Sultan Tarlaci

Electrophysiological evaluation of pharyngeal phase of swallowing in patients with Parkinson's disease

We studied the various physiological aspects of oropharyngeal swallowing in Parkinsons disease (PD). Fifty‐eight patients with PD were investigated by clinical and electrophysiological methods that measured the oropharyngeal phase of swallowing. All patients except 1 had mild to moderate degree of disability score. Dysphagia was demonstrated in 53% of all patients in whom the test of dysphagia limit was abnormal. All PD patients with or without dysphagia displayed the following abnormalities: (1) the triggering of the swallowing reflex was prolonged probably due to inadequate bolus control in the mouth and tongue and/or a specific delay in the execution of the swallowing reflex; (2) the duration of the pharyngeal reflex time was extremely prolonged due to slowness of the sequential muscle movements, especially those of the suprahyoid‐submental muscles; (3) cricopharyngeal muscle of the upper oesophageal sphincter was found to be electrophysiologically normal; and (4) the electrophysiological phenomena in PD patients could not be strongly correlated with the degree of the disability and clinical score of the PD. It was concluded that various motor disorders of PD have considerable influence on oropharyngeal swallowing: hypokinesia, reduced rate of spontaneous swallowing, and the slowness of segmented but coordinated sequential movements rather than any abnormalities in the central pattern generator of the bulbar center. Some compensatory mechanisms in the course of PD may explain the benign nature of swallowing disorder until the terminal stage of the disease. Similarly, the swallowing problems of PD are not only related with the dopamine deficiency; some other nondopaminergic mechanisms may also be involved.

Electrodiagnostic methods for neurogenic dysphagia

OBJECTIVE Swallowing mechanisms and neurogenic dysphagia have not been systematically studied by the EMG technique. It is desirable to evaluate neurogenic dysphagia for diagnostic and possibly for therapeutic purposes using electrophysiological methods. METHODS The following methods were described: mechanical upward/downward movements of the larynx were detected using a piezoelectric sensor, while submental integrated EMG activity was recorded during dry and wet swallowing. The EMG activity of cricopharyngeal muscle of the upper oesophageal sphincter was also recorded in some normal subjects and patients. Piecemeal deglutition and the dysphagia limit were determined in all patients to detect dysphagia objectively. In this study 75 normal subjects and 177 neurological patients with various degrees of dysphagia were investigated. RESULTS Voluntarily triggered oropharyngeal swallowing was commonly pathological in the majority of patients, with or without overt dysphagia. The dysphagia limit appeared to be an objective measure of the degree of dysphagia in more than 90% of patients. Pathophysiological mechanisms were different in at least three groups of patients with neurogenic dysphagia. In the group of patients with muscular disorders, laryngeal elevators were involved while the CP-sphincter was intact. The second group included patients with the clinical signs of corticobulbar fibre involvement such as amyotrophic lateral sclerosis and pseudobulbar palsy. In these patients, there was incoordination between paretic laryngeal elevators and hyperreflexic CP-sphincter. In the third group (patients with Parkinsons disease), the swallowing reflex was delayed and prolonged. CONCLUSIONS EMG methods described in the present study are very useful for the diagnosis of neurogenic dysphagia, objectively and quickly. They are important to understand the physiological mechanisms for deglutition and its disorders.

Generalized tonic-clonic status epilepticus: causes, treatment, complications and predictors of case fatality.

Abstract We retrospectively reviewed the clinical course of 66 patients treated for generalized tonic-clonic status epilepticus at the Ege University neurological intensive care unit from 1988 to 1997. Seventy-two per cent of the study group had a pre-existing seizure disorder, and antiepileptic drug withdrawal was the most prominent cause of status epilepticus. The other causes included drug toxicity, central nervous system infection, cerebrovascular disease, tumour and trauma. Seventy-three per cent of all patients responded to the first-line therapy (diazepam and/or phenytoin), and the remainder were considered to have refractory status epilepticus and required pentobarbital anaesthesia. Overall case fatality was 21%, but death could be attributed directly to status epilepticus and/or treatment complication in 10% of the study group. Major determinants of fatal outcomes were: increasing age, longer duration of status epilepticus before initiation of therapy and central nervous system infection as a causal factor.

Voluntary and Reflex Influences on the Initiation of Swallowing Reflex in Man

The electrophysiological features of voluntarily induced and reflexive/spontaneous swallows were investigated. In normal subjects, swallows were elicited by infusing water either into the mouth (1–3 ml) or directly into the oropharyngeal region through a nasopharyngeal cannula (0.3–1 ml). For water infused orally, subjects were either requested to swallow voluntarily or instructed to resist swallowing and maintain the horizontal head position until swallowing occurred reflexively. Spontaneous saliva swallowing was investigated in patients with severe dysphagia who had a prominent clinical picture of suprabulbar palsy. Comparisons between different swallowing types were made by measuring the time interval between the onset of submental electromyographic activity (SM-EMG) and the onset of the upward movement of the larynx recorded by a movement sensor. This interval was less than 100 ms, even frequently less than 50 ms, in reflexive/spontaneous swallows, while in voluntarily induced swallows it was substantially longer. The rising time of submental muscles excitation was also shorter in reflexive/spontaneous swallows. It was suggested that the triggering of voluntarily induced swallows commences more than 100 ms before the onset of swallowing reflex and that this mechanism is under the control of corticobulbar–pyramidal pathways. If the swallowing reflex is triggered within such a short period of time following the onset of SM-EMG, the central control by the bulbar swallowing center should be effective until the end of oropharyngeal swallowing.

Mechanisms of Dysphagia in Suprabulbar Palsy With Lacunar Infarct

BACKGROUND AND PURPOSE The objective of the present study was to investigate the neural mechanisms of dysphagia in suprabulbar palsy (SBP) with multiple lacunar infarct. METHODS We evaluated the swallowing disorders of patients with SBP (n=34) and age-matched healthy control subjects (n=35) by means of an electrophysiological method that recorded the oropharyngeal swallowing patterns. With this method, dysphagia limit, the triggering of voluntarily initiated swallows, duration of laryngeal relocation time, and total duration of oropharyngeal swallowing were recorded and measured. In addition, the EMG behavior of the cricopharyngeal (CP) muscle of the upper esophageal sphincter was also assessed. RESULTS In patients with SBP, the dysphagia limit in all except 1 patient was pathological with limits of <20-mL bolus volume, which is contrary to normal subjects, in whom the dysphagia limit exceeds the 20-mL bolus volume. Either triggering of swallowing reflex was delayed (P<0.04), or the swallow could hardly be triggered in 7 patients on the voluntary attempts for 3 mL water. Whenever the reflex swallowing could be triggered, it was slow and prolonged (P<0.01). The CP muscle of the upper esophageal sphincter appeared to have become hyperreflexic and incoordinated with laryngeal movements during swallowing. CONCLUSIONS It was proposed that the progressive involvement of the excitatory and inhibitory corticobulbar fiber systems linked with the bulbar swallowing center is mainly responsible for the triggering difficulties of the swallowing reflex and for the hyperreflexic/incoordinated nature of the CP sphincter. In addition, the dysfunction of the extrapyramidal system has a specific role in the slowing of oropharyngeal swallowing and the accumulation of saliva in the mouth.

Effect of mucosal anaesthesia on oropharyngeal swallowing

The effect of the topical anaesthesia of the oropharyngeal mucosae was studied in order to evaluate the role of the mucosal sensory receptors on the oropharyngeal swallowing in 12 adult volunteers. Laryngeal vertical movements were detected by a piezoelectric sensor and electromyography of the submental muscle complex were simultaneously recorded. All subjects were instructed to swallow doses of water, gradually increasing in quantity from 3–20 mL and any recurrence of the signals related to swallowing within 8 s was accepted as a sign of dysphagia and its limit value measured. Before the topical anaesthesia of the oropharyngeal mucosae by xylocaine puffs; the dysphagia limit was never observed with less than 20 mL water. During topical mucosal anaesthesia lasting 4–6 min among the subjects, the dysphagia limit was less than 20 mL water and the recurrence of swallows two or more times was mainly recorded with 3–5 mL water. Five of the subjects demonstrated the clinical and electrophysiological signs of laryngeal aspiration at the earlier period of the topical anaesthesia. It is concluded that the sensory inputs from the mucosal receptors are important to trigger voluntary swallowing and their absence or dysfunction may contribute to oropharyngeal dysphagia and laryngeal aspiration.

Cricopharyngeal sphincter muscle responses to transcranial magnetic stimulation in normal subjects and in patients with dysphagia

OBJECTIVE Cricopharyngeal (CP) muscle of the upper oesophageal sphincter (UES) has a significant role in the pharyngo-esophageal phase of deglutition. The linkage between the CP muscle of UES and the motor cortex has not been previously studied electrophysiologically in healthy humans and in patients with neurogenic dysphagia. METHODS Needle recordings of EMG responses were carried out from the CP sphincter muscle following transcranial magnetic stimulation (TMS) over the vertex around the Cz electrode position (cortical MEP), and on the parieto-occipital skull and the occiput ipsilaterally (peripheral MEP) in 14 healthy control subjects and in 26 patients with and without neurogenic dysphagia. Needle recordings obtained from the cricothyroid muscle of the larynx were also evaluated in six healthy subjects. RESULTS The cortical motor latency of CP sphincter muscle was 10.7+/-0.5 ms with an amplitude of 0.8+/-0.2 mV in healthy subjects. Both the latency and amplitude of CP-MEP were facilitated during swallowing. The peripheral MEP of the CP muscle was very stable in all normal subjects (5.1+/-0.3 ms; 1.3+/-0.3 mV) and swallowing did not influence these parameters. The cortically elicited CP-MEP was significantly longer than the cortical MEPs obtained from the cricothyroid muscle of the larynx. In 10 dysphagic patients with corticobulbar tract involvement (6 ALS and 4 pseudobulbar palsy) and with pathologic and hyperreflexic EMG of the CP-sphincter muscle, the cortical MEP of CP muscle of the upper esophageal sphincter could not be elicited, although the peripheral CP-MEPs were obtained. TMS never produced a swallowing movement in neither healthy subjects nor patients. CONCLUSION The CP muscle of the upper esophageal sphincter can produce MEPs by cortical TMS and by stimulation at the root/nerve levels of vagus nerve. The MEP latency values and central motor delay suggest that there is an oligosynaptic corticobulbar pathway to the motoneurons of CP muscles. When the pathway is affected by a pathology (i.e. ALS or pseudobulbar palsy) the CP sphincter becomes hyperreflexic due to disinhibition and the cortical MEP of the CP muscle disappears due to degeneration of the corticobulbar pathway. These mechanisms appear to be responsible for the pathogenesis of dysphagia.

Oropharyngeal swallowing in craniocervical dystonia

Objective: To clarify the pathophysiology of dysphagia by electrophysiological methods. Method: Electrophysiological methods related to oropharyngeal swallowing were used to investigate 25 patients with cervical dystonia and 25 age matched normal volunteers. Results: Dysphagia was suspected in 36% of patients with cervical dystonia on the basis of clinical assessment. The incidence of dysphagia increased to 72% on electrophysiological evaluation of pharyngeal swallowing. Submental muscle electromyographic (EMG) and laryngeal relocation times were significantly prolonged and the triggering time to swallowing reflex was significantly delayed. Some abnormalities seen in cricopharyngeal sphincter muscle EMG indicated that the striated sphincter muscle is hyperreflexive in some patients. Conclusion: Neurogenic dysphagia was more prominent and longer lasting than mechanical dysphagia, which was transient and varied from patient to patient. Although these electrophysiological methods were not suitable for detecting anatomical changes during swallowing, as in videofluoroscopic studies, observations supported the neurogenic cause of dysphagia in patients with any kind of cervical dystonia.

The electromyographic behavior of the thyroarytenoid muscle during swallowing.

The electromyographic (EMG) behavior of the laryngeal adductors (e.g., the thyroarytenoid [TA] muscle) during swallowing has been scarcely studied. However, the detailed analysis of TA muscle is important to understand the physiology of swallowing. We investigated 14 healthy adult subjects. Activation of the TA laryngeal adductor muscle was compared with the mechanically measured laryngeal up-down movement and with the onset of excitation of laryngeal elevators, such as submental (SM) muscles, during swallowing. The laryngeal adductor of TA and laryngeal elevators of SM muscles were electromyographically (integrated/rectified) recorded. The vertical laryngeal movements during swallowing were recorded using a piezoelectric sensor. The EMG behavior of the TA muscle revealed three different activities during swallowing. The basic activity was stable; it almost started with the upward movement of larynx and after the SM-EMG onset. A fore-burst was recorded just before the upward movement of the larynx and a late-burst appeared just after the downward movement. The fore-burst was proposed to be related with oral-laryngeal reflexes, and the late-burst could be a rebound activity after a short expiration of swallowing, while the basic activity is accepted to be a part of activity of central-pattern generator of swallowing program.

Diagnostic value of “dysphagia limit” for neurogenic dysphagia: 17 years of experience in 1278 adults

OBJECTIVE Neurogenic dysphagia (ND) is a prevalent condition that accounts for significant mortality and morbidity worldwide. Screening and follow-up are critical for early diagnosis and management which can mitigate its complications and be cost-saving. The aims of this study are to provide a comprehensive investigation of the dysphagia limit (DL) in a large diverse cohort and to provide a longitudinal assessment of dysphagia in a subset of subjects. METHODS We developed a quantitative and noninvasive method for objective assessment of dysphagia by using laryngeal sensor and submental electromyography. DL is the volume at which second or more swallows become necessary to swallow the whole amount of bolus. This study represents 17 years experience with the DL approach in assessing ND in a cohort of 1278 adult subjects consisting of 292 healthy controls, 784 patients with dysphagia, and 202 patients without dysphagia. A total of 192 of all patients were also reevaluated longitudinally over a period of 1-19 months. RESULTS DL has 92% sensitivity, 91% specificity, 94% positive predictive value, and 88% negative predictive value with an accuracy of 0.92. Patients with ALS, stroke, and movement disorders have the highest sensitivity (85-97%) and positive predictive value (90-99%). The clinical severity of dysphagia has significant negative correlation with DL (r=-0.67, p<0.0001). CONCLUSIONS We propose the DL as a reliable, quick, noninvasive, quantitative test to detect and follow both clinical and subclinical dysphagia and it can be performed in an EMG laboratory. SIGNIFICANCE Our study provides specific quantitative features of DL test that can be readily utilized by the neurologic community and nominates DL as an objective and robust method to evaluate dysphagia in a wide range of neurologic conditions.