Aims: The aim of this study was to test the utility of blink reflex in detecting sub-cranial neuropathy in the early course of Guillain Barre syndrome (GBS).
Study Design: The study was a case control study with 5 clinically diagnosed patients of GBS and 5 age and sex matched healthy controls.
Place and Duration of Study: Department of Physiology, Pt. B.D. Sharma, Rohtak, Haryana, India. The duration was six months.
Methodology: A total of 5 patients (4 men, 1 women; age range 9-70 years) clinically diagnosed patients of GBS in 1st week of illness, sent for electro-diagnostic evaluation to the department of Physiology from the department of Medicine were included. Motor conduction studies (median, ulnar, tibial & peroneal), sensory conduction studies (median & sural nerves), F wave studies and blink reflex analysis were carried out on both cases and 5 healthy controls.
Results: Out of the Five patients, four had decreased conduction velocity (CV) & amplitude for median & ulnar nerves while 1 patient had normal CV & amplitude. Three patients had a decrease in CV & amplitude for tibial & peroneal nerves; one patient had decreased CV & amplitude for tibial nerve while one had conduction block for both nerves. Decreased sensory CV was seen in all 5 patients in the upper limb; while 3 had normal sural nerve CV. Two patients had decreased sural nerve velocity. F wave was completely absent (prolonged F wave latency) in 3 patients in the upper limb; in 2 cases it was decreased. In the lower limb, f wave was completely absent. A statistically significant increase in R1 latency of blink reflex was seen in all 5 patients on both right & left sides. Increased latency of R2 (ipsilateral) & R2 (contralateral) were also seen.
Conclusion: The abnormalities of blink reflex most likely represent demyelination in either the facial and/or the trigeminal nerves reflecting the multifocal nature of demyelination in GBS. So blink Reflex can be a useful tool for detection of clinically silent cranial neuropathy in GBS.
In the last years, several clinical studies have shown the usefulness of N-acetylcysteine (NAC) in psychiatric diseases including a role in some drug abuse disorders. Although the glutathione replenishment and the antioxidant activity of NAC have been suggested as the principal mechanisms to improve such a wide range of conditions, these actions seem to be unspecific and insufficient to explain all reported effects. The present paper proposes that cysteinet (cysteine network) may be deregulated in psychiatric diseases explaining the wide-range beneficial actions of NAC supplementation.
Traditionally, the right hemisphere has been considered as non-dominant because of absence of significant alterations in cognitive functioning after lesions. Recent studies have shown that right hemisphere plays an active role in cognitive processes, such as spatial global analysis, recognition and evocation of auditory patterns, motor sequences, recognition of faces and emotions. The objectives of the study consisted in providing qualitative analysis of neuropsychological deficits in a male patient with brain damage in right frontotemporal region due to an automobile accident and to describe the effects of the program of neuropsychological rehabilitation. A pretest-posttest research design was used. The neuropsychological assessment evaluation was carried out through qualitative protocols for Spanish speaking patients. Final assessment pointed out positive changes in the process of intellectual activity on perceptive and verbal levels. The patient managed to return to university studies. Our results show that it is possible to define the mechanisms, which underline the clinical syndrome in cases brain injury in right hemisphere. Predominant difficulties consisted in loss of involuntary regulation and mild difficulties with the global perception of information on perceptive and verbal level. These difficulties were reflected in all kinds of complex intellectual activity, which became milder after the work with the program for rehabilitation.
Cognitive and psychological deficits may be frequent in patients with epileptic disorders. The study was aimed at assessing the cognitive (memory and academic achievement) and psychological (anxiety and depression) deficits associated with epileptic disorders. The study also examined the effect of socio-economic status of the patient in ameliorating the cognitive and psychological deficits associated with the epileptic disorder. One hundred (n=100) respondents consisting of epileptic children (n=50) visiting the neurological clinic at the Korle Bu Teaching Hospital and healthy control group (n=50) from West African Basic School were selected to respond to questionnaires measuring cognitive and psychological deficits. Data were analysed using the MANOVA. Results of the study indicated higher psychological deficits among epileptic children compared to healthy control group. There was no significant difference in cognitive deficits between epileptic children and healthy control group. Lower socioeconomic status was found to ameliorate the cognitive deficits associated with epilepsy but did not have any significant impact on the psychological deficits. Findings suggest that though epilepsy has no negative significant impact on cognitive deficits, poor socio-economic factors can deteriorate the cognitive deficits associated with epileptic disorder.
Aims: Although epilepsy is a common disease, the pathological process has not been sufficiently elucidated. Previous studies have reported that blood-brain barrier (BBB) damage is involved in epileptogenesis. Our aim was to non-invasively and sequentially evaluate BBB damage in a mouse model of generalised seizure, using Gadolinium (Gd)-enhanced magnetic resonance imaging using T1 weighting (GdET1WI). In addition, we assessed whether or not valproate (VPA) could prevent BBB damage.
Methods: Mice were kindled with the daily intraperitoneal administration of 40 mg/kg pentylenetetrazole (PTZ). After each PTZ injection, convulsive behaviours were observed, and seizures were scored from 0 to 5. Five consecutive scores of 4 or 5 were required to ensure kindling. We evaluated the changes in the BBB damage using the signal intensity (SI) ratio of GdET1WI. The SI was sequentially measured at baseline, score 1, score 3, PTZ-kindled, and 1-week post-kindled after PTZ withdrawal. In addition, the SI was measured in mice pretreated with VPA before PTZ injection.
Results: The SI values (means±standard error of the mean) at score 1, score 3, PTZ-kindled, and post-kindled increased to 0.70%±0.22%, 7.17%±1.86%, 7.43%±1.60%, and 6.82%±1.27%, respectively, compared to baseline. All values (except at score 1) were significantly higher than those at baseline (p-value < 0.05). We did not observe significant differences between score 3 or post-kindled and PTZ-kindled. In VPA-pretreated mice, the SI significantly increased to 8.77%±1.57% compared to baseline, although convulsions were fully controlled.
Conclusion: Our data suggest that BBB damage started before PTZ-induced kindling was acquired. The BBB damage was irreversible after PTZ-induced kindling. In addition, VPA prevented epileptic convulsive seizures but could not suppress BBB damage in PTZ-kindled mice.
