Evaluation of depressive mood and cognitive functions in patients with acromegaly under somatostatin analogue therapy.

AIMS: Acromegaly is caused by a pituitary adenoma that releases excess growth hormone (GH) and a concomitant increase in insulin-like growth factor 1 (IGF-1). Acromegaly results not only in phenotypic changes, but also in neurologic complications as peripheral neuropathy and cognitive dysfunction. This study aimed to compare depressive mood and cognitive function in patients with acromegaly and in healthy controls as well as to determine the factors underlying cognitive dysfunction in the acromegalic patients. MATERIALS AND METHODS: This study included 42 patients with acromegaly that were receiving somatostatin analogue therapy and 44 healthy controls. Memory, attention, visuospatial function, inhibitory function, abstract thinking, verbal fluency, and depressive mood were measured in the patients and controls. RESULTS: Patients with acromegaly had lower learning (p = 0.01), planning (p = 0.03), complex attention and inhibitory function (p = 0.04) scores than the controls. There was no significant difference in depressive mood between the patients and controls (p > 0.05). Gamma knife radiosurgery did not negatively affect cognitive function (p > 0.05). CONCLUSION: The present findings show that acromegaly negatively affects learning, attention, and planning.

Peripheral nervous system assessment in acromegaly patients under somatostatin analogue therapy.

PURPOSE: Acromegaly is known to affect peripheral nervous system (PNS) causing carpal tunnel syndrome (CTS) and polyneuropathy. The frequency of these disorders and the evaluation methods vary among studies. In the present study, we aimed to examine PNS of acromegaly patients under somatostatin analogue (SSA) therapy. METHODS: Forty-eight acromegaly patients (26 F/22 M, 45.58 ± 11.6 years) under SSA treatment and 44 healthy controls (25 F/19 M, 47.46 ± 8.7 years) were assessed by symptom questionnaires, neurologic examination and electrophysiological studies. RESULTS: 87.5 % of the acromegaly patients had at least one abnormal finding regarding PNS. With the incorporation of palm-wrist median nerve conduction velocity method, we detected CTS in 50 % of patients. Polyneuropathy was less frequent (29.2 %). Both conditions were independent from the coexisting diabetes mellitus (p = 0.22 for CTS, p = 0.71 for polyneuropathy). Polyneuropathy but not CTS was more common among biochemically uncontrolled acromegaly patients rather than those under control (p = 0.03; p = 0.68, respectively). CONCLUSION: Our findings emphasize the high prevalence of peripheral nervous system involvement in acromegaly patients under SSA therapy and importance of neurological evaluation of these patients. Early diagnosis and treatment of the disease may reduce the PNS involvement.

Visual evoked potential abnormalities in migraine patients.

BACKGROUND: Visual processing in migraine has been targeted indicating that the visual pathways are involved in the migraine pathophysiology. We aimed to assess the nature of visual evoked potential (VEP) changes in migraine patients and to evaluate the role of VEP in the diagnosis of migraine. MATERIALS AND METHODS: We examined 31 female and 10 male patients with a migraine headache diagnosis according to the criteria of the International Headache Society. Control subjects had neither migraine and other types of primary headache nor familial history. VEP were elicited using a checkerboard by monocular and binocular pattern reversal stimulation. The latencies of N75, P100 and N145 and peak-to-peak amplitude of N75-P100 were measured. We compared VEP latencies and amplitudes of the monocular and binocular stimulation within each population. RESULTS: The N75 and P100 latencies were found to be significantly longer in the study group than the control group (p = 0.014 and p = 0.034, respectively) while the amplitudes in the study group were lower (p = 0.014). N145 latency was found to be longer in patients with longer duration of disease (p < 0.05). P100 latency was found to be significantly longer in patients with aura than the patients without aura (p = 0.029). N75 latency, recorded by left monocular stimulation, was elongated and the amplitude was diminished with left hemicranial headache. CONCLUSION: Measurement of VEP latency and amplitude is a valuable and reliable test for the diagnosis of migraine. Our results reflect a persisting dysfunction of precortical visual processing which might be relevant in the pathogenesis of migraine.

Brainstem auditory evoked potentials and middle latency auditory evoked potentials in patients with impaired glucose tolerance.

AIMS: The aim was to investigate the effects of impaired glucose tolerance (IGT) on the central nervous system via brainstem auditory evoked potentials (BAEPs) and middle latency auditory evoked potentials (MLAEPs), and on the peripheral nervous system via nerve conduction studies (NCS). METHODS: Thirty patients with IGT and 20 control subjects underwent NCS, BAEPs and MLAEPs. RESULTS: Tibial distal motor latencies were significantly prolonged in the IGT group; no differences in other parameters, including BAEPs and MLAEPs, were observed between the IGT and control subjects. CONCLUSION: Brainstem involvement may not be seen in IGT patients as in DM. The was no obvious electrophysiological finding indicating peripheral nervous system disfunction in our patients.

A comparison of sural nerve conduction studies in patients with impaired oral glucose tolerance test.

OBJECTIVE: Monitoring of the sural nerve is a sensitive method for detection of neuropathies. We examined different methods of studying sural nerve conduction in a group of patients with impaired glucose tolerance (IGT) in the same study. MATERIALS AND METHODS: Several parameters of sural nerve were investigated in 20 patients. First, sensory nerve conduction studies of the sural nerve were performed on the distal-leg and the proximal-leg segments. Second, dorsal sural nerve studies were conducted. Third, the sural/radial sensory nerve action potential (SNAP) amplitude ratios were calculated. The results were compared with those obtained from 21 healthy controls. RESULTS: Abnormal results revealing peripheral neuropathy were found in only one patient and dorsal sural SNAP was absent in another patient (5%). Although the results of nerve conduction studies were within normal ranges except the patient with peripheral neuropathy, the lower extremity nerves and especially sural nerves have been found to be more affected and the parameters revealed large differences between groups (P < 0.05). Only dorsal sural nerve latency related to fasting blood glucose level in patients (<0.05). DISCUSSION AND CONCLUSIONS: Sural nerve studies should be of value to determine neuropathy in IGT patients. This study supported the idea that IGT is a transitional state before diabetes and also the importance of the dorsal sural nerve latencies for early detection of neuropathy.

Assessment of spatial-contrast function and short-wavelength sensitivity deficits in patients with migraine.

AIMS: To study spatial-contrast function and short-wavelength sensitivity deficits in a migraine population with a disease duration of 30 years or less. MATERIALS AND METHODS: In this prospective, cross-sectional study, we evaluated 28 subjects with migraine headache and 15 nonheadache healthy controls. Visual fields were evaluated using the Humphrey Field Analyzer 750i and the 30-2, blue and yellow threshold programme. Contrast sensitivity (CS) was measured at 1.5, 3, 6, 12, and 18 cpd spatial frequencies, using the Functional Acuity Contrast Test (F.A.C.T.). The results of the visual field parameters (mean defect (MD) and pattern standard defect (PSD)) and CS were compared with 15 age-equivalent normal subjects. RESULTS: Short-wavelength amplitude perimetry (SWAP) parameters and CS scores at all spatial frequencies were significantly altered in the migraine patients when compared with the control subjects. Visual field parameters correlated significantly with contrast sensitivity scores: positively for MD (r=0.39, P=0.01; r=0.43, P=0.005; r=0.56, P=0.0001; r=0.45, P=0.003; r=0.48, P=0.0001) and negatively for PSD (r=-0.45, P=0.003; r=-0.45, P=0.003; r=-0.51, P=0.001; r=-0.53, P=0.0001; and r=-0.67, P=0.0001) at all (1.5, 3, 6,12, and 18 cpd) spatial frequencies, respectively. Migraine duration correlated negatively with MD (r=-0.42, P=0.04) and positively with PSD (r=0.42, P=0.03). CONCLUSION: Migraineurs had significantly altered visual field and contrast function at all spatial frequencies to the normal population. These defects share some features with early stages of glaucoma and may relate a possibility for a common vascular disease pathogenesis in these two conditions.

Median sep and blink reflex in thyroid diseases.

Pathological disturbances of thyroid hormones is associated with central and peripheral nervous system disturbances. The aim of this study is to evaluate median nerve stimulated somatosensory evoked potential (SEP) and blink reflex of thyroid patients (hypo and hyperthyroidism). Median SEP was performed in 40 patients (21 with hyperthyroidism and 19 with hypothyroidism). We evaluated the latencies of N9, N11, N13, P9, P11, P14, N20 and P25 waves and the N9-N20, N9-N13, N13-N20 and P14-N20 interpeak latencies. We compared the results of patients with the control group (26 persons). We found that the N20 latency was longer in patients with hyperthyroidism than in the control group and the difference was statistically significant. There was not any statistically significant difference regarding the N9, N11, N13, P9, P11, P14, N20 and P25 latencies and the N9-N20, N9-N13, N13-N20 and P14-N20 interpeak latencies between hypothyroid patients and controls. We performed the blink reflex study in 28 of 40 patients (14 patients with hyperthyroidism and 14 patients with hypothyroidism). Comparing the R1, R2, CR2 (contralateral R2) latencies and durations of the patients and controls, we found that R2 and CR2 duration was shorter in patients with hyperthyroidism. This difference was statistically significant.

Myasthenia gravis with thymoma and autoimmune haemolytic anaemia. A case report.

Myasthenia gravis is an autoimmune disorder that affects the neuromuscular junction and leads to weakness of the skeletal muscles. Associated autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis and pernicious anaemia are present in approximately 5% of the myasthenic patients. This report presents a 64-year-old man with autoimmune haemolytic anemia associated with myasthenia gravis and thymoma. The patient developed a severe Coomb's positive autoimmune haemolytic anaemia, which was resistant to treatment with large doses of prednisone. Haemolytic anaemia entered remission one month following thymectomy, and the patient has maintained a normal haemoglobin and a negative Coomb's test without the need for steroid or immunosuppressive therapy. In conclusion, thymectomy may induce a striking improvement of therapyresistant autoimmune haemolytic anemia in patients with MG and thymoma, but in terms of remission, a long follow-up is needed as autoimmune diseases can show spontaneous fluctuations.

Motor neuron degeneration due to aluminium deposition in the spinal cord: a light microscopical study.

For a long time, aluminium has been considered as an indifferent element from a toxicological point of view. In recent years, it became clear that aluminium is a potential toxic agent in humans and has been implicated in the pathogenesis of several clinical disorders, such as dementia, respiratory tract disorders and allergic reactions. Chronic exposure to aluminium fumes, inhalation of aluminium and aluminium-oxide powder increase the risk to develop serious central nervous system pathology, in particular Alzheimer's disease and amyotrophic lateral sclerosis (ALS). In the present study, 3 experimental and 1 control group of rats were used to study the effects of aluminium on the central nervous system. Aluminium was injected intracisternally as a single dose (50 micrograms for group I, 100 micrograms for group II and 300 micrograms for group III) to the experimental groups (n = 5 in each group). The same dose was given at 3 months after the first injection to all groups. The control group (n = 5) was intracisternally given a physiological salt solution. Electromyography (EMG) was applied to the rats of the experimental groups. Rats were decapitated at 3 months after the second injections. Spinal cord samples from lumbar and cervical regions were removed and histological examination was performed. Light microscopical investigations revealed severe degeneration in motor neurons of the rats treated with 300 micrograms. Neurofibrillary tangle formation, chromatolysis and abnormal localization of the nuclei were found in swollen perikarya. Extreme loss of motor neurons with "ghost cell" appearance was found in that group. Sections of spinal cords of rats treated with lower doses of aluminium showed a moderate degree of motor neuron damage. EMGs of rats treated with the high dose of aluminium revealed severe acute denervation whereas treatment with lower doses resulted in moderate denervation. We conclude that aluminium may cause severe motor neuron damage in rat spinal cord resembling ALS.

Antiglutamatergic therapy in Alzheimer's disease--effects of lamotrigine. Short communication.

It has been proposed that excitotoxic damage by glutamatergic hyperactivity is responsible for neurodegeneration in Alzheimer's disease. Lamotrigine (LTG) inhibits presynaptic glutamate release and is considered to be effective in treatment of other neurodegenerative disorders by its cerebroprotective properties. We used LTG in 11 patients with the diagnosis of probable Alzheimer's disease. 300 mg/day administration of LTG improved word recognition, naming and depressed mood on Alzheimer Disease Assessment Scale (ADAS).