Cricopharyngeal myotomy in neurogenic oropharyngeal dysphagia.

OBJECTIVE: Cricopharyngeal myotomy as an independent procedure has been performed on fourteen patients with a variety of neuromuscular disorders, suffering from neurogenic oropharyngeal dysphagia in the interval between 1994-1997. All of them were referred from a neurophysician or physiatrist after failure of improvement by medical treatment. METHODS: The selection of patients for operation was based mainly on clinical evaluation and simple exclusion criteria without manometric studies. RESULTS: There was dramatic improvement in twelve, with recurrent laryngeal nerve palsy and temporary pharyngeal fistula in two patients. No mortality was recorded. CONCLUSION: We conclude that cricopharyngeal myotomy is a simple, safe and effective procedure with acceptable morbidity. It should be considered as a rehabiliation procedure for patients with dysphagia due to various neurologic disorders based on simple, clinical exclusion criteria without the need for the tedious, time consuming and expensive manometric studies.

Dysfunction of sensory nerves during attacks of hypokalemic periodic paralysis.

Reversible electrophysiologic abnormalities of sensory nerve function were found by chance in three patients with hypokalemic periodic paralysis, a disorder previously considered to affect the function of muscle membranes only. A formal, prospective study was therefore conducted. Serial nerve conduction studies were done in ten additional patients. Amplitude of sensory action potentials was significantly smaller during paralytic attacks, but did not differ from controls after normalization of serum potassium concentration. These apparently novel findings might be explained by previous electrodiagnostic studies either not involving the testing of sensory nerves at all, or not being repeated after recovery from an attack. Involvement of sensory nerves in hypokalemic periodic paralysis is suggested to arise through dorsal root ganglia having an incomplete blood-nerve barrier and sensory neurons being particularly vulnerable to derangements affecting nerve cell metabolism. Neuronal inexcitability is postulated to occur consequent upon possible inactivation of the sodium-potassium pump by the low concentration of extracellular potassium. In patients with acute areflexic limb weakness, the diagnosis of hypokalemic periodic paralysis should not be excluded by abnormal results of sensory nerve conduction studies.

Intrathecal synthesis of IgG in benign intracranial hypertension: a re-examination.

In a previous retrospective study, 4 of 9 patients with benign intracranial hypertension were unexpectedly positive for intrathecal synthesis of immunoglobulin (Ig) G by quantitative measurement (log IgG index). This was remarkable as the only disease among many studied that showed such a discrepancy. A further study was done, now prospectively. Log IgG index values were elevated in 2 of the 11 new cases. As before, qualitative measurement (isoelectric focusing) gave uniformly negative results. Five of the 6 instances where the log IgG index was elevated could be accounted for, in fact, by abnormal values of constituent variables other than cerebrospinal fluid IgG. Quantitative tests for intrathecal synthesis of IgG can give misleading results on their own. Immunological mechanisms most probably are not involved in the pathogenesis of benign intracranial hypertension.