Cardiac syncope due to pain: report of a case responsive to duloxetine treatment.

Neurocardiogenic syncope comprises situations triggered by neurological reflexes resulting in abnormal responses of the neurocardiovascular system that cause loss of consciousness. A vast number of clinical conditions may cause this disorder including pain, defecation, micturition, swallowing, cough, sudden fear or excitement, exercise, and long-time standing. Treatment options for syncope prevention are not satisfactory. Several agents were used for pharmacological treatment without success. Selective inhibitors of neuronal norepinephrine transporter (NET) like duloxetine may play a role in neurally mediated syncope by increasing synaptic norepinephrine levels. Therefore, we report the effect of duloxetine in a patient with pain-induced syncope resistant to standard regimens.

Intramedullary hydatid cyst of the cervical spine.

Hydatid disease (Echinococcosis) is a common parasitic infection caused by Echinococcus granulosus mainly in sheep-raising areas of the world. Liver, lungs and brain are the predominantly involved organs. However, 0.5-1% of the hydatid disease involves the spine and in 90% of the cases it is confined to the bone and the epidural space. Although intramedullary involvement is extremely rare, in this report, we present a 55-year-old female patient who was diagnosed with a cervical intramedullary hydatid cyst during magnetic resonance imaging of the cervical vertebrae. Accordingly, we imply that particularly in endemic areas, hydatid cyst disease should be kept in mind for the differential diagnosis of spinal mass lesions.

Effects of the antiepileptic drugs on peripheral nerve function.

OBJECTIVE: We aimed to compare the effects of antiepileptic drugs and provide findings of peripheral nerve impairment using standard electrophysiological techniques. MATERIALS AND METHODS: Young adult outpatients with epilepsy on monotherapy for no less than 6 months with carbamazepine (CBZ), valproic acid (VPA), oxcarbazepine (OXC) and topiramate (TPM) were examined. Patients who had any other disease that could effect nerve conduction studies and who had neuropathic symptoms were excluded. RESULTS: Each group contained 15 patients and 20 healthy subjects were examined as the control group. Prolonged latency of median sensory nerve (P = 0.004), ulnar sensory nerve (P = 0.01) and sural nerve (P = 0.003) with a diminished nerve conduction velocity was observed in the CBZ group (P = 0.014, P = 0.002, P = 0.025, respectively). No correlation was found between VPA, OXC and TPM and the nerve conduction studies (P > 0.05). CONCLUSIONS: Valproic acid, oxcarbazepine and topiramate don't have effects on nerve conduction studies. Mild electrophysiological changes contribute to carbamazepine therapy.

Plasma osteoprotegerin concentrations in type 2 diabetic patients and its association with neuropathy.

BACKGROUND AND AIMS: To investigate the association of plasma osteoprotegerin (OPG) levels with diabetic neuropathy. METHODS: Forty-two diabetic patients (21 female and 21 male) and twenty-four non-diabetic healthy control subjects (12 female and 12 male) were included in the study. All consecutive diabetic patients who came for routine follow-up at our outpatient clinic were invited to participate in this clinical study. We studied EMG and neuropathy symptom score in all study subjects. Fasting plasma glucose, HbA1 C, hs-CRP, OPG levels and lipid profile were measured for each subject. RESULTS: Serum fasting glucose, HbA1c, HOMA-IR, total cholesterol, triglyserid, LDL-Cholesterol, HDL-Cholesterol, lipoprotein (a), apolipoprotein-b, hs-CRP, OPG levels, and neuropathy symptom score were statistically higher in diabetic patients than in healthy control subjects. Plasma OPG levels was statistically higher in diabetic patients than it was in nondiabetic control subjects. However, plasma OPG levels were not significantly different between diabetic patients without neuropathy and healthy control subjects. On the other hand, OPG levels were statistically higher in diabetic patients with neuropathy than in patients without neuropathy. In addition to that serum fasting glucose, HbA1c, hs-CRP, diabetes duration, neuropathy symptom score were statistically higher in diabetic patients with neuropathy than they were in patients without neuropathy. In total group of subjects, plasma OPG levels were correlated significantly with age, diabetes duration, HbA1c, total cholesterol, HDL-cholesterol, lipoprotein (a), apolipoprotein b, hs-CRP. In diabetic patients, plasma OPG correlated significantly with age, diabetes duration, neuropathy symptom score, HbA1c, lipoprotein (a), apolipoprotein b levels. CONCLUSIONS: The major findings of this study were that the plasma OPG concentrations were higher in type 2 diabetic patients than OPG concentrations in healthy control subjects and they were positively correlated with diabetic neuropathy. This finding supports the growing concept that OPG acts as an important regulator in the development of vascular dysfunction in diabetes.

Reversible myelopathy with vitamin B12 deficiency.

Vitamin B12 deficiency causes haematological, gastrointestinal, psychiatric and neurological diseases. Subacute combined degeneration (SCD) of the spinal cord, characterised by degeneration of the lateral and posterior columns, is often found due to vitamin B12 deficiency. We report SCD occurring in a 57-year-old man who presented with a 2.5-month history of gradually progressing tingling in the fingers and toes and neck ache. Laboratory data revealed vitamin B12 deficiency and magnetic resonance (MR) imaging of the cervical spinal cord demonstrated abnormal hyperintense signal changes on T2-weighted imaging of the posterior columns. In our case, follow-up MR imaging findings correlated well with clinical outcome after treatment with vitamin B12 supplements. Neurological symptoms in vitamin B12 deficiency are frequent. Early spinal MR imaging assists in the early diagnosis and treatment of the disease.

The sensitivity of clinical diagnostic methods in the diagnosis of diabetic neuropathy.

This study assessed the sensitivity of various methods for the clinical diagnosis of diabetic peripheral neuropathy. A total of 147 randomly selected patients with diabetes mellitus and 65 age- and sex-matched healthy controls were evaluated by various clinical (the neuropathy symptom score [NSS], the neuropathy disability score [NDS], vibration perception thresholds [VPTs], Tinel's sign and Phalen's sign), laboratory (fasting plasma glucose and glycosylated haemoglobin levels) and electro-physiological (nerve conduction studies, H-reflex and F-wave measurements) methods. In the patient group, 8.2% had an abnormal NSS, 28.5% had a positive Phalen's sign, 32.6% had a positive Tinel's sign, 42.8% had an abnormal VPT and 57.1% had an abnormal NDS. Significant correlations were found between electro-physiologically confirmed neuropathy and the two provocation tests and abnormal VPTs. In conclusion, assessment with a complete neurological examination and standard electrophysiological tests is very important for the diagnosis of diabetic peripheral neuropathy and the prevention of morbidity in patients with or without symptoms.

Relationship between tuberculous otomastoiditis and tuberculous meningitis.

OBJECTIVE: The aim of this study was to determine the correlation between tuberculous meningitis and tuberculous otomastoiditis. MATERIALS AND METHODS: Meningeal involvement sites were investigated by magnetic resonance imaging in 32 patients (21 males, 11 females) who had previously been diagnosed with tuberculous meningitis. Clinical and laboratory findings and responses to anti-tuberculous treatment were evaluated, and the presence of concomitant tuberculous otomastoiditis was also investigated. RESULTS: The meningeal involvement site was unilateral (in the sylvian fissure and the perimesencephalic cistern) in 28 patients (87.5 per cent), and bilateral and widespread in four patients (12.5 per cent). Tuberculous otomastoiditis was found in 11 of the patients with tuberculous meningitis (34.3 per cent). Otomastoiditis was on the same side as the meningeal involvement in nine of these 11 patients. Bilateral otomastoiditis with meningeal involvement was observed in two patients. CONCLUSIONS: Tuberculous meningitis is frequently accompanied by otomastoiditis, although the exact causal relationship between the two conditions is unclear. Since meningitis is a serious clinical condition, concomitant otomastoiditis generally remains unrecognised. Tuberculosis should be considered in the differential diagnosis of patients with otitis or otomastoiditis who do not respond to antibiotic therapy.