ABSTRACT
Background and Objectives@#There is growing interest in the use of the Level-specific (LS) CE-Chirp® stimulus in auditory brainstem response (ABR) due to its ability to produce prominent ABR waves with robust amplitudes. There are no known studies that investigate the test-retest reliability of the ABR to the LS CE-Chirp® stimulus. The present study aims to investigate the test-retest reliability of the ABR to the LS CE-Chirp® stimulus and compare its reliability with the ABR to standard click stimulus at multiple intensity levels in normal-hearing adults. @*Subjects and Methods@#Eleven normal-hearing adults participated. The ABR test was repeated twice in the same clinical session and conducted again in another session. The ABR was acquired using both the click and LS CE-Chirp® stimuli at 4 presentation levels (80, 60, 40, and 20 dBnHL). Only the right ear was tested using the ipsilateral electrode montage. The reliability of the ABR findings (amplitudes and latencies) to the click and LS CE-Chirp® stimuli within the same clinical session and between the two clinical sessions was calculated using an intra-class correlation coefficient analysis (ICC). @*Results@#The results showed a significant correlation of the ABR findings (amplitude and latencies) to both stimuli within the same session and between the clinical sessions. The ICC values ranged from moderate to excellent. @*Conclusions@#The ABR results from both the LS CE-Chirp® and click stimuli were consistent and reliable over the two clinical sessions suggesting that both stimuli can be used for neurological diagnoses with the same reliability.
ABSTRACT
Objective: our hypothesis was that an EEG recording of 20 minutes' duration would yield more information than a 10-minute EEG in capturing epileptiform abnormalities
Methods: the study was conducted in electrophysiology section of neurology department of services hospitals, Lahore during 2012. Total 171 consecutive EEG patients were evaluated
Results: we prospectively studied 171 consecutive EEGs [patients of 16-29 years old] of 20 minutes' duration performed at Services Hospital. Although the majority [89%] of interracial EEG abnormalities can be identified within the first 20 minutes of a routine EEG, extending the time of a routine EEG may increase the yield. The single electrical abnormality was found to appear between 11 to 14 minutes
Conclusion: it should be emphasized that every EEG should be done for at least 20 minutes duration as recommended, especially when the first 10 minutes are normal
ABSTRACT
Objective: to investigate the patients of opt c atrophy to find the cause
Material and Methods: this descriptive study was conducted at department of neurology, Mayo Hospital Lahore and department of medicine, Wapda Teaching Hospital, Lahore. Patients of all ages and both sexes with optic atrophy were included. Patients of pure eye diseases like glaucoma and those having any contraindication to essential investigations were excluded. First 118 patients were studied. After history and physical examination some initial and predetermined tests were performed on all patients. Further advance investigations were performed to reach the diagnosis on case to case basis. All the data obtained was processed for the results
Results: out of these 118 patients, 75 [63.56%] were male and 43 [36.44%] were female. Mean age was 43.97 +/- 17.54 years [range 3 to 71 years]. Causes of optic atrophy included, Tumours in 29 [24.58%], demyelinating diseases in 19 [16.10%], infections in 18 [15.25%], methanol toxicity in 11 [9.32%] and ischemic optic neuropathies in 9 [7 .63%] patients. Hydrocephalus and hereditary optic neuropathies, each in 4 [3.39%] patients while non-neoplastic compressive lesions, drugs and trauma, each in 3 [2.54 %] patients caused optic atrophy. Nine patients had rare causes while six patients remained undiagnosed
Conclusion: tumours, demyelinating diseases, infections, methanol toxicity and ischemic optic neuropathies were the frequent causes of optic atrophy. Methanol toxicity is more common in our society as compared to the rest of the world
ABSTRACT
Objective: The Urticaria caused by NSAIDs wasstudied for their antioxidant enzyme activity andmalondialdehyde [MDA] concentration
Methodology: Patients were divided into twogroups; group one act as a control and the remaininggroup was urticaria patients. The levels of theThiobarbituric acid reactive substances [TBARS, asa marker of lipid peroxidation], superoxidedismutase [SOD], glutathione [GSH] and catalase[CAT] in the serum were estimated. The enzymaticactivity was estimated and compared with differentcategories of NSAIDs
Results: In present studyCAT, SOD and lipid peroxidation product [MDA]were statistically different from that of healthycontrol and showed significant changes [p< 0.05]while GSH showed a non-significant [p>0.05]value
Conclusion: It is concluded thatantioxidative system of the body is accelerated andshows variations in the patient of Urticaria.Moreover, present study shows the co-ordinatedenzymatic mechanism and the interrelationshipbetween enzymatic activities in allergy
ABSTRACT
Creutzfeldt-Jakob disease is a prion related disease, characterized by rapidly progressive dementia, associated with myoclonus and ataxia. A 55-year-old male, who initially developed depressive symptoms and obsessive-compulsive disorder one year before presentation, and in due course, developed ataxia, forgetfulness and disorientation in time and space followed by myoclonic jerks with increasing difficulty in walking, finally becoming bed bound and developing startle response to sound and touch, presented in mute and bed bound state. On the basis of typical clinical syndrome, suggestive electroencephalography and magnetic resonance imaging, and absence of any other cause, diagnosis of Creutzfeldt-Jakob disease was made
Subject(s)
Humans , Male , Dementia , Myoclonus , Ataxia , Depression , Obsessive-Compulsive Disorder , Confusion , Electroencephalography , Magnetic Resonance ImagingABSTRACT
Three cases with transient episodes of ataxia and dysarthria are described. The episodes lasted for 10-20 seconds with frequency from 20-200/day. The primary diagnosis was multiple sclerosis in two cases and acute disseminated encephalomyelitis in one case. An electroencephalogram [EEG] recorded during the episodes in these patients was normal. All patients responded to low doses of carbamazepine with complete amelioration of episodes. Recovery from relapse was associated with spontaneous cessation of these paroxysmal symptoms