Hyperkalaemia mimicking acute Guillain-Barre syndrome.

Abstract

Recurrent confusion and ataxia triggered by pyrexia in a case of occult multiple sclerosis It has long been known that an increase in body temperature may worsen reversibly the signs and symptoms of multiple sclerosis, probably by the production of conduction block in partially demyelinated nerve axons. We present the case of a man whom we believe has multiple sclerosis, who has a nine year history of brief episodes of profound neurological dysfunction, always in association with pyrexial illnesses. The unusual feature of this case is that, until recently, between these attacks our patient remained subjectively well, and that there was no history suggesting episodes of acute demyelination.A 44 year old man was admitted in May 1992 with a 12 hour history of increasing confusion, blurring of vision, and ataxia, associated with a fever. On admission he was pyrexial at 39°C, but there were no signs of localised infection or any features of meningism. He was drowsy and mildly confused. The cranial nerves were normal apart from bilateral failure of adduction with ataxic nystagmus of the abducting eyes typical of an internuclear ophthalmoplegia, down-beat nystagmus on down-gaze, and up-beat nystagmus on up-gaze. There was a mild bilateral ptosis and a slight left upper motor neuron facial weakness. Bulbar function was intact. In the limbs power was normal, but tone was slightly increased generally and the reflexes were exaggerated, particularly on the left. The left plantar reflex was extensor, the right flexor. There was pronounced cerebellar ataxia in all four limbs, again more pronounced on the left, and he was unable to walk unassisted. Sensation was normal. The only abnormal investigations were a noticeable peripheral neutrophilia (granulocyte count 11 -6 x 109/1), and a raised C reactive protein concentration of 77 mg/l (normal range 0-10). Cerebrospinal fluid contained 1 white blood cell/mm', 0-21 g/l protein, and 4-7 mmol/l glucose.The Further analysis of the CSF collected on his admission showed the presence of oligoclonal IgG bands that were absent from plasma, although the CSF IgG:albumin ratio was normal at 0-20 (normal range 0-0 25). An MRI of the brain two days after his discharge showed the presence of multiple areas of increased signal intensity in the periventricular regions, the corpus callosum, the base of the fourth ventricle, the left cerebellar peduncle, and the lower medulla. The appearances were typical of widespread demyelination caused by multiple sclerosis. Repeat MRI five months later appeared identical. Visual evoked responses recorded eight months after his admission were of grossly increased latency.In

Acute Reversible Tetraplegia Induced by Hyperkalemia in a Patient with Paravertebral Mass due to Lymphoma

“…Although the precise mechanism of secondary hyperkalemic paralysis remains unclear, the persistent state of depolarization in the neurons is believed to be responsible for the reversible neuromuscular paralysis. It manifests clinically with an ascending pattern, from the lower extremities followed by a progression into the trunk and arms closely resembling the Guillian Barré syndrome [1,2]. In our patient, as well as most of other cases in the literature, there was no compromise of respiratory muscles, cranial nerves or sphincter tone [3].…”

Angiotensin converting enzyme inhibitor induced hyperkalaemic paralysis

“…3 Cerebrospinal fluid has been examined in four patients and has been normal in every case 23 9Most cases described earlier have had an onset of muscle weakness over days. In our patient, the muscle weakness was more abrupt in onset.…”

“…3 5 8 In two cases where neurophysiological studies have been carried out, reduced nerve conduction velocities have been found suggesting nerve mediated weakness 23 Cerebrospinal fluid has been examined in four patients and has been normal in every case 23 9Most cases described earlier have had an onset of muscle weakness over days.…”

“…No cases have yet been reported to the Committee on Safety of Medicines in the UK. Hyperkalaemia leading to paralysis has been reported in renal failure,3 4trauma,5 6 spironolactone intake,2 7 8treatment with amiloride/hydrochlorthiazide,9 10 and trimethoprim-sulfamethoxazole therapy 11. We describe what we believe to be the first reported case of hyperkalaemic paralysis secondary to treatment with an angiotensin converting enzyme (ACE) inhibitor.…”

Hyperkalemic Recurrent Bilateral Lower Extremity Weakness in a Patient on Hemodialysis

“…This type of paralysis resembles the one that is observed in Guillain-Barre Syndrome [12, 13]. It has been reported that this entity has been observed in patients with end-stage renal disease on hemodialysis or it has been precipitated as a result of antibiotic therapy [7] or in the context of drug use and abuse [6, 8].…”