Preservative solution for skeletal muscle biopsy samples.

CONTEXT: Muscle biopsy samples must be frozen with liquid nitrogen immediately after excision and maintained at -80°C until analysis. Because of this requirement for tissue processing, patients with neuromuscular diseases often have to travel to centers with on-site muscle pathology laboratories for muscle biopsy sample excision to ensure that samples are properly preserved. AIM: Here, we developed a preservative solution and examined its protectiveness on striated muscle tissues for a minimum of the length of time that would be required to reach a specific muscle pathology laboratory. MATERIALS AND METHODS: A preservative solution called Kurt-Ozcan (KO) solution was prepared. Eight healthy Sprague-Dawley rats were sacrificed; striated muscle tissue samples were collected and divided into six different groups. Muscle tissue samples were separated into groups for morphological, enzyme histochemical, molecular, and biochemical analysis. STATISTICAL METHOD USED: Chi-square and Kruskal Wallis tests. RESULTS: Samples kept in the KO and University of Wisconsin (UW) solutions exhibited very good morphological scores at 3, 6, and 18 hours, but artificial changes were observed at 24 hours. Similar findings were observed for the evaluated enzyme activities. There were no differences between the control group and the samples kept in the KO or UW solution at 3, 6, and 18 hours for morphological, enzyme histochemical, and biochemical features. The messenger ribonucleic acid (mRNA) of ß-actin gene was protected up to 6 hours in the KO and UW solutions. CONCLUSION: The KO solution protects the morphological, enzyme histochemical, and biochemical features of striated muscle tissue of healthy rats for 18 hours and preserves the mRNA for 6 hours.

Reduced breath holding index in patients with chronic migraine.

Migraine is a neurovascular disorder characterized by autonomic nervous system dysfunction and severe headache attacks. Studies have shown that changes in the intracranial vessels during migraine have an important role in the pathophysiology. Many studies have been conducted on the increased risk of stroke in patients with migraine, but insufficient data are available on the mechanism underlying the increase. This study aimed to evaluate basal cerebral blood flow velocity and vasomotor reactivity in patients with chronic migraine. We evaluated 38 patients with chronic migraine. Three of them were excluded because they had auras and four of them were excluded because of their use of medication that can affect cerebral blood flow velocity and breath holding index (beta or calcium channel blockers). Our study population consisted of 31 patients with chronic migraine without aura and 29 age- and gender-matched healthy individuals who were not taking any medication. The mean blood flow velocity and breath holding index were measured on both sides from the middle cerebral artery and posterior cerebral artery, with temporal window insonation. The breath holding index for middle cerebral artery and posterior cerebral artery was significantly lower in the migraine group compared to that of the control group (p < 0.05).The vasomotor reactivity indicates the dilatation potential of a vessel, and it is closely related to autoregulation. According to our results, the vasodilator response of cerebral arterioles to hypercapnia was lower in patients with chronic migraine. These findings showed the existence of impairments in the harmonic cerebral hemodynamic mechanisms in patients with chronic migraine. This finding also supports the existing idea of an increased risk of stroke in patients with chronic migraine due to impaired vasomotor reactivity.

A sledgehammer on the brachial plexus: thoracic outlet syndrome, subclavius posticus muscle, and traction in aggregate.

Reported here is a 30-year-old man who was seen because of pain and weakness in the upper extremities after a tractional injury. Physical examination revealed significant atrophy in the left deltoid and right intrinsic hand muscles, generalized hypoesthesia, decreased deep tendon reflexes bilaterally, and decreased strength in various muscle groups. Roos (right) and hyperabduction (bilateral) tests were positive. Electrodiagnostic studies were consistent with bilateral brachial plexopathy. Cervical radiographs showed long transverse process of C7 on the right side and a small rudimentary rib articulating with C7 on the left side. Brachial plexus magnetic resonance imaging demonstrated an aberrant muscle and compressive brachial plexus injury on the left side. Surgery via transaxillary approach was performed on the left side. The occurrence of traumatic brachial plexopathy in the presence of underlying thoracic outlet syndrome and subclavius posticus muscle is discussed for the first time in the literature.