Farid Ullah Shah, Mohammad Salih, Iftikhar Ahmed Malik.
Clinical evaluation of patients with acute flaccid motor weakness.
Pak J Med Res Jan ;41(2):58-63.

Objectives: To differentiate Guillain Barre` syndrome from hypokalemicperiodic paralysis on basis of clinical features and simple laboratory investigations like serum potassium level, E.C.G, blood gases analysis. Patients and methods: Patients presented between January 1999 to June 2000 to the department of Neurology of Pakistan Institute of Medical Sciences Islamabad were included in this study. Patients more than 13 years of age and of both sexes, who were conscious, with lower motor neuron type of weakness, which developed within a period of four weeks with no sensory level, were included in this study. All patients who were unconscious, who were having sensory level, in whom weakness developed in a period of more than four weeks, patients with diabetic neuropathy, acute renal failure, porphypria and lead poisoning were excluded. Results: Out of 33 patients, 22 (66.7%) were suffering from Guillain Barre’ syndrome ( G B S) , 5(15.1%) from hypokalemic periodic paralysis (HPP), 4(12.1%) from hypokalemic paralysis ( HP) with hypokalemia secondary to renal tubular acidosis type-1 and 2(6.1%) from critical illness neuropathy(CIN). All 22 patients with GBS developed distal weakness except one patient. Serum potassium level was 3.9 to 4.6 mmol/l (mean level 4.72 mmol/l). Respiratory failure was present in 9(40.9%) patients; bulbar palsy in 13 (59.1%) patients and 2(9.1%) patients expired. All patients with HPP developed proximal as well as distal weakness. Serum potassium level was 1.5-mmol/l to2.5mmol/l (mean 2.06 mmol/l). Two (40%) patients developed respiratory failure and 2(40%) bulbar palsy. One (20%) patient expired. Family history and history of repeated episodes of weakness was positive in 3(60%) patients. While in 2(40%) patients, there was no family history and no past history of weakness. Cause of hypokalemia was renal tubular acidosis type -1, in all HP patients. All developed both proximal as well as distal weakness. Serum potassium level was 1.9 to 2.9 mmol/l (mean 2.22 mmol/l). Respiratory failure was present in 2(50%) patients and 2(50%) patients developed bulbar palsy. Two (50%) patients expired. Critical illness neuropathies were present in two patients. Both patients were on mechanical ventilator. One patient (50%) expired. Conclusion: Certain clinical and laboratory criteria differentiate HPP from GBS, which includes Positive family history and similar episodes of weakness in the past, rapid onset of weakness in hours, quick recovery in 24 to 72 hours, and low serum potassium during the episodes of weakness.

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