy (AIDP) type. We report a case of acute motor axonal neuropathy (AMAN) type GBS following herpes zoster in a 27-year-old male who presented with bilateral lower limb weakness and left sided lower motor neuron type facial nerve palsy a week after herpes zoster infection.

Bruns Garland Syndrome as the first presentation of type 2 diabetes: two case reports and a practical approach to diagnosis.

BACKGROUND: Diabetes is a global health problem causing a significant burden on the healthcare systems both due to the disease itself and associated complications. Diabetic radiculoplexus neuropathies or Bruns-Garland syndrome constitutes a rare form of microvascular complications, more commonly affecting the lumbosacral plexus and, very rarely, the cervical plexus. We describe two Sri Lankan males who presented with diabetic lumbosacral radiculoplexus neuropathy and diabetic cervical radiculoplexus neuropathy as the initial manifestation of diabetes. CASE DESCRIPTION: Case 1: a 49-year-old Sri Lankan hotel chef presented with subacute painful weakness and wasting of the left upper arm for 3 months and weight loss. Left upper limb proximal muscles were wasted with diminished power and reflexes. A nerve conduction study showed comparative amplitude reduction. An electromyogram revealed positive sharp waves, frequent fibrillations, and high amplitude polyphasic motor unit potentials with reduced recruitment in proximal muscles of left upper limb. Case-2: a 47-year-old Sri Lankan carpenter presented with subacute progressive asymmetrical painful weakness and wasting of bilateral thighs for 5 months and weight loss. Lower limb proximal muscles were wasted with reduced power and knee jerks. The nerve conduction study was normal. The electromyogram was similar to case 1 involving both quadratus femoris muscles, which was more prominent on the left side. The work up for an underlying etiology revealed only elevated fasting blood glucose and HbA1c, suggesting a new diagnosis of diabetes associated with neurological symptoms. Patient 1 was diagnosed with diabetic cervical radiculoplexus neuropathy and patient 2 with diabetic lumbosacral radiculoplexus neuropathy. Both showed significant improvement following optimization of glycemic control together with symptomatic treatment and physiotherapy. CONCLUSION: Diagnosis of diabetic radiculoplexus neuropathy requires a comprehensive workup to rule out other sinister pathologies. This case report has a dual importance; it describes diabetic radiculoplexus neuropathy as the very first manifestation of two previously healthy people, giving rise to a new diagnosis of diabetes and, at the same time, reporting on diabetic cervical radiculoplexus neuropathy, which is extremely rare and has never been previously reported in Sri Lanka.

Chlorpyrifos-induced delayed myelopathy and pure motor neuropathy: a case report.

INTRODUCTION: Organophosphate (OP) poisoning is known to cause delayed neurological manifestations. Chlorpyrifos, an OP, causes a delayed syndrome that is characterized by a motor sensory polyneuropathy. Pure motor neuropathy with intact sensory conduction is rarely documented. Rapidly evolving delayed myelopathy is extremely uncommon. CASE REPORT: A healthy 15-year-old female was admitted to hospital with cholinergic crisis due to ingestion of a large dose of chlorpyrifos (OP). She was treated with atropine and recovered completely without any neurological symptoms or signs. She came to hospital 6 weeks later with upper and lower motor neuron signs involving the lower limbs without sensory loss. By the end of 7 weeks, there was urinary incontinence. At 2-month follow-up, she had progressive spasticity. Electrophysiological studies revealed a pure motor neuropathy. Spine magnetic resonance imaging showed early signs of thoracic cord atrophy. Other causes of myelopathy were excluded. CONCLUSIONS: Chronic neurotoxicity due to OP poisoning is dependent on several factors: chemical composition of the OP, dose systematized, and the administration of anitcholinergics for cholinergic crisis. The pathology of OP-induced delayed neuropathy involves a central-peripheral distal axonopathy. Peripheral distal axonopathy results in a predominantly motor polyneuropathy. Axonopathy of the central nervous system results in myelopathic features that makes for a poorer prognosis.