Sub-acute sensory neuronopathy as a preceding sign of recurrence in colon carcinoma

Subacute sensory neuronopathy is a paraneoplastic syndrome, which occurs mostly in lung, breast, ovarian malignancies and lymphoma. A 75-yr-old woman who was at the twentieth month of her postoperative follow-up owing to colon adenocarcinoma admitted with subacute sensory neuronopathy. Six months later from the first, neuropathic symptoms liver metastases developed. To the best of our literature review subacute sensory neuronopathy as a preceding sign of recurrence in colon adenocarcinoma has not previously been reported. We conclude that, in the case of subacute sensory neuronopathy without an obvious underlying etiological factor, an occult malignity should always be researched in clinical practice.     

Sub-acute sensory neuronopathy as a preceding sign of recurrence in colon carcinoma

Subacute sensory neuronopathy is a paraneoplastic syndrome, which occurs mostly in lung, breast, ovarian malignancies and lymphoma. A 75-yr-old woman who was at the twentieth month of her postoperative follow-up owing to colon adenocarcinoma admitted with subacute sensory neuronopathy. Six months later from the first, neuropathic symptoms liver metastases developed. To the best of our literature review subacute sensory neuronopathy as a preceding sign of recurrence in colon adenocarcinoma has not previously been reported. We conclude that, in the case of subacute sensory neuronopathy without an obvious underlying etiological factor, an occult malignity should always be researched in clinical practice.     

Microscopic polyangiitis presenting with medullary infarct

Microscopic polyangiitis is a small vessel vasculitis which is rarely associated with ischemic stroke. Cerebrovascular disease has rarely been reported in connection with this disease. It may cause fatal hemorrhage, hemorrhagic conversion and multiple lacunar infarcts. We report here a 55-year-old woman with left medullary oblangata infarction without any symptoms of microscopic polyangiitis. During hospitalization, retinal ischemia, mononeuritis multiplex and pulmonary infiltration developed. Sural nerve biopsy was concomitant with small vessel vasculitis. Elevated CRP and sedimentation and positive P-ANCA led to confirmation of a diagnosis of microscopic polyangiitis. Our patient is a rare case of microscopic polyangiitis presenting with medullary infarction. Although the characteristics of this disease are well-known, the first symptom can be a medullary infarction, which has not been reported in literature before.     

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 muscle's 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.     

Hereditary Thrombophilic Factors in Stroke Due to Cerebral Infarct

BackgroundThe stroke is the third most common cause of all deaths. In new studies, the importance of hereditary thrombophilic factors on stroke is emphasized. The aim of this study is to determine the role of hereditary thrombophilic factors including factor V Leiden A1691G (FVL), prothrombin G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T gene mutations in patients with stroke because of cerebral infarct.MethodsTwenty-four patients with stroke and 53 controls with risk factor for stroke were enrolled. Polymerase chain reaction was used to detect these mutations.ResultsHeterozygote FVL mutation in 2 (8.3%) patients and MTHFR mutation in 10 (41.7%) patients were detected. In the control group, there were 2 (3.8%) patients with heterozygote FVL mutation and 15 (28.3%) patients with MTHR mutation. Both FVL and MTHFR gene mutations were detected in 1 patient and 2 controls, respectively. Prothrombin gene mutation was not found in 2 groups. There were not statistically significant differences for all 3 mutations in-between 2 groups (P > 0.05). Odds ratios were 0.431 (0.074–2.504, 95% CI) for FVL mutation and 0.553 (0.221–1.381, 95% CI) for MTHFR mutation, respectively.ConclusionAlthough our study group was small, hereditary thrombophilic factors might not be risk factors for stroke because of cerebral infarct.     

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.     

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

We studied the various physiological aspects of oropharyngeal swallowing in Parkinson's 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.     

The relationship between protein C, protein S and cytokines in acute ischemic stroke

OBJECTIVE: The role of inflammation in the pathogenesis of acute ischemic stroke is well known, but its association with the clinical picture is as yet unclear. MATERIAL AND METHODS: In our study, we measured the serum levels of the proinflammatory cytokines interleukin-1beta (IL-1beta), tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) within the first 50 h of stroke in 60 acute stroke patients, and examined the association with the natural anticoagulants protein C and free protein S. We compared the results with a control group that consisted of 30 volunteers. We also correlated their levels with the clinical outcomes by using the Canadian Neurological Scale (CNS). RESULTS: Neither stroke patients nor the control group had any elevations in IL-1beta serum levels. However, the levels of serum IL-6 were significantly higher in stroke patients (13.7 +/- 19.46 vs. 4.3 +/- 15.88, p = 0.002). In addition, the protein S levels of patients were lower than those of the controls (84.36 +/- 27.97 vs. 95.9 +/- 25.64, p = 0.007). Although IL-6 showed negative correlation with protein S (r = -0.504, p = 0.000), the other studied cytokines TNFalpha and IL-1beta did not correlate with these natural anticoagulants. Another negative correlation was found between IL-6 and CNS scores (r = -0.451, p = 0.000). In addition, both protein C and protein S positively correlated with CNS (r = 0.263, p = 0.042; r = 0.381, p = 0.003). There was also a positive correlation between protein C and protein S (r = 0.408, p = 0.001). CONCLUSIONS: Our results suggest that TNFalpha and IL1beta serum levels are not elevated in the acute phase of stroke and have no correlation with the natural anticoagulants protein C and protein S. However, a decrease in free protein S may be related to elevated IL-6 levels. In addition, increased levels of IL-6 and reduced levels of protein C and protein S may play a role in acute ischemic stroke severity.     

Iron deficiency anemia and restless legs syndrome: is there an electrophysiological abnormality?

OBJECTIVE: The pathogenesis of restless legs syndrome (RLS) is unknown. Although iron deficiency anemia (IDA) is related with RLS, the mechanism of this relationship is still unknown. Therefore, we decided to examine some neurophysiological parameters that reflect the function of brainstem, spinal cord and peripheral nervous system. MATERIALS AND METHODS: 34 patients diagnosed with IDA at the hematology department were questioned with a structured battery for RLS and additional symptoms. Of those, 14 patients had symptoms of RLS, while remaining 20 had no signs of this disorder. In both groups, electrophysiological examination including motor and sensory nerve conduction, F-responses, H-reflex, blink-reflex, and mixed nerve silent periods was performed. RESULTS: Neurological examination of all patients was normal. The two groups were identical for age and sex, and the difference between both groups concerning motor and sensory nerve conduction, F-wave, H-reflex, blink-reflex, and mixed nerve silent periods was insignificant. CONCLUSION: Results suggest that IDA does not cause electrophysiological changes in the peripheral nerves, spinal cord and brainstem, and therefore, measurement of these parameters in IDA patients does not seem effective for the confirmation of RLS.